Prosecution Insights
Last updated: April 19, 2026
Application No. 17/801,434

Compositions and Methods for Treatment of Cytokine Storm and Cytokine Release Syndrome

Final Rejection §103§112§DP
Filed
Aug 22, 2022
Examiner
ADLAM, CHANTAL PETA-GAYE
Art Unit
1622
Tech Center
1600 — Biotechnology & Organic Chemistry
Assignee
Yinuoke Medicine Science Technology Company Ltd.
OA Round
2 (Final)
49%
Grant Probability
Moderate
3-4
OA Rounds
3y 8m
To Grant
73%
With Interview

Examiner Intelligence

Grants 49% of resolved cases
49%
Career Allow Rate
27 granted / 55 resolved
-10.9% vs TC avg
Strong +24% interview lift
Without
With
+24.2%
Interview Lift
resolved cases with interview
Typical timeline
3y 8m
Avg Prosecution
31 currently pending
Career history
86
Total Applications
across all art units

Statute-Specific Performance

§101
2.5%
-37.5% vs TC avg
§103
36.3%
-3.7% vs TC avg
§102
12.7%
-27.3% vs TC avg
§112
20.9%
-19.1% vs TC avg
Black line = Tech Center average estimate • Based on career data from 55 resolved cases

Office Action

§103 §112 §DP
DETAILED ACTION This action is in response to papers filed on 02/03/2026. Claims 1-10, 18-19, 21, and 23 of Zhang et al., 17801434 (08/22/2022) are pending examination on the merits: claims 1-2, 10, 18 and 21 are amended. Claims 1-10, 18-19, 21, and 23 are rejected. 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 . Priority This application is a 371 of PCT/US2021/019462 (02/24/2021) which claims benefit of 62/980,652 (02/24/2020). Election/Restrictions REQUIREMENT FOR UNITY OF INVENTION In a response filed on 06/23/2025, Applicant elected without traverse, Group I invention: claims 1-10, 18-19, 21, and 23, drawn to a method of treating cytokine storm and/or cytokine release syndrome; and preventing or treating body weight loss and/or diarrhea associated with cytokine storm and/or cytokine release syndrome. Applicant’s Remarks at page 5. Group II, claims 11-16, drawn to a non-elected pharmaceutical composition have since been canceled. Withdrawn Claim Rejections The rejection of Claims 1-10, 18-19, 21, and 23 under 35 U.S.C. 112(b) is withdrawn in view of Applicant’s amendment to claim 1 to recite in part “(R)-ketorolac, (S)-ketorolac, or a racemic mixture…”. Applicant’s Remarks at page 5. The rejection of claims 21 and 23 are rejected under 35 U.S.C. 112(a) is withdrawn in view of Applicant’s amendment to the claim, removing the term “preventing”. Applicant’s Remarks at page 6. Claim Interpretation Claim 21 recites “A method of preventing or treating body weight loss and/or diarrhea associated with cytokine storm...”. Regarding the word preventing, as per the Specification para. [0047]: “As used herein, the terms "treating," "treat," or "treatment" refer to either preventing, providing symptomatic relief, or curing a patient's disorder, condition, or disease. The Specification in Example 4 on page 19 solely discusses treatment and no prevention. Claim 21 and dependent claim 23 are therefore interpreted as “A method of treating body weight loss and/or diarrhea associated with cytokine storm and/or cytokine release syndrome (CRS) in a subject in need thereof…”. 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. Claims 1-10, 18-19, 21, and 23 are rejected under 35 U.S.C. 103 as being unpatentable over Barberich et al., US 5,382,591 A (“Barberich”), in view of Lisboa et al., (2017), Surgery, Volume 161, Number 4, pp. 1164-1173 (“Lisboa”). Claims 1, 9-10, and 18-19 are rejected under 35 U.S.C. 103 as being unpatentable over Barberich et al., US 5,382,591 A (“Barberich”), in view of Lisboa et al., (2017), Surgery, Volume 161, Number 4, pp. 1164-1173 (“Lisboa”). Regarding claim 1, Barberich teaches the use of R-ketorolac as an analgesic and anti-inflammatory NSAID (col 5, In 1-11: "The magnitude of a prophylactic or therapeutic dose of R-ketorolac in the acute or chronic management of disease will vary with the severity of the condition to be treated, and the route of administration. The dose, and perhaps the dose frequency, will also vary according to the age, body weight, and response of the individual patient. In general, the total daily dose range for R-ketorolac, for the conditions described herein, is from about 15 mg to about 500 mg, in single or divided doses. Preferably, a daily dose range should be between about 30 mg to about 250 mg, in single or divided doses."). Barberich however, does not specifically teach a method of treating cytokine storm and/or cytokine release syndrome (CRS) in a subject in need thereof, and use of R-ketorolac to reduce the blood serum concentration of at least one of IL-1 beta, TNF-alpha, IL-6, IL-7, IL- 10, MCP-1, MIP-1A, LIF, G-CSF, and GM-CSF in the subject. Lisboa teaches a) administering a therapeutically effective amount of ketorolac to the subject (page 1168, col 1-2, para 1 - "3 patients were administered ketorolac 15 mg or 30 mg (Toradol, Roche