Prosecution Insights
Last updated: October 04, 2026
Application No. 18/748,675

BIOCHIP SENSOR FOR DETECTING OF MOLECULES

Final Rejection §103
Filed
Jun 20, 2024
Priority
Dec 22, 2021 — provisional 63/292,502 +1 more
Examiner
SUN, CAITLYN MINGYUN
Art Unit
1645
Tech Center
1600 — Biotechnology & Organic Chemistry
Assignee
Bar-Ilan University
OA Round
2 (Final)
64%
Grant Probability
Moderate
3-4
OA Rounds
8m
Est. Remaining
75%
With Interview

Examiner Intelligence

Grants 64% of resolved cases
64%
Career Allowance Rate
207 granted / 326 resolved
+3.5% vs TC avg
Moderate +12% lift
Without
With
+11.9%
Interview Lift
resolved cases with interview
Typical timeline
3y 0m
Avg Prosecution
67 currently pending
Career history
392
Total Applications
across all art units

Statute-Specific Performance

§101
1.5%
-38.5% vs TC avg
§103
52.0%
+12.0% vs TC avg
§102
16.6%
-23.4% vs TC avg
§112
27.9%
-12.1% vs TC avg
Black line = Tech Center average estimate • Based on career data from 326 resolved cases

Office Action

§103
DETAILED ACTION Response to Amendment This is a final office action in response to a communication filed on July 19, 2026. Claims 1-19 are pending in the application. Status of Objections and Rejections All objections and rejections under 35 U.S.C. §112 from the previous office action are withdrawn in view of Applicant’s amendment. The amended limitation “processor” in claims 12 and 14 does not invoke 35 U.S.C. 112(f). Some rejections under 35 U.S.C. §103 are maintained. New grounds of rejections are necessitated by the amendments. Claim Rejections - 35 USC § 103 The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action. Claim(s) 1-9 and 11-19 is/are rejected under 35 U.S.C. 103 as being unpatentable over Bollman (US 2016/0139114) in view of Sayler (US 2003/0027241) and Sayler-1 (US 2007/0072174), supported by Majeed (US 2020/0316139) and Kim (US 2018/0155699) as evidence. Regarding claim 1, Bollman teaches a biochip (¶31) for detection of a marker molecule in a sample (¶¶18-19: detecting pathogenic material in a sample; further, this limitation in preamble is deemed to be a statement with regard to the intended use and are not further limiting in so far as the structure of the product is concerned. In article claims, a claimed intended use must result in a structural difference between the claimed invention and the prior art in order to patentably distinguish the claimed invention from the prior art. MPEP § 2111.02(II)), the biochip comprising one or more chambers (Fig. 3; ¶78: individual wells 18), each chamber comprising a biosensor module (e.g., Fig. 2; ¶71: the detection molecule 8 immobilized through a linking molecule 13 on a carrier 2) and a detection module (e.g., Fig. 2; ¶73: a detection reagent 16a equipped with a marker 28 and capable of binding the target molecule 9 that is bound to the detection molecule 8), wherein the biosensor module comprises a receptor (Fig. 2; ¶66: detection molecule 8) capable of binding the marker molecule (Fig. 2; ¶66: respective target molecule 9), and a reporter, wherein the reporter is induced by the binding of the marker molecule to the receptor (e.g., Fig. 2: the formed complex composed of detection molecule 8 and target molecule 9); and wherein the detection module comprises a reporter substrate (¶29: an enzyme substrate), wherein enzymatic interaction between the reporter and the reporter substrate (¶¶51-52: the target molecule is a quorum sensing-associated enzyme; e.g., beta-galactosidase) produces an electrochemical output signal (¶34: an electrochemical signal convert can convert the binding into a change of resistance, the impedance or the electric current) indicative of presence of the marker molecule in the sample (¶74: to qualitatively detect the target molecule 9 in the sample 6), and wherein the marker molecule is associated with a gastrointestinal disease or disorder (as evidenced by Majeed ¶2, lactase (beta-D-galactosidase) is an endogenous enzyme which catalyzes the hydrolysis of lactose, and the shortage of lactase in small intestine would cause lactose intolerance and inflammatory bowel disease to experience gastrointestinal symptoms after lactose ingestion). Bollman further discloses quorum sensing target molecules are bacteria or substances that are produced in an intensified way due to an increased concentration