Prosecution Insights
Last updated: April 19, 2026
Application No. 18/246,756

Antibody Binding to Human IL-33, Preparation Method Therefor, and Use Thereof

Non-Final OA §112
Filed
Mar 27, 2023
Examiner
LANDSMAN, ROBERT S
Art Unit
1647
Tech Center
1600 — Biotechnology & Organic Chemistry
Assignee
Sunshine Guojian Pharmaceutical (Shanghai) Co., Ltd.
OA Round
1 (Non-Final)
81%
Grant Probability
Favorable
1-2
OA Rounds
2y 4m
To Grant
94%
With Interview

Examiner Intelligence

Grants 81% — above average
81%
Career Allow Rate
1007 granted / 1239 resolved
+21.3% vs TC avg
Moderate +13% lift
Without
With
+13.0%
Interview Lift
resolved cases with interview
Typical timeline
2y 4m
Avg Prosecution
43 currently pending
Career history
1282
Total Applications
across all art units

Statute-Specific Performance

§101
3.8%
-36.2% vs TC avg
§103
18.6%
-21.4% vs TC avg
§102
15.0%
-25.0% vs TC avg
§112
38.5%
-1.5% vs TC avg
Black line = Tech Center average estimate • Based on career data from 1239 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 . 1. Formal Matters A. In the response filed 12/17/25, Applicants elected Group I, without traverse, drawn to the indicated species. However, upon further review, all species have been examined. This restriction is deemed proper and is, therefore, made FINAL. B. Claims 1, 3, 4, 6, 7, 10-22, 24 and 25 are pending. Claim 25 is withdrawn as being drawn to a non-elected invention. Claims 1, 3, 4, 6, 7, 10-22 and 24 are the subject of this Office Action. 2. Claim Objections A. Though not incorrect, it is unclear why, in claim 1, the characteristics are labeled with a “t” before each number (e.g. “(t1)”). B. Though not incorrect, it is noted that the use of number and letters in the outline form of the claims is inconsistent since claims 3 and 22 use “(a)” and “(b)”, whereas claim 20 uses “a)” and “b)”. C. Though not incorrect, clarification is requested regarding claim 11, which recites that the heavy chain constant region “further comprises” SEQ ID NO:13. This claim depends from claim 10, which already recites a heavy chain constant region. Therefore, it is unclear if claim 11 is intended to claim a heavy chain constant region in addition to that of claim 10, or if the intent is “wherein the heavy chain constant region of claim 10 is SEQ ID NO:13”. It is noted that lines 8-10 of page 8 of the specification appear to indicate that there is a single heavy chain constant region, which, in one embodiment, is SEQ ID NO:13. Lines 20-21 of page 7 state that another preferred embodiment is IgG1, 2, 3 or 4. It does not appear that these are intended to both be used in the same antibody. 3. Claim Rejections - 35 USC § 112(a) – written description The following is a quotation of the first paragraph of 35 U.S.C. 112(a): (a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention. The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112: The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention. A. Claims 1, 4, 10-13, 18-22 and 24 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention. The claims are broadly drawn to antibodies only required to comprise L-CDR2. However, the specification only teaches that antibodies which specifically bind to IL-33 comprise 6 defined CDRs (see claim 3). The specification does not teach antibodies that comprise fewer than all 6 CDRs defined by SEQ ID NO. The nature of the invention is engineered antibodies where the relative level of skill of those in the art is deemed to be high. The state of the prior art is such that it is well-established in the art that the formation of an intact antigen-binding site of antibodies routinely requires the association of the complete heavy and light chain variable regions of a given antibody, each of which consists of three CDRs or hypervariable regions, which provide the majority of the contact residues for the binding of the antibody to its target epitope (Paul, William E.), under the heading “Fv Structure and Diversity in Three Dimensions”). The amino acid sequences and conformations of each of the heavy and light chain CDRs are critical in maintaining the antigen binding specificity and affinity, which is characteristic of the immunoglobulin. It is expected that all of the heavy and light chain CDRs in their proper order and in the context of framework sequences which maintain their required conformation, are required in order to produce a protein having antigen-binding function and that proper association of heavy and light chain variable regions is required in order to form functional antigen binding sites (Paul, page 293, first column, lines 3-8 and line 31 to column 2, line 9 and lines 27-30). Even minor changes in the amino acid sequences of the heavy and light variable regions, particularly in the CDRs, may dramatically affect antigen-binding function as evidenced by Rudikoff et al. Rudikoff et al. teach that the alteration of a single amino acid in the CDR of a phosphocholine-binding myeloma protein resulted in the loss of antigen-binding function. Colman P. M. et al teaches that even a very conservative substitution may abolish binding or may have very little effect on the binding affinity (see pg. 35, top of left column and pg. 33, right column). Additionally, Bendig M. M. et al. reviews that the general strategy for “humanizing” antibodies involves the substitution of all six CDRs from a rodent antibody that binds an antigen of interest, and that all six CDRs are involved in antigen binding (see entire document, but especially Figures 1-3). Similarly, the skilled artisan recognized a “chimeric” antibody to be an antibody in which both the heavy chain variable region (which comprises the three heavy chain CDRs) and the light chain variable region (which comprises the three light chain CDRs) of a rodent antibody are recombined with constant region sequences from a human antibody of a desired isotype (see entire document, but especially Figures 1-3). While there are some publications which acknowledge that CDR3 is important, the conformations of other CDRs as well as framework residues influence binding. MacCallum et al. analyzed many different antibodies for interactions with antigen and state that although CDR3 of the heavy and light chain dominate, a number of residues outside the standard CDR