Inc, Nutley, NJ)."), and b) reducing a blood serum concentration of at least one of IL-1beta, TNF-alpha, IL-6, IL-7, IL-10, MCP-1, MIP-1A, LIF, G-CSF, and GMCSF in the subject (page, 1168, col 1-2, para 1 - "3 patients were administered ketorolac 15 mg or 30 mg (Toradol, Roche Inc, Nutley, NJ)."; page 1168, col 2. para 1 - "When compared with the control group, we found that patients using NSAIDs had significantly lesser serum levels of IL-2, IL-6, IL-8, and MCP-1 (Fig 1, A)."). Lisboa, does not specifically teach ketorolac reduces cytokine release. However, Lisboa teaches NSAIDs including ketorolac maintain the stability of cytokine levels (page 1168, col 2, para 1 - "Linear regression illustrated how patients using NSAIDs maintained stability of the levels of these cytokines throughout operative debridement until primary closure of wounds was achieved (Fig 1, B-E). In addition to the linear regression, a nonparametric multivariate analysis of variance, which was used as a confirmatory test, showed the level of these same cytokines was greater in the absence of NSAID treatment (P =.02) based on time from injury."). Since Barberich teaches the use of R-ketorolac as an analgesic and anti-inflammatory NSAID, and Lisboa teaches that ketorolac, maintains the stability of cytokine levels, indicating the inhibition of further cytokine release and thus a reduction in cytokine release, it would have been obvious to one of ordinary skill in the art to have applied the combined teachings of Lisboa and Barberich to use a therapeutically effective dose of R-ketorolac to reduce cytokine levels and cytokine release, in order to treat cytokine release syndrome or cytokine storm of a given subject and arrive at the claimed invention with reasonable expectation of success. Additionally, obviousness does not require absolute predictability, but a reasonable expectation of success. See MPEP 2143.02. Claim 1 is obvious over Barberich and Lisboa. Regarding claims 9-10, Barberich in view of Lisboa teaches the method of claim 1. Barberich also teaches the therapeutically effective amount of (R)-ketorolac is about 1 mg to about 5 mg, about 5 mg to about 1000 mg, about 5 mg to about 800 mg, about 5 mg to about 500 mg, about 5 ma to about 200 mg, about 5 mg to about 100 mg, about 5 mg to about 50 mg, about 5 mg to about 25 mg, about 10 mg to about 1000 mg, about 10 mg to about 800 mg, about 10 mg to about 500 mg, about 10 mg to about 200 mg, about 10 mg to about 100 mg, or about 10 mg to about 50 mg (col 5, In 1-11 - "The magnitude of a prophylactic or therapeutic dose of R-ketorolac in the acute or chronic management of disease will vary with the severity of the condition to be treated, and the route of administration. The dose, and perhaps the dose frequency, will also vary according to the age, body weight, and response of the individual patient. In general, the total daily dose range for R-ketorolac, for the conditions described herein, is from about 15 mg to about 500 mg, in single or divided doses. Preferably, a daily dose range should be between about 30 mg to about 250 mg, in single or divided doses."). In the case where the claimed ranges “overlap or lie inside ranges disclosed by the prior art” a prima facie case of obviousness exists. In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976). Claims 9-10 are obvious. Regarding claim 18, Barberich in view of Lisboa teaches the method of claim 1. Barberich also discloses the use of racemic ketorolac as an analgesic and anti-inflammatory NSAID (col 6, In 44-45 - "The medications used are two dose levels of R(-) ketorolac and two dose levels of racemic ketorolac."; col 6, In 60-63 - "Groups of 6-10 rats are injected with either vehicle, racemic ketorolac (30, 15, 5 and 1 mg/kg/day), S-ketorolac (30, 15, 5 and 1 mg/kg/day) and R-ketorolac (30, 15, 5 and 1 mg/kg/day)"). Claim 18 is also obvious. Regarding claim 19, Barberich in view of Lisboa teaches the method of claim 1. Barberich also discloses administering a therapeutically effective amount of enantiomerically pure (S)- ketorolac to the subject (col 2, In 37-47 - "Caldwell et al., Biochem. Pharmacol, 37: 105-114 (1988) allege that "at best, the R-isomers of aryl alkanoic acids function as prodrugs for the therapeutically active S-forms when the racemic drug is administered and add to both the therapeutic and toxic effects of the active S-enantiomers. This reference further contends that, "at worst, the R-enantiomers are undesirable impurities in the active drug" causing difficulties due to non-stereoselective toxicity and further alleges that the use of the S-isomers should provide safer and more effective use of this class of drugs."). It would have therefore been obvious to select and use a therapeutically effective amount of enantiomerically pure (S)-ketorolac to the subject and arrive at the claimed invention. Claim 19 is also obvious. Claims 