of quorum sensing molecules (¶25), but fails to teach the biosensor module is a synthetic one or the receptor is a genetically modified bacteria expressed receptor or the reporter is a reporter gene, wherein expression is induced by the binding of the marker molecule to the receptor, wherein the genetically modified bacteria is configured to produce the reporter gene in response to uptake of the marker molecule or the reporter substrate is a reporter gene substrate so that the enzymatic interaction is between the expressed reporter gene and the reporter gene substrate to produce an electrochemical output signal. However, Sayler teaches detecting bacteria based on recognition and infection of one or more selected strains of bacteria with bacteriophage genetically modified to cause production of an inducer molecule in the bacterium following phage infection ([Abstract]), by providing a novel internally amplified bioluminescent bacteriophage/bioreporter system (¶17). For example, a bacteriophage genetically modified carries a luxI gene, which encodes a protein product, resulting in the production of AHL (¶18). Upon infection, the phage luxI gene is transcribed in the bacterium, with resultant expression of the LuxI protein by the infected target cell (¶18). Following infection, the uptake of AHL molecules induces production of bioluminescent proteins in the bioreporter cells (¶19), and the bioluminescent is amplified due to the presence of the lux-modified bioreporter cells (¶20). As shown in Fig. 1, the expressed product of the LuxI gene has an expressed product that is AHL synthetase, which acts as an inducer of the bioluminescent reaction (¶34). The expressed complex product (Fig. 1; ¶34: black and white circles) binds to the promoter site of the luxI gene (Fig. 1: black box), which further induces transcription to carry out the biochemical reactions resulting in the production of 490 run light (Fig. 1; ¶34). Although Sayler does not teach using electrochemical signal, Sayler-1 teaches a recombinant bacteriophage-based system for rapid detection of a bacteria, using lux-I encoded LuxI proteins for generation of a specific AHL signaling molecule, which generates bioluminescent signal (¶5), and besides chemiluminescent signal, electrochemical signal can also be implemented (¶36). It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified Bollman by incorporating genetically engineered bacteria (e.g., lux genes) for expressing a promoter site capable of uptaking and binding AHL for generating bioluminescent or electrochemical signals as taught by Sayler and Sayler-1 because incorporation of lux genes would cause infection a particular pathogenic strain of bacteria and produce gene products (¶37). Here, the claimed limitations are obvious because all the claimed elements were known in the prior art and one skilled in the art could have combined the elements as claimed by known methods with no change in their respective functions, and the combination yielded nothing more than predictable results. MPEP 2143(I)(A). Further, the designation “wherein the marker molecule is associated with a gastrointestinal disease or disorder” is directed to a material or article worked upon. "Expressions relating the apparatus to contents thereof during an intended operation are of no significance in determining patentability of the apparatus claim." Ex parte Thibault, 164 USPQ 666, 667 (Bd. App. 1969). Furthermore, "[i]nclusion of material or article worked upon by a structure being claimed does not impart patentability to the claims." In re Young, 75 F.2d. 25 USPQ 69 (CCPA 1935) (as restated in In re Otto, 312 F.2d 937, 136 USPQ 458, 459 (CCPA 1963)). MPEP 2115. Regarding claim 2, Bollman teaches wherein the detection module is a quantitative detection module and/or qualitative detection module (¶74: not only to qualitatively detect the target molecule 9, but also to quantitatively determine the quantity of target molecule 9 in the sample). Regarding claim 3, Bollman teaches wherein an intensity and/or strength of the output signal is indicative of the concentration of the marker molecule in the sample (Fig. 4; ¶85: the strength of the electric current that correlates and provides quantitative information about the quantity of the target molecule 9, 10, e.g., concentration). Regarding claim 4, Bollman