Prosecution Insights
Last updated: April 19, 2026
Application No. 18/532,395

MULTIFUNCTIONAL PROTEIN MOLECULES COMPRISING DECORIN AND USE THEREOF

Final Rejection §103
Filed
Dec 07, 2023
Examiner
LU, CHENG
Art Unit
1642
Tech Center
1600 — Biotechnology & Organic Chemistry
Assignee
Catalent Pharma Solutions LLC
OA Round
4 (Final)
55%
Grant Probability
Moderate
5-6
OA Rounds
3y 5m
To Grant
99%
With Interview

Examiner Intelligence

Grants 55% of resolved cases
55%
Career Allow Rate
111 granted / 202 resolved
-5.0% vs TC avg
Strong +67% interview lift
Without
With
+67.0%
Interview Lift
resolved cases with interview
Typical timeline
3y 5m
Avg Prosecution
64 currently pending
Career history
266
Total Applications
across all art units

Statute-Specific Performance

§101
2.5%
-37.5% vs TC avg
§103
29.7%
-10.3% vs TC avg
§102
13.0%
-27.0% vs TC avg
§112
32.5%
-7.5% vs TC avg
Black line = Tech Center average estimate • Based on career data from 202 resolved cases

Office Action

§103
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 . DETAILED ACTION The amendment filed November 25, 2025 in response to the Office Action of August 29, 2025 is acknowledged and has been entered. Claims 6, 9, 11 and 13 have been amended. Claims 2, 4-9, 11 and 13-17 are pending. Claims 16 and 17 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected inventions or species, there being no allowable generic or linking claim. Claims 2, 4-9, 11 and 13-15 are currently under consideration as drawn to the elected invention. In view of claim amendments, the 112(b) rejection for claims 6, 9, 11 and 13-15 are hereby withdrawn. MAINTAINED/MODIFIED REJECTIONS Claim Rejections - 35 USC § 103 In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status. The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action: A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made. The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows: 1. Determining the scope and contents of the prior art. 2. Ascertaining the differences between the prior art and the claims at issue. 3. Resolving the level of ordinary skill in the pertinent art. 4. Considering objective evidence present in the application indicating obviousness or nonobviousness. This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention. Claims 2, 4-9, 11, and 13-15 are rejected under 35 U.S.C. 103 as being unpatentable over Hubbell (Hubbell et al., WO 2018/195386, Filing Date: 04/20/2018, of record) in view of Jarvinen (Jarvinen et al., BioMed Research International, Vol 2015, Article ID 654765, Publication Year: 2015, of record), Bleck (Bleck et al., US 2012/0238727 A1, Appl. No.: 13/419,045, Publication Date: 09/20/2012, of record) and Kontermann (Kontermann et al., Archives of Biochemistry and Biophysics, 526 (2012), 194-205, Publication Date: 03/16/2012, of record). Hubbell teaches extracellular matrix (ECM)-affinity peptide ([0005]). In some embodiments, the ECM-affinity peptide comprises a decorin peptide, such as SEQ ID NO: 16 ([0006], [0095]). As shown below, SEQ ID NO: 16 comprises a sequence which is 99.8% identical to SEQ ID NO: 7 of the instant application and comprises amino acids Asp45-Lys359 or Leu155-Val260 of full length decorin: RESULT 13 BFT48908 DE Decorin peptide (17-359), SEQ ID 16. Query Match 99.8%; Score 1712; Length 343; Best Local Similarity 99.7%; Matches 328; Conservative 1; Mismatches 0; Indels 0; Gaps 0; Qy 1 DEAAGIGPEVPDDRDFEPSLGPVCPFRCQCHLRVVQCSDLGLDKVPKDLPPDTTLLDLQN 60 |||:|||||||||||||||||||||||||||||||||||||||||||||||||||||||| Db 15 DEASGIGPEVPDDRDFEPSLGPVCPFRCQCHLRVVQCSDLGLDKVPKDLPPDTTLLDLQN 74 Qy 61 NKITEIKDGDFKNLKNLHALILVNNKISKVSPGAFTPLVKLERLYLSKNQLKELPEKMPK 120 |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||| Db 75 NKITEIKDGDFKNLKNLHALILVNNKISKVSPGAFTPLVKLERLYLSKNQLKELPEKMPK 134 Qy 121 TLQELRAHENEITKVRKVTFNGLNQMIVIELGTNPLKSSGIENGAFQGMKKLSYIRIADT 180 |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||| Db 135 TLQELRAHENEITKVRKVTFNGLNQMIVIELGTNPLKSSGIENGAFQGMKKLSYIRIADT 194 Qy 181 NITSIPQGLPPSLTELHLDGNKISRVDAASLKGLNNLAKLGLSFNSISAVDNGSLANTPH 240 |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||| Db 