2-9 are rejected under 35 U.S.C. 103 as being unpatentable over Barberich and Lisboa, as applied to claims 1, 9-10, and 18-19 above, and further in view of Novik et al., US 20190175649A1 (“Novik”). Regarding claim 2, Barberich in view of Lisboa teaches the method of claim 1, yet does not teach the cytokine storm and/or CRS is secondary to at least one of a viral infection, bacterial infection, cancer, and/or cancer treatment. Novik teaches the cytokine storm and/or CRS is secondary to at least one of a viral infection, bacterial infection, cancer, and/or cancer treatment (para. [0010] - "The relatively high death rate in young people, with presumably healthy immune systems, in the 1918 H1N1 influenza pandemic and the more recent bird flu H5N1 infection are attributed to cytokine storms. This syndrome has been also known to occur in advanced or terminal cases of severe acute respiratory syndrome (SARS), Epstein-Ban virus-associated hemophagocytic lymphohistiocytosis, gram-negative sepsis, malaria and numerous other infectious diseases, including Ebola infection. Cytokine storm may also stem from non-infectious causes, such as acute pancreatitis, severe burns or trauma, or acute respiratory distress syndrome."; para [0507] - "In another embodiment, a solid tumor consists of an abnormal mass of cells which may stem from different tissue types such as liver, colon, breast, or lung, and which initially grows in the organ of its cellular origin. However, such cancers may spread to other organs through metastatic tumor growth in advanced stages of the disease."). Since Barberich and Lisboa teaches reduction of cytokines with ketorolac, as applied to claim 1, and Novik teaches CRS is associated with viral infection, bacterial infection, and cancer, it would have been obvious to one of ordinary skill in the art to have applied combined teachings of Barberich, Lisboa and Novik to treat CRS associated complications, in order to effectively treat CRS patient and reduce the serum concentrations of indicated cytokines in a given subject; thus arriving at the claimed invention. Claim 2 is obvious. Regarding claim 3, Barberich and Lisboa in view of Novik teach the method of claim 2, and Novik teaches the viral infection is caused by one or more of a coronavirus, influenza, Epstein-Barr virus, respiratory syncytial virus, dengue virus, zika virus, west Nile virus, variola virus, cytomegalovirus, and HIV [para [0205] - "In one embodiment, an infection causes the cytokine release syndrome or cytokine storm in the subject. In one embodiment, the infection is an influenza infection. In one embodiment, the influenza infection is H1N1. In another embodiment, the influenza infection is an H5N1 bird flu. In another embodiment, the infection is severe acute respiratory syndrome (SARS). In another embodiment, the subject has Epstein-Ban virus-associated hemophagocytic lymphohistiocytosis (HLH). In another embodiment, the infection is sepsis. In one embodiment, the sepsis is gram-negative. In another embodiment, the infection is malaria. In another embodiment, the infection is an Ebola virus infection. In another embodiment, the infection is variola virus. In another embodiment, the infection is a systemic Gram-negative bacterial infection. In another embodiment, the infection is Jarisch-Herxheimer syndrome."). Claim 3 is also obvious. Regarding claim 4, Barberich and Lisboa in view of Novik teach the method of claim 2, and Novik teaches bacterial infection is caused by gram positive toxins (para [0211] - "In one embodiment, the trigger for the release of inflammatory cytokines is a lipopolysaccharide (LPS), Gram-positive toxins, fungal toxins, glycosylphosphatidylinositol (GPI) or modulation of RIG-1 gene expression.”). Note: group A streptococcus belongs to gram positive bacteria. Claim 4 is obvious. Regarding claim 5, Barberich and Lisboa in view of Novik teach the method of claim 2, and Novik teaches the cancer is an advanced stage cancer. (para [0507] - "In another embodiment, a solid tumor consists of an abnormal mass of cells which may stem from different tissue types such as liver, colon, breast, or lung, and which initially grows in the organ of its cellular origin. However, such cancers may spread to other organs through metastatic tumor growth in advanced stages of the disease."). Claim 5 is obvious. Regarding claim 6, Barberich and Lisboa in view of Novik teach the method of claim 5, and Novik teaches the cancer is pancreatic cancer, lung cancer, or colorectal cancer (para [0507] - "In another embodiment, a solid tumor consists of an abnormal mass of cells which may stem from different tissue types such as liver, colon, breast, or lung, and which initially grows in the organ of its cellular origin. However, such cancers may spread to other organs through metastatic tumor growth in advanced stages of the disease."). Claim 6 is obvious. Regarding