in view of Sayler and Sayler-1 teaches the biochip comprising at least two chambers (e.g., Bollman, Fig. 3: four detection fields 7), each chamber comprising a receptor (Fig. 3: detection molecule 8) capable of binding a different marker molecule (Fig. 3: detection molecule 8 binding target 10; ¶79: a different quorum sensing-associated target molecule 10 can be detected in each detection field 7), wherein the receptor is a genetically modified bacteria expressed receptor capable of binding a different marker molecule (Sayler, ¶34: the complex (black and white circles) binds to the promoter site of the luxI gene (black box); Bollman, ¶32: the detection molecules specifically bind a different quorum sensing target molecule in each detection field). Regarding claim 5, the designation “wherein a ratio between the output signal of each of the at least two chambers is indicative of a ratio between different bacterial populations in the sample and/or type of a gastrointestinal disease” is deemed to be functional limitation in apparatus claims. MPEP 2114 (II). "[A]pparatus claims cover what a device is, not what a device does." Hewlett-Packard Co. v. Bausch & Lomb Inc., 909 F.2d 1464, 1469, 15 USPQ2d 1525, 1528 (Fed. Cir. 1990) (emphasis in original). A claim containing a "recitation with respect to the manner in which a claimed apparatus is intended to be employed does not differentiate the claimed apparatus from a prior art apparatus" if the prior art apparatus teaches all the structural limitations of the claim. Ex parte Masham, 2 USPQ2d 1647 (Bd. Pat. App. & Inter. 1987). Regarding claim 6, the designation “wherein combined outputs of the at least two chambers is indicative of a specific bacterial population in the sample and thus of a disease status of the patient” is deemed to be functional limitation in apparatus claims. MPEP 2114 (II). "[A]pparatus claims cover what a device is, not what a device does." Hewlett-Packard Co. v. Bausch & Lomb Inc., 909 F.2d 1464, 1469, 15 USPQ2d 1525, 1528 (Fed. Cir. 1990) (emphasis in original). A claim containing a "recitation with respect to the manner in which a claimed apparatus is intended to be employed does not differentiate the claimed apparatus from a prior art apparatus" if the prior art apparatus teaches all the structural limitations of the claim. Ex parte Masham, 2 USPQ2d 1647 (Bd. Pat. App. & Inter. 1987). Regarding claim 7, Bollman teaches the biochip comprising at least two fluidly separate chambers (Fig. 3: individual wells 18), each chamber configured to separately receive samples at different time points (Fig. 1: indicating the sample 6 flow through application field 5 and arrives at each detection fields at different time points). Further, the designation “each chamber configured to separately receive samples at different time points” is deemed to be functional limitation in apparatus claims. MPEP 2114 (II). "[A]pparatus claims cover what a device is, not what a device does." Hewlett-Packard Co. v. Bausch & Lomb Inc., 909 F.2d 1464, 1469, 15 USPQ2d 1525, 1528 (Fed. Cir. 1990) (emphasis in original). A claim containing a "recitation with respect to the manner in which a claimed apparatus is intended to be employed does not differentiate the claimed apparatus from a prior art apparatus" if the prior art apparatus teaches all the structural limitations of the claim. Ex parte Masham, 2 USPQ2d 1647 (Bd. Pat. App. & Inter. 1987). Regarding claim 8, Bollman teaches wherein the output signal is an electric signal (¶26: verification of whether a target molecule has bonded with the at least one detection molecules can be done in many ways, for example, by means of electrically). Regarding claim 9, Bollman in view of Sayler and Sayler-1 teaches wherein the reporter gene is beta-galactosidase (Bollman, ¶51). Regarding claim 11, Bollman. Sayler, and Sayler-1 disclose all limitations of claim 1. Bollman and Sayler-1 do not disclose the biochip further comprising a DNA probe encoding a transporter of said marker molecule. However, Sayler teaches the bioreporter strain is constructed using a promoterless gene cassette and allowing for direct insertion of promoter fragments (¶45). The cassette refers to a recombinant DNA construct made from a vector and inserted DNA sequences (¶7). It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified Bollman and Sayler-1 by incorporating a DNA probe for inserting a promoter capable of binding to the target molecule as taught by Sayler because it would provide the binding site to carry out the biochemical reactions resulting in the signal to be detected (¶34). Here, the claimed limitations are obvious because all the claimed elements were known in the prior art and one skilled in the art could have combined the elements as claimed by known methods with no change in their respective functions, and the combination yielded nothing more than predictable results. MPEP 2143(I)(A). Regarding claim 12, Bollman teaches a microbiome analysis system (¶31) comprising a biochip (¶31) for detection of a marker molecule in a sample (¶¶18-19: detecting pathogenic material in a sample), the biochip comprising one or more chambers (Fig. 3; ¶78: individual wells 18), each chamber comprising a biosensor module (e.g., Fig. 2; ¶71: the detection molecule 8 immobilized through a linking molecule 13 on a carrier 2) and a detection module (e.g., Fig. 2; ¶73: a detection reagent 16a equipped with a marker 28 and capable of binding the target molecule 9 that is bound to the detection molecule 8), wherein the biosensor module comprises a receptor (Fig. 2; ¶66: detection molecule 8) capable of binding a marker molecule (Fig. 2; ¶66: respective target molecule 9), and a reporter, wherein the reporter is induced by the binding of the marker molecule to the receptor (e.g., Fig. 2: the formed complex composed of detection molecule 8 and target molecule 9); and wherein the detection module comprises a reporter gene substrate (¶29: an enzyme substrate), wherein enzymatic interaction between the reporter and the reporter substrate (¶¶51-52: the target molecule is a quorum sensing-associated enzyme; e.g., beta-galactosidase) produces an electric output signal (¶26: verification of whether a target molecule has bonded with the at least one detection molecules can be done in many ways, for example, by means of electrically; ¶34: an electrochemical signal convert can convert the binding into a change of resistance, the impedance or the electric current); a processor (Fig. 4; ¶84: a measurement unit 21) configured to receive the output signal and to provide an indication regarding presence of the marker molecule in the sample (¶84: the binding signal 12 can be displayed and quantified by the measurement unit 21, i.e., a digital measurement unit). Bollman further discloses quorum sensing target molecules are bacteria or substances that are produced in an intensified way due to an increased concentration of quorum sensing molecules (¶25), but fails to teach the biosensor module is a synthetic one or the receptor is a genetically modified bacteria expressing the receptor or the reporter is a reporter gene wherein expression is induced by the binding of the marker molecule to the receptor, wherein the genetically modified bacteria is configured to produce the reporter gene in response to uptake of the marker molecule or the reporter substrate is a reporter gene substrate so that the enzymatic interaction is between the expressed reporter gene and the reporter gene substrate. However, Sayler teaches detecting bacteria based on recognition and infection of one or more selected strains of bacteria with bacteriophage genetically modified to cause production of an inducer molecule in the bacterium following phage infection ([Abstract]), by providing a novel internally amplified bioluminescent bacteriophage/bioreporter system (¶17). For example, a bacteriophage genetically modified carries a luxI gene, which encodes a protein product, resulting in the production of AHL (¶18). Upon infection, the phage luxI gene is transcribed in the bacterium, with resultant expression of the LuxI protein by the infected target cell (¶18). Following infection, the uptake of AHL molecules induces production of bioluminescent proteins in the bioreporter cells (¶19), and the bioluminescent is amplified due to the presence of the lux-modified bioreporter cells (¶20). As shown in Fig. 1, the expressed product of the LuxI gene has an expressed product that is AHL synthetase, which acts as an inducer of the bioluminescent reaction (¶34). The expressed complex product (Fig. 1; ¶34: black and white circles) binds to the promoter site of the luxI gene (Fig. 