definitions make antigen contacts (see page 733, right col.) and non-contacting residues within the CDRs coincide with residues as important in defining canonical backbone conformations (see page 735, left col.). The fact that not just one CDR is essential for antigen binding or maintaining the conformation of the antigen binding site, is underscored by Casset et al., which constructed a peptide mimetic of an anti-CD4 monoclonal antibody binding site by rational design and the peptide was designed with 27 residues formed by residues from 5 CDRs (see entire document). Casset et al. also states that although CDR H3 is at the center of most if not all antigen interactions, clearly other CDRs play an important role in the recognition process (page 199, left col.) and this is demonstrated in this work by using all CDRs except L2 and additionally using a framework residue located just before the H3 (see page 202, left col.). In fact, even regarding CDR3, Scheffer et al. states “[t]herefore, many studies attempt to predict AIR-antigen binding exclusively based on the heavy/beta chain CDR3 sequences. Yet, the underlying rules determining whether an AIR can bind an antigen of interest remain unknown.” Furthermore, even within CDR3, Scheffer concludes “we have shown that there indeed exist motifs composed of a few amino acids in fixed positions of the antibody CDRH3, whose presence is nearly sufficient to predict antigen binding in a mutagenesis dataset where other variable regions were kept the same”. Applicants do not appear to show such a motif, nor would bind be predictable in the presence of changes to other CDRs. Additionally, Valdes-Trescano (Section 2.3) states “[a]t the sequence region level, we observed a considerable variation in the accuracy of CDR modeling, especially for CDR3”. Further, Chen et al. teach that the substitution of a single amino acid can totally ablate antigen and that the same substitution in closely related antibodies can have opposite effects binding (e.g., see entire document, including Figure I). For example, the authors compared the effects of identical substitutions in related antibodies DI6 and TI5, and as shown in Figure 3, some substitutions increased antigen binding in one antibody while ablating it in the other. As such, it is unpredictable which combination of random substitution has the recited function. Finally, Ye teaches that “[t]he final data set contained 1157 antibodies and 57 antigens that were combined in 5041 antibody-antigen pairs. The best performance for the prediction of interactions was obtained by using the nearest neighbor method with the BLOSUM62 matrix, which resulted in around 82% accuracy on the full data set. These results provide a useful frame of reference, as well as protocols and considerations, for machine learning and data set creation in the prediction of antibody-antigen binding. However, in this approach, “[s]everal machine learning approaches were compared to predict antibody-antigen interaction from protein sequences”. Therefore, even with a study using 1157 antibodies and 57 antigens, the best prediction was 82%. Again, it is noted that several machine learning approaches were used, showing that prediction can still be difficult and dependent on the prediction method used. Thus, the state of the art recognized that it would be highly unpredictable that a specific binding member comprising an antibody comprising fewer than all six CDRs of a parental antibody with a desired specificity would retain the antigen-binding function of the parental antibody. One of ordinary skill in the art could not predictably extrapolate the teachings in the specification, limited to antibodies that comprise all 6 wild-type CDRs to antibodies that comprise fewer than 6 defined CDRs from the parental antibody. In summary, in view of the lack of the predictability of the art to which the invention pertains as evidenced by the above references, the lack of guidance and direction provided by applicant, and the absence of working examples, the Examiner concludes that undue experimentation would be required to practice the invention as claimed. B. Claim 1 is rejected under 35 U.S.C. 112(a) as containing subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor(s), at the time the application was filed, had possession of the claimed invention. The claims do not provide a lower limit for the KD values (i.e. the claim recites “less than 1 nM”). Therefore, the claims read on “superbinders”, which can have affinity values in the femptomolar range, or lower (i.e. higher affinity). 3. Conclusion A. Claims 1, 4, 10-13, 18-22 and 24 are not allowable. B. Claims 3, 6, 7 and 14-17 are objected to since they depend from rejected base claims, but are otherwise allowable. Advisory information Any inquiry concerning this communication or earlier communications from the examiner should be directed to ROBERT S LANDSMAN whose telephone number is 571-272-0888. The examiner can normally be reached M-F 8 AM – 6 PM (eastern). 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, Joanne Hama, can be reached at 571-272-2911. 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 the Patent Application Information Retrieval (PAIR) system. Status information for published applications may be obtained from either Private PAIR or Public PAIR. Status information for unpublished applications is available through Private PAIR only. For more information about the PAIR system, see http://pair-direct.uspto.gov. Should you have questions on access to the Private PAIR system, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). /ROBERT S LANDSMAN/Primary Examiner, Art Unit 1647
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Prosecution Timeline

Mar 27, 2023
Application Filed
Feb 03, 2026
Non-Final Rejection — §112 (current)

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Study what changed to get past this examiner. Based on 5 most recent grants.

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Prosecution Projections

1-2
Expected OA Rounds
81%
Grant Probability
94%
With Interview (+13.0%)
2y 4m
Median Time to Grant
Low
PTA Risk
Based on 1239 resolved cases by this examiner. Grant probability derived from career allow rate.

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