claim 7, Barberich and Lisboa in view of Novik teach the method of claim 2, and Novik teaches the cancer treatment comprises at least one of chemotherapy, radiotherapy, and immunotherapy (para [0002] - "While standard treatments for cancer are surgery, chemotherapy, and radiation therapy, improved methods, such as targeted immunological therapies, are currently being developed and tested."). Regarding claim 8, Barberich and Lisboa in view of Novik teach the method of claim 7, and Novik teaches immunotherapy comprises antibody therapy or CART cell treatment (para [0213] - "In another embodiment, the subject has cytokine release syndrome or cytokine storm secondary to receipt of immunotherapy, which in one embodiment is immunotherapy with super-agonistic CD28-specific monoclonal antibodies (CD28SA). In one embodiment, the CD28SA is TGN1412. In another embodiment, the immunotherapy is CAR T cell therapy."). Claims 21 and 23 are rejected under 35 U.S.C. 103 as being unpatentable over Barberich et al., US 5,382,591 A (“Barberich”) and Lisboa et al., as applied to claims 1, 9-10, and 18-19, in further view of Samal et al., Sci Rep 5, 9982 (2015) (“Samal”). Regarding claim 21, Barberich in view of Lisboa teachings regarding the reduction in cytokines is discussed and applied here as above in claim 1. Barberich also discloses administering a therapeutically effective amount of (R)-ketorolac (or racemic or (S)-ketorolac) to the subject (col 5, In 1-11 - "The magnitude of a prophylactic or therapeutic dose of R-ketorolac in the acute or chronic management of disease will vary with the severity of the condition to be treated, and the route of administration. The dose, and perhaps the dose frequency, will also vary according to the age, body weight, and response of the individual patient. In general, the total daily dose range for R ketorolac, for the conditions described herein, is from about 15 mg to about 500 mg, in single or divided doses. Preferably, a daily dose range should be between about 30 mg to about 250 mg, in single or divided doses."). Barberich does not specifically teach administering a therapeutically effective amount of (R)-ketorolac (or racemic or (S)-ketorolac) to the subject and reducing occurrence or severity of body weight loss in the subject. Samal teaches ketorolac administration in mice does not lead to severity of body weight loss (pg 5, col 1, para 1 -"After having visible tumors on the tongue, the animals were given IP injection with Ketorolac salt (20 mg/kg and 30 mg/kg) two times in a week for 3 weeks. At the end of the experiment, we found decreased tumor burden in case of the treated groups as compared to the control groups (Figure 6 ac Top panel). Tumor load was outlined as a digital image (Figure 6 lower panel). To monitor the toxicity related issues, we measured the body weight; the weight remained unaffected and is unaffected throughout the course of treatment (Supplementary Figure 1). "; pg 9, col 1, para 6 - "The Ketorolac treatment was given as IP injection twice in a week for 3 weeks. During each treatment mice were monitored for weight loss or any kind of sickness."; supplemental data pg 3, para 2 - "To monitor the toxicity related issues caused by ketorolac salt, we measured the body weight of each BALB/c mice in grams during the whole treatment period and plotted in graphs. As shown in Supplementary Fig. 1 the weight remains same and is unaffected throughout the course of treatment even at 30mg/kg of body weight."; page 4, Supplementary Fig 1 - "Weight of each BALB/c mice in grams during the whole treatment period plotted in graphs. The above graphs represent the weight of BALB/c mice taken at the indicated days (Day1 to Day 21)."). Since Barberich teaches administering a therapeutically effective amount of (R)-ketorolac (or racemic or (S)-ketorolac) to the subject, Lisboa teaches that ketorolac, maintain the stability of cytokine levels, indicating the inhibition of further cytokine release and thus a reduction in cytokine release, and Samal teaches ketorolac administration in mice does not lead to severity of body weight loss, it would have been prima facie obvious to one of ordinary skill in the art to have applied the method taught by Barberich wherein the subject is administered an effective dose of R-and/or S-Ketorolac as an analgesic and anti-inflammatory agent, in order to maximize the treatment efficacy of ketorolac to reduce occurrence or severity of body weight loss in the subject with CRS and arrive at the claimed invention with reasonable expectation of success. Claim 21 is obvious. Regarding claim 23, Barberich in view of Samal make obvious the method of claim 21. Barberich also teaches the therapeutically effective amount of (R)-ketorolac is about I mg to about 5 mg, about 5 mg to about 1000 mg, about 5 mg to about 800 mg, about 5 mg to about 500 mg, about 5 ma to about 200 