1: black box), which further induces transcription to carry out the biochemical reactions resulting in the production of 490 run light (Fig. 1; ¶34). Although Sayler does not teach using electrochemical signal, Sayler-1 teaches a recombinant bacteriophage-based system for rapid detection of a bacteria, using lux-I encoded LuxI proteins for generation of a specific AHL signaling molecule, which generates bioluminescent signal (¶5), and besides chemiluminescent signal, electrochemical signal can also be implemented (¶36). It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified Bollman by incorporating genetically engineered bacteria (e.g., lux genes) for expressing a promoter site capable of uptaking and binding AHL for generating bioluminescent or electrochemical signal as taught by Sayler and Sayler-1 because incorporation of lux genes would cause infection a particular pathogenic strain of bacteria and produce gene products (¶37) for amplifying the bioluminescent signal (¶38). Here, the claimed limitations are obvious because all the claimed elements were known in the prior art and one skilled in the art could have combined the elements as claimed by known methods with no change in their respective functions, and the combination yielded nothing more than predictable results. MPEP 2143(I)(A). Regarding claim 13, Bollman in view of Sayler and Sayler-1 teaches wherein the biochip comprises at least two chambers (Fig. 3: individual wells 18), each chamber comprising a receptor (Fig. 3: detection molecule 8) capable of binding a different marker molecule (Fig. 3: detection molecule 8 binding target 10; ¶79: a different quorum sensing-associated target molecule 10 can be detected in each detection field 7), wherein the receptor is a genetically modified bacteria expressed receptor capable of binding a different marker molecule (Sayler, ¶34: the complex (black and white circles) binds to the promoter site of the luxI gene (black box); Bollman, ¶32: the detection molecules specifically bind a different quorum sensing target molecule in each detection field). Regarding claim 14, the designation “wherein the processor is configured to provide a clinical indication/safety indication, based on an integrated analysis of the outputs obtained from each of the at least two chambers” is deemed to be functional limitation in apparatus claims. MPEP 2114 (II). "[A]pparatus claims cover what a device is, not what a device does." Hewlett-Packard Co. v. Bausch & Lomb Inc., 909 F.2d 1464, 1469, 15 USPQ2d 1525, 1528 (Fed. Cir. 1990) (emphasis in original). A claim containing a "recitation with respect to the manner in which a claimed apparatus is intended to be employed does not differentiate the claimed apparatus from a prior art apparatus" if the prior art apparatus teaches all the structural limitations of the claim. Ex parte Masham, 2 USPQ2d 1647 (Bd. Pat. App. & Inter. 1987). Regarding claim 15, Bollman teaches a method for evaluating the presence of a marker molecule (¶1: rapid test for detecting pathogenic material), the method comprising: a. providing a biochip (¶31) comprising one or more chambers (Fig. 3; ¶78: individual wells 18), each chamber comprising a biosensor module (e.g., Fig. 2; ¶71: the detection molecule 8 immobilized through a linking molecule 13 on a carrier 2) and a detection module (e.g., Fig. 2; ¶73: a detection reagent 16a equipped with a marker 28 and capable of binding the target molecule 9 that is bound to the detection molecule 8), wherein the biosensor module comprises a receptor (Fig. 2; ¶66: detection molecule 8) capable of binding the marker molecule (Fig. 2; ¶66: respective target molecule 9), and a reporter, wherein the reporter is induced by the binding of the marker molecule to the receptor (e.g., Fig. 2: the formed complex composed of detection molecule 8 and target molecule 9); and wherein the detection module comprises a reporter substrate (¶29: an enzyme substrate), wherein enzymatic interaction between the reporter and the reporter substrate (¶¶51-52: the target molecule is a quorum sensing-associated enzyme; e.g., beta-galactosidase) produces an electrochemical output signal (¶34: an electrochemical signal convert can convert the binding into a change of resistance, the impedance or the electric current) indicative of presence of the marker molecule (¶74: to qualitatively detect the target molecule 9 in the sample 6); b. contacting the biochip with a biological sample (Fig. 1; ¶63: a sample 6 is applied into an application field 5 and transported along the flow direction through four detection fields 7); c. detecting the electrochemical output signal produced by the biochip in response to said contacting (Fig. 4; ¶84: the binding signal 12, as the emitted electric current, due to binding between the targe molecules 9, 10 and the detection molecule 8 can be displayed and quantified by the measurement unit 21), d. providing an indication related to presence of the marker molecule in the sample (¶84: displayed and quantified by the measurement unit 21), wherein the marker molecule (¶51: e.g., the enzyme activities of beta-galactosidase) is associated with a gastrointestinal disease or disorder (as evidenced by Majeed ¶2, lactase (beta-D-galactosidase) is an endogenous enzyme which catalyzes the hydrolysis of lactose, and it the shortage of lactase in small intestine would cause lactose intolerance and cause inflammatory bowel disease to experience gastrointestinal symptoms after lactose ingestion). Bollman further discloses quorum sensing target molecules are bacteria or substances that are produced in an intensified way due to an increased concentration of quorum sensing molecules (¶25), but fails to teach the biosensor module is a synthetic one or the receptor is a genetically modified bacteria expressed receptor or the reporter is a reporter gene, wherein expression is induced by the binding of the marker molecule to the receptor, wherein the genetically modified bacteria is configured to produce the reporter gene in response to uptake of the marker molecule or the reporter substrate is a reporter gene substrate so that the interaction is between the expressed reporter gene and the reporter gene substrate. However, Sayler teaches detecting bacteria based on recognition and infection of one or more selected strains of bacteria with bacteriophage genetically modified to cause production of an inducer molecule in the bacterium following phage infection ([Abstract]), by providing a novel internally amplified bioluminescent bacteriophage/bioreporter system (¶17). For example, a bacteriophage genetically modified carries a luxI gene, which encodes a protein product, resulting in the production of AHL (¶18). Upon infection, the phage luxI gene is transcribed in the bacterium, with resultant expression of the LuxI protein by the infected target cell (¶18). Following infection, the uptake of AHL molecules induces production of bioluminescent proteins in the bioreporter cells (¶19), and the bioluminescent is amplified due to the presence of the lux-modified bioreporter cells (¶20). As shown in Fig. 1, the expressed product of the LuxI gene has an expressed product that is AHL synthetase, which acts as an inducer of the bioluminescent reaction (¶34). The expressed complex product (Fig. 1; ¶34: black and white circles) binds to the promoter site of the luxI gene (Fig. 1: black box), which further induces transcription to carry out the biochemical reactions resulting in the production of 490 run light (Fig. 1; ¶34). Although Sayler does not teach using electrochemical signal, Sayler-1 teaches a recombinant bacteriophage-based system for rapid detection of a bacteria, using lux-I encoded LuxI proteins for generation of a specific AHL signaling molecule, which generates bioluminescent signal (¶5), and besides chemiluminescent signal, electrochemical signal can also be implemented (¶36). It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified Bollman by incorporating genetically engineered bacteria (e.g., lux genes) for expressing a promoter site capable of uptaking and binding AHL for generating bioluminescent or electrochemical signals as taught by Sayler and Sayler-1 because incorporation of lux genes would cause infection a particular pathogenic strain of bacteria and produce gene products (¶37) for amplifying the bioluminescent signal (¶38). Here, the claimed limitations are obvious because all the claimed elements were known in the prior art and one skilled in the art could have combined the elements as claimed by known methods with no change in their respective functions, and the combination yielded nothing more than predictable