Prosecution Insights
Last updated: April 19, 2026
Application No. 18/246,512

ANTI-INFLAMMATORY CYTOKINES AND METHODS OF USE

Non-Final OA §112
Filed
Mar 23, 2023
Examiner
MERTZ, PREMA MARIA
Art Unit
1674
Tech Center
1600 — Biotechnology & Organic Chemistry
Assignee
The University of Chicago
OA Round
1 (Non-Final)
72%
Grant Probability
Favorable
1-2
OA Rounds
2y 10m
To Grant
99%
With Interview

Examiner Intelligence

Grants 72% — above average
72%
Career Allow Rate
539 granted / 754 resolved
+11.5% vs TC avg
Strong +36% interview lift
Without
With
+35.6%
Interview Lift
resolved cases with interview
Typical timeline
2y 10m
Avg Prosecution
16 currently pending
Career history
770
Total Applications
across all art units

Statute-Specific Performance

§101
5.9%
-34.1% vs TC avg
§103
21.7%
-18.3% vs TC avg
§102
13.9%
-26.1% vs TC avg
§112
41.2%
+1.2% vs TC avg
Black line = Tech Center average estimate • Based on career data from 754 resolved cases

Office Action

§112
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 without traverse of Group II (claims 91, 92, 95, 96, 98, 99, 118-121, and 133-141; species: multiple sclerosis) in the reply filed on 1/2/2026 is acknowledged. Pursuant to an interview with the Examiner on 2/2/2026, amended claims 91, 140, (2/10/2026), previously presented claims 118-120, 133, 139, and new claims 143-152, (2/10/2026) were submitted. Claims 91, 118-120, 133, 139-140, and 143-152 are pending and under consideration by the Examiner. Claims 1-90, 92-117, 121-132, 134-138, and 141, have been canceled. Information Disclosure Statement 3. The information disclosure statements (IDS) submitted on 3/20/2025, 2/12/2025, and 7/10/2023 are in compliance with the provisions of 37 CFR 1.97 and have been considered by the examiner. Applicant is reminded of their duty to disclose to the Office all information known to the person to be material to patentability as defined in 37 CFR 1.56. As stated therein, “[e]ach individual associated with the filing and prosecution of a patent application has a duty of candor and good faith in dealing with the Office, which includes a duty to disclose to the Office all information known to that individual to be material to patentability as defined in this section”. Claim Rejections - 35 USC § 112(a), scope of enablement 4. The following is a quotation 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 35 U.S.C. 112 (pre-AIA ), first paragraph: 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. 4a, Claims 91, 118-120, 133, 139-140, and 143-152 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for a method of reducing inflammation in a subject with multiple sclerosis (MS), the method comprising administering to the subject in need thereof, by subcutaneous, intradermal, or intramuscular administration, an effective amount of a composition comprising an anti- inflammatory cytokine operatively linked to an albumin protein, wherein the anti-inflammatory cytokine is IL-33, does not reasonably provide enablement for a method for treating MS or its subtypes in a subject wherein the MS subtypes comprise secondary-progressive MS (SPMS), relapsing-remitting MS (RRMS), clinically isolated syndrome, late-stage MS, spino-optical MS, primary-progressive MS (PPMS), active, not-active, worsening, and/or not worsening, comprising administering to the subject an effective amount of a composition comprising an anti- inflammatory cytokine operatively linked to an albumin protein, wherein the anti-inflammatory cytokine is IL-33 (SA-IL-33). The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the invention commensurate in scope with these claims. “There are many factors to be considered when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any necessary experimentation is 'undue'. These factors include, but are not limited to: (A) The breadth of the claims; (B) The nature of the invention; (C) The state of the prior art; (D) The level of one of ordinary skill; (E) The level of predictability in the art; (F) The amount of direction provided by the inventor; (G) The existence of working examples; and (H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure. In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988)”. See MPEP § 2164.01. Claims 91, 118-120, 133, 139-140, and 143-152, are drawn to a method of treating MS in a subject wherein the MS comprises secondary-progressive MS (SPMS), relapsing-remitting MS (RRMS), clinically isolated syndrome, late-stage MS, spino-optical MS, primary-progressive MS (PPMS), active, not-active, worsening, and/or not worsening, comprising administering to the subject an effective amount of a composition comprising an anti- inflammatory cytokine operatively linked to an albumin protein, wherein the anti-inflammatory cytokine is IL-33 (See claims 91, 33). The instant specification, page 73, [0190], discloses: “SA-IL-33 and SA-IL-4 prevent EAE disease progression and development Myelin oligodendrocyte glycoprotein (MOG)35-55 experimental autoimmune encephalomyelitis (EAE) mice were injected every other day for 10 days from day 8 after immunization with phosphate-buffered saline (PBS) subcutaneously (s.c.), SA-IL-33 (13-39 g, based on IL-33, as shown in FIG. 12A) subcutaneous, or SA-IL-4 (10 g, IL-4 base) or dosed with FTY720 1 mg/kg daily by oral administration. n = 6-7 per group. FIG. 12A shows the clinical score progression for all groups. SA-IL-33 and SA-IL-4 treatment significantly reduced disease progression and severity compared with the PBS-treated group. FIG. 12B shows body weight progression for all groups.” Furthermore, the instant specification, page 95, [0242], discloses Example 9, SA-IL-33 for treating multiple sclerosis (EAE) and FIGURES 32-42, which further demonstrate aspects of SA-IL-33 experiments in mice. However, the specification fails to provide sufficient guidance as to how to treat a subject with more serious and