195 NITSIPQGLPPSLTELHLDGNKISRVDAASLKGLNNLAKLGLSFNSISAVDNGSLANTPH 254 Qy 241 LRELHLDNNKLTRVPGGLAEHKYIQVVYLHNNNISVVGSSDFCPPGHNTKKASYSGVSLF 300 |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||| Db 255 LRELHLDNNKLTRVPGGLAEHKYIQVVYLHNNNISVVGSSDFCPPGHNTKKASYSGVSLF 314 Qy 301 SNPVQYWEIQPSTFRCVYVRSAIQLGNYK 329 ||||||||||||||||||||||||||||| Db 315 SNPVQYWEIQPSTFRCVYVRSAIQLGNYK 343 Thus, the decorin peptide taught by Hubbell comprises the TGF-β domain of claims 7 and 8. Hubbell teaches an ECM-affinity peptide operatively linked to a CTLA4 antibody, or to a PD-L1 antibody, or a PD-1 antibody ([15], claims 1, 50, 51). Hubbell teaches various antibodies can be linked to an ECM-affinity peptide, including Bevacizumab ([0089]), a VEGF antibody as evidenced by paragraph [0100] of the instant publication (US2024/0150452 A1). Hubbell teaches the method making decorin anti-PD-L1 and decorin-anti-CTLA conjugates ([0238] and [0239]), which have enhanced anti-tumor activity ([0073], Fig. 44). As evidenced by [0032], αPD-L1 and αCTLA4 refer to antibodies. Regarding linked to the c-terminal end of a heavy chain of the antibody, Hubbell further teaches that the peptide is covalently linked to the antibody. Linkers such as amino acid sequences may be inserted between the peptide and antibody sequence. In some embodiment, the linker can be joined to a heavy chain immediately after the last amino acid at the C-terminus of the Heavy chain. The length of the linker sequence may vary without significantly affecting the function or activity of the fusion protein ([0007]). Hubbell’s teachings are set forth above. However, Hubbell does not teach decorin comprises a mutation such as serine to alanine at position 4, or decorin lacks modification by glycosaminoglycans molecules at position 4, or explicitly teach that the decorin molecule is linked to the c-terminal end of a heavy chain of the antibody. Jarvinen teaches that decorin (DCN) is the best characterized member of the small leucine-rich proteoglycan (SLRP) family of extracellular matrix (ECM) proteins (introduction). Jarvinen teaches that DCN influences various cellular functions such as proliferation, spreading, migration, and differentiation, and inflammation (Introduction). Jarvinen teaches that mammalian DCN contains a 42 kDa protein core and a single glycosaminoglycan (GAG) chain, attached to a serine residue near the N terminus (Introduction). Jarvinen teaches that DCN has an antiangiogenic effect on tumor angiogenesis (page 4 § 7. DCN in angiogenesis). Jarvinen teaches that administration of DCN can inhibit tumor growth and progression in vivo, including lung, colon, squamous cell carcinomas, prostate and pancreatic cancer (pages 4-5 § 8 DCN as a Therapeutic anticancer drug in vivo). Jarvinen teaches that most of the anticancer effects of DCN have been generated with recombinant DCN with no GAG attached to it, and most of the interactions DCN has with growth factors or their receptors are through direct binding to the DCN core protein (page 5 § 10 Limitations of DCN). Jarvinen teaches that the GAGs attached to a serine residue at position 4 of DCN, and it is possible to produce recombinant DCN without GAG attached to it by simply mutating the serine residue critical for the GAG attachment, which can simplify production process for recombinant DCN protein (pages 6-7 bridging paragraph). Jarvinen teaches that DCN fusion protein can be produced through recombinant technology (page 7, § 11 Recombinant DCN variant with enhanced biological activity). Bleck teaches decorin protein comprises a mutation at position 4 of the mature decorin core protein (claim 5), wherein the mutation is a serine to alanine mutation (claim 6). Bleck teaches that a serine to alanine modification was made at amino acid 4 of mature decorin. The mutation prevents a GAG from being attached to the decorin molecule (Example 1, [0048]). Kontermann teaches various formats to linker a peptide (various cytokines) to antibody, including linked to C-terminal of heavy chains (see Fig. 2(b) and Fig. 3). It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to