results. MPEP 2143(I)(A). Regarding claim 16, the designation “wherein the indication is related to a gastrointestinal disease or disorder, and wherein the level of the marker molecule corresponds to the stage of the gastrointestinal disease or disorder” does not further limit the method as claimed because it is the intended result of the step “providing an indication related to presence of the marker molecule in the sample.” Claim scope is not limited by claim language that suggests or makes optional but does not require steps to be performed. In method claims, it is the overall method steps that are given patentable weight not the intended result thereof because the intended result does not materially alter the overall method. Here, this designation is not given patentable weight when it simply expresses the intended result of a process step positively recited. MPEP 2111.04. Regarding claim 17, as evidenced by Majeed, wherein the gastrointestinal disease or disorder is inflammatory bowel disease (¶2). Regarding claim 18, Bollman teaches wherein the biological sample is urine (¶71: for example, a blood sample, urine sample, etc.). Regarding claim 19, as evidenced by Kim, wherein the biological sample is obtained from a food, a beverage, a water source or any combination thereof (¶3: Beta-galactosidases are widely found in mammalian organs, plant seeds, bacteria, fungi, and yeasts; e.g., in the food industry, beta-galactosidases from yeasts). Claim(s) 10 is/are rejected under 35 U.S.C. 103 as being unpatentable over Bollman in view of Sayler and Sayler-1, and further in view of Tabor (US 2018/0258459). Regarding claim 10, Bollman, Sayler, and Sayler-1 disclose all limitations of claim 9, and Bollman further discloses wherein the reporting agent is beta-galactosidase (¶51). Bollman, Sayler, and Sayler-1 do not disclose the report gene substrate is p-aminophenyl-β-D-galactopyranoside. However, Tabor teaches common spectroscopically active reporter proteins and their detection (p. 4, Table 1 -continued), for example, for β-Galactosidase as a reporter protein, the substrate is galactopyranosides, such as 4-aminophenyl-β-D-galactopyranoside. It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified Bollman, Sayler, and Sayler-1 by substituting the reporter gene substrate with p-aminophenyl-β-D-galactopyranoside as taught by Tabor because it is a well-known substrate for the reporter protein β-galactosidase. The suggestion for doing so and the selection of a known material, which is based upon its suitability for the intended use, are within the ambit of one of ordinary skill in the art. MPEP § 2144.07. Response to Arguments Applicant’s arguments have been considered but are unpersuasive. Applicant argues Bollman does not teach or suggest using living genetically modified bacteria as the sensing element (Response, p. 9, para. 3), and Sayler does not cure the deficiencies of Bollman (p. 9, para. 4) because the claims require no phage infection or the detection uses an electrochemical signal (pp. 9-10: bridging para.). This argument is moot because both Bollman and Sayler-1 teach using electrochemical signal for biosensing, and Sayler-1 uses the same bacteriophage-based system of Sayler, so that the bacteriophage-based system does not only generate bioluminescent signal (Sayler-1, ¶5), but also electrochemical signal (¶36). Conclusion THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a). A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any extension fee 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 CAITLYN M SUN whose telephone number is (571)272-6788. The examiner can normally be reached M-F: 8:30am - 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, Luan Van can be reached on 571-272-8521. 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. /C. SUN/Primary Examiner, Art Unit 1795
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Prosecution Timeline

Jun 20, 2024
Application Filed
Apr 22, 2026
Non-Final Rejection mailed — §103
Jul 19, 2026
Response Filed
Sep 17, 2026
Final Rejection mailed — §103 (current)

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Prosecution Projections

3-4
Expected OA Rounds
64%
Grant Probability
75%
With Interview (+11.9%)
3y 0m (~8m remaining)
Median Time to Grant
Moderate
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