advanced MS conditions as recited in claim 133. The instant invention is based on findings that administering to an animal model of MS/EAE induced with a MOG35-55 peptide in complete Freund's adjuvant (MOG35-55/CFA Emulsion), followed by i.p. administration of pertussis toxin in PBS-first on the day of immunization and again the following day, reduced the severity of MS and SA IL-33 treatment in the chronic phase of EAE reduced the clinical score, increased body weight, and reduced immune-cell infiltration (See page 96, [0247]; FIGURES 37A-F). Applicant extrapolates the above findings to the claimed method for treating MS comprising secondary-progressive MS, relapsing-remitting MS, clinically isolated syndrome, late-stage MS, spino-optical MS, primary-progressive MS, active, not-active, worsening, and/or not worsening, by administering to the subject anti- inflammatory cytokine IL-33 operatively linked to an albumin protein. The Ransohoff publication ( Nature Neuroscience 15(8):1074-1077, Aug. 2012) is being included in the record because it shows that positive results in the treatment of EAE animals are still regarded in the contemporary art as an unreliable predictor of the efficacy of a protocol in the treatment of MS. The first paragraph in the right hand column on page 1075 therein states that there were more than 8,800 EAE papers listed in PubMed as of March of 2012, showing that EAE is routinely used in the art to study autoimmune demyelination. However, the sentence bridging pages 1075 to 1076 therein states that “[f]or the most part, EAE has proven poorly predictive of treatment success in MS, particularly as concerns manipulations of inflammatory cytokines”. The text in the third paragraph, left hand column, on page 1076 of the Ransohoff publication lists various reasons as to why EAE is not reliably representative of MS. The following paragraph concludes with the statement that, whereas “EAE provides a remarkably flexible, potent and rapid platform for research”, “ [i]ts predictive value for treatment efficacy has been poor, however, and it performs best when asking mechanistic research questions”. The Constantinescu et al. publication (British Journal of Pharmacology, 164, pages 1079-1106, 2011) is being relied upon because it provides a discussion of the reliability of the mouse EAE model in evaluating methods of treating MS in humans. As explained in the text on page 1093, right hand column, first full paragraph of this reference, “EAE results, especially those taken in relative isolation, cannot easily predict the success of a given therapeutic intervention in MS. For an immunological intervention in EAE to be matched in MS, the appropriate MS population (i.e. RRMS) needs to be tested”. That text further states that “ [h]owever, the development of pure progressive EAE models to mimic primary progressive MS is problematic”. The Constantinescu et al. publication, much like the Ransohoff et al. publication discussed above, shows that the mouse EAE model is extremely useful in the development and evaluation of potentially useful methods of treating multiple sclerosis in humans. However, both of these references clearly show that the demonstration of efficacy of a treatment protocol in that model does not demonstrate possession of a method of treating MS and its subtypes in humans. The specification fails to provide sufficient guidance as to enable one of skill in the art to practice the invention as it pertains to a method of treating MS comprising secondary-progressive MS, relapsing-remitting MS, clinically isolated syndrome, late-stage MS, spino-optical MS, primary-progressive MS, active, not-active, worsening, and/or not worsening, by administering to the subject anti-inflammatory cytokine IL-33 operatively linked to an albumin protein. Furthermore, Applicant fails to provide specific guidance as to the dosage of the claimed SA-IL-33 protein to be administered, and thus would be effective to treat symptoms of MS subtypes in secondary-progressive MS, relapsing-remitting MS, clinically isolated syndrome, late-stage MS, spino-optical MS, primary-progressive MS, active, not-active, worsening, and/or not worsening MS. The specification fails to provide sufficient guidance as to enable one of skill in the art to practice the invention as it pertains to a method as recited in claim 133. The practice of the claimed method without the need for substantial undue experimentation and additional inventive contribution requires the disclosure of an effective route, duration and quantity of administration of SA-IL-33 to an individual suffering from the various MS subtypes and this information is not provided by the instant specification. The text on pages 63-65 of the instant specification clearly fails to supply the guidance that would be needed by a routine practitioner and essentially constitutes nothing more than an invitation to engage in additional experimentation. The instant specification has also failed to disclose how these parameters are to be determined, how a similar method was practiced in the art with a different agent or to provide even a single working example, prophetic or actual, of the claimed method. In the absence of this guidance a practitioner would have to resort to a substantial amount of undue experimentation involving the variation in the amount and duration of administration of SA-IL-33 of the instant invention. The instant situation is directly analogous to that which was addressed in In re Colianni, 195 U.S.P.Q. 150,(CCPA 1977), which held that a "[d]isclosure that calls for application of "sufficient" ultrasonic energy to practice claimed method of fusing bones but does not disclose what "sufficient" dosage of ultrasonic energy might be or how those skilled in the art might select appropriate intensity, frequence, and duration, and contains no specific examples or embodiment