make a protein molecule comprising at least one decorin molecule having at least 95% sequence identity to SEQ ID NO: 7 linked to an anti-VEGF antibody as taught by Hubbell, and to link to the c-terminal end of a heavy chain of an antibody through a linker because it is a well-known and easily-implemented strategy to link a peptide to antibody as taught by Hubbell and Kontermann, and to substitute wild-type decorin with a decorin variant with a mutation at position 4 and lacking modification by GAG at position 4 as taught by Jarvinen, and to further pick a mutation as a serine to alanine mutation as taught by Bleck, because Jarvinen teaches most of the anticancer effects of DCN have been generated with recombinant DCN with no GAG attached to it, and the GAGs attached to a serine residue at position 4 of DCN, and it is possible to produce recombinant DCN without GAG attached to it by simply mutating the serine residue critical for the GAG attachment, which can simplify production process for recombinant DCN protein, and Bleck teaches decorin with the mutation (S4A) prevents modification by glycosaminoglycans molecules at position 4 of the mature decorin core protein. One of ordinary skill in the art would have reasonable expectation of success to reach the claimed invention, given that all components and methods of heavy chain C-terminal fusion are well known and widely used in the art as evidenced by Hubbell, Kontermann and Jarvinen. The motivation is to make more potent and effective anti-cancer agent with a well-tested strategy. Regarding claims 6 and 9, the format (Fig. 2(b) taught by Kontermann would comprise two copies of the decorin molecules. Regarding claim 11, Hubbell teaches recombinant fusion of decorin with the antibodies ([0224], [0229]). In some embodiments, nucleotides encoding for an ECM-affinity polypeptide and/or an ECM-affinity polypeptide fused to antibody heavy or light chain ([0102]). Regarding claim 13-15, Hubbell teaches a nucleotide encoding the ECM-affinity polypeptide fused to the antibody ([0102]); vector comprises the nucleotide ([0110]); and host cells and expression system (pages 34 and 35). Response to Arguments For the rejection of claims 2, 4-9, 11 and 13-15 under 35 U.S.C. 103, Applicant argues: Hubbell does not teach attachments of decorin ( or indeed any of the disclosed ECM affinity peptides) to the C terminal end of the heavy chain of the antibody with a peptide linker. Instead, the cited paragraph from Hubbell teaches attachment of fynomer domain at the Nor C terminal: In an embodiment, a fynomer domain is joined to a Heavy (H) chain or Light (L) chain immediately after the last amino acid at the amino( H2)-terminus or the carboxy(C)-terminus of the Heavy (H) chain or the Light (L) chain. A fynomer domain is not decorin (or an ECM affinity peptide) and instead is a small protein derived from the human Fyn SH3 domain. This is the sole mention of fynomer domains in Hubbell and the only reference to attachment of any peptide or protein at the C terminal end of the heavy chain. Applicant first argues that Hubbell only teaches fynomer domain attached at the C-terminus of heavy chain or light chain. Applicant’s arguments have been fully considered but they are not persuasive. Contrary to applicant’s arguments, Hubbell’s teachings are not limited to fynomers. Hubbell clearly teaches that the peptide (including decorin) can be covalently linked to the antibody. Linkers such as amino acid sequences may be inserted between the peptide and antibody sequence. In some embodiment, the linker can be joined to a heavy chain immediately after the last amino acid at the C-terminus of the Heavy chain. The length of the linker sequence may vary without significantly affecting the function or activity of the fusion protein ([0005]-[0007]). In addition, Kontermann teaches various formats to linker a peptide (various cytokines) to antibody, including linked to C-terminal of heavy chains (see Fig. 2(b) and Fig. 3). Thus, as set forth above, one of ordinary skill in the art would link a decorin molecule to the c-terminal