mg, about 5 mg to about 100 mg, about 5 mg to about 50 mg, about 5 mg to about 25 mg, about 10 mg to about 1000 mg, about 10 mg to about 800 mg, about 10 mg to about 500 mg, about 10 mg to about 200 mg, about 10 mg to about 100 mg, or about 10 mg to about 50 mg (col 5, In 1-11 - "The magnitude of a prophylactic or therapeutic dose of R-ketorolac in the acute or chronic management of disease will vary with the severity of the condition to be treated, and the route of administration. The dose, and perhaps the dose frequency, will also vary according to the age, body weight, and response of the individual patient. In general, the total daily dose range for R-ketorolac, for the conditions described herein, is from about 15 mg to about 500 mg, in single or divided doses. Preferably, a daily dose range should be between about 30 mg to about 250 mg, in single or divided doses."). In the case where the claimed ranges “overlap or lie inside ranges disclosed by the prior art” a prima facie case of obviousness exists. In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976). Claim 23 is also obvious. Applicant’s Arguments In Applicant’s Remarks filed on 02/03/2026, Applicant argues the prior art: Barberich, Lisboa, Novik, and Samal. Applicant argues the prima facie case highlighting the differences between the prior arts relied upon and the claimed invention discussed by the Examiner above. Applicant essentially argues that the prior art references cited– alone or in combination with one another – do not teach a method of treating cytokine storm and/or cytokine release syndrome wherein there is a reduction in the release of cytokines. Applicant’s Remarks at pages 6-9. Examiner’s Response Applicant’s arguments are acknowledged, but are not found to be persuasive. Applicant argues the references individually and argues the differences between the prior art references relied upon and the claimed invention discussed by the Examiner above. The Examiner respectfully points out that the prima facie case of obviousness is made based on the combination of references discussed and applied in the above prima facie case rejections. The rejections are maintained using the same rationale discussed above. . Double Patenting The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969). A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b). The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13. The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer. Claims 1-10, and 18-19 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 43 of co-pending Application No. 19105807 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because both claim 43 of the reference application, and instant claims 1-10, and 18-19 teach a method of treating colon cancer by administering R-ketorolac (c.f., instant claims 1-2, and 5-6). The difference between the reference application and the instant claims is that the reference application teaches a method of preparing R-ketorolac and the use of R-ketorolac in treating colon cancer (as per claim 43), while the instant claims teach a method of treating colon cancer using said R-ketorolac. It is prima facie obvious to use R-Ketorolac for treating colon cancer as discussed above in view of Barberich and Lisboa. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented. Applicant’s Arguments/Examiner’s Response Applicant argues that the rejection should be held in abeyance until allowable subject matter is identified. Applicant’s Remarks at page 9. In response to Applicant’s arguments, the Examiner acknowledges the argument, but it is not found to be persuasive for the same reasons discussed above. The rejection is maintained. Conclusion No claims are allowed. Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a). A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action. Any inquiry concerning this communication or earlier communications from the examiner should be directed to CHANTAL ADLAM whose telephone number is (571)270-0923. The examiner can normally be reached Monday - Friday 8:00 am - 5:00 pm. Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, JAMES HENRY ALSTRUM-ACEVEDO can be reached on (571) 272-5548. 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 A/Examiner, Art Unit 1622 March 12, 2026 /JAMES H ALSTRUM-ACEVEDO/Supervisory Patent Examiner, Art Unit 1622
Read full office action

Prosecution Timeline

Aug 22, 2022
Application Filed
Oct 20, 2025
Non-Final Rejection — §103, §112, §DP
Feb 03, 2026
Response Filed
Mar 12, 2026
Final Rejection — §103, §112, §DP (current)

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Prosecution Projections

3-4
Expected OA Rounds
49%
Grant Probability
73%
With Interview (+24.2%)
3y 8m
Median Time to Grant
Moderate
PTA Risk
Based on 55 resolved cases by this examiner. Grant probability derived from career allow rate.

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