by way of illustration of how claimed method is to be practiced does not meet requirements of 35 U.S.C. 112 first paragraph". Applicant is enabled for a method for reducing inflammation by administering IL-33 linked to albumin in an animal model of MS/EAE induced with a MOG35-55 peptide. However, the specification fails to provide sufficient guidance to enable a skilled artisan to practice the full scope of the claimed method without undue experimentation because the specification fails to teach treatment of secondary-progressive MS, relapsing-remitting MS, clinically isolated syndrome, late-stage MS, spino-optical MS, primary-progressive MS, active, not-active, worsening, and/or not worsening MS by administering IL-33 linked to albumin. When considered as a whole, the art of record shows that positive results obtained from the application of a protocol to the treatment of EAE was not considered a reliable predictor of the efficacy of that protocol in the treatment of MS at the time of the instant invention and continues to be regarded as unreliable. The fact that EAE is routinely employed to study mechanisms involved in autoimmune demyelination does not change the fact that it is recognized in the art as notoriously unreliable in predicting the efficacy of a protocol in the treatment of MS and more serious MS conditions. The references cited above show that one of ordinary skill in this art would not reasonably conclude that the in vivo treatment protocols described in the working examples of the instant specification, which employ a mouse EAE model system, can be expected to be effective in the treatment of all MS subtypes comprising secondary-progressive MS (SPMS), relapsing-remitting MS (RRMS), clinically isolated syndrome, late-stage MS, spino-optical MS, primary-progressive MS (PPMS), active, not-active, worsening, and/or not worsening MS. A patent is granted for a completed invention, not the general suggestion of an idea and how that idea might be developed into the claimed invention. In the decision of Genentec, Inc, v. Novo Nordisk, 42 USPQ 2d 100,(CAFC 1997), the court held that: “[p]atent protection is granted in return for an enabling disclosure of an invention, not for vague intimations of general ideas that may or may not be workable” and that “[t]ossing out the mere germ of an idea does not constitute enabling disclosure”. The court further stated that “when there is no disclosure of any specific starting material or of any of the conditions under which a process is to be carried out, undue experimentation is required; there is a failure to meet the enablement requirements that cannot be rectified by asserting that all the disclosure related to the process is within the skill of the art”, “[i]t is the specification, not the knowledge of one skilled in the art, that must supply the novel aspects of an invention in order to constitute adequate enablement”. Therefore, in view of the lack of guidance in the specification, the unpredictability of the invention, the breadth of the claims, and the status of the prior art, undue experimentation would be required by a skilled artisan in order to practice the claimed invention as it pertains to a method for treating MS subtypes comprising PPMS, SPMS relapsing-remitting MS, clinically isolated syndrome, late-stage MS, spino-optical MS, active, not-active, worsening, and/or not worsening MS, by administering to the subject anti-inflammatory cytokine IL-33 operatively linked to an albumin protein, and one cannot following the guidance presented therein and practice the claimed method without first making a substantial inventive contribution. Claim Rejections - 35 USC § 112(b) 4. 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. 4a. Claims 91, 118-120, 133, 139-140, and 143-152 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. Claim 91 recites the limitation "the anti-inflammatory cytokine" in line 5. There is insufficient antecedent basis for this limitation in the claim. Claim 133 is vague and indefinite because it recites “not-active, worsening, and/or not worsening” rather than the proper “not-active MS, worsening MS, and/or not worsening MS”. Claims 118-120, 139-140, and 143-152 are rejected as vague and indefinite insofar as they depend on the above rejected claim 91 for its limitations. Conclusion No claim is allowed. Claims 91, 118-120, 133, 139-140, and 143-152, are rejected. Advisory Information Any inquiry concerning this communication or earlier communications from the examiner should be directed to PREMA MARIA MERTZ whose telephone number is (571)272-0876. The examiner can normally be reached on Monday to Thursday from 7:30am to 6:00pm. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, VANESSA FORD, can be reached at telephone number 571-272-0857. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300. Information regarding the status of an application may be obtained from Patent Center. Status information for published applications may be obtained from Patent Center. Status information for unpublished applications is available through Patent Center for authorized users only. Should you have questions about access to Patent Center, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). 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) Form at https://www.uspto.gov/patents/uspto-automated- interview-request-air-form. /PREMA M MERTZ/ Primary Examiner, Art Unit 1674
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Prosecution Timeline

Mar 23, 2023
Application Filed
Jan 27, 2026
Interview Requested
Feb 02, 2026
Examiner Interview Summary
Mar 08, 2026
Non-Final Rejection — §112 (current)

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Prosecution Projections

1-2
Expected OA Rounds
72%
Grant Probability
99%
With Interview (+35.6%)
2y 10m
Median Time to Grant
Low
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