end of a heavy chain of an antibody through a linker because it is a well-known and easily-implemented strategy to link a peptide to antibody as taught by Hubbell and Kontermann. Applicant further argues: There is no teaching in Hubbell that decorin can be attached to the C terminal of the heavy chain and that such attachment would provide a functional decorin activity. This directly undermines the Examiner's argument that Hubbell and Konterman establish that decorin would have activity when linked to the C terminal end of the heavy chain of the antibody. As admitted by the Examiner in a previous office action "Based on teachings from Bowie and Bork, the positions of linkage and the method of linkage between decorin and antibody/functional fragment thereof could impact the function of the protein molecules. Consequently, the effects of a decorin (and its linked to an antibody or functional fragment cannot be predicted." Paragraph [0007] of Hubbell as cited by the Examiner does not teach or suggest that decorin (or any ECM matrix peptide) can be attached the C terminal end of the heavy chain of an antibody. Thus, there is no reasonable expectation of success. Applicant further argues that one of ordinary skill would not have had a reasonable expectation of success. In particular, Applicant cited previous Office Action to argue the unpredictability. Applicant’s arguments have been fully considered but they are not persuasive. Based on the teachings from Bowie and Bork (see 112(a) of Office Action 09/17/2024), one of ordinary skill in the art would not randomly insert or connect a decorin at a random position of antibody, because this could impact function of the antibody and/or decorin. The 112(a) rejection was withdrawn in view of the claim amendments of 01/30/2025, in which claim 1 recites “wherein the decorin molecule is linked to the c-terminal end of a heavy chain of the antibody”. Thus, contrary to applicant’s arguments, the statement in the previous Office Action does not “directly undermines the Examiner's argument that Hubbell and Konterman establish that decorin would have activity when linked to the C terminal end of the heavy chain of the antibody”. As set forth above, Kontermann explicitly describes the format for peptide-antibody fusion, through a peptide linker at the c-terminal of heavy chain. Thus, this is not linking a decorin to antibody to a random position of an antibody. Instead, as evidenced by Hubbell and Kontermann, the antibody-peptide fusion at the C-terminal end of heavy chain of an antibody has been widely used in the art, thus one of skilled in the art would have had a reasonable expectation that a decorin fused to c-terminal of heavy chains of an antibody would generate a protein molecule with better properties as set forth above. In addition, in the field of biological technology, no invention has absolute certainty of success before experimental tests. Thus, only a reasonable expectation of success (not absolute) would have motivated an artisan to make the claimed fusion protein. Given the teachings from references, an ordinary skilled in the art would have would have had a reasonable expectation of success in producing the claimed invention. Conclusion No claims are allowed. 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 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 CHENG LU whose telephone number is (571)272-0334. The examiner can normally be reached Monday-Friday 8-5. 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, Samira Jean-Louis can be reached at (571)270-3503. 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. /CHENG LU/ Examiner, Art Unit 1642 /SAMIRA J JEAN-LOUIS/ Supervisory Patent Examiner, Art Unit 1642
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Prosecution Timeline

Dec 07, 2023
Application Filed
May 07, 2024
Response after Non-Final Action
Oct 25, 2024
Non-Final Rejection — §103
Jan 30, 2025
Response Filed
Apr 08, 2025
Final Rejection — §103
Jul 09, 2025
Request for Continued Examination
Jul 15, 2025
Response after Non-Final Action
Aug 25, 2025
Non-Final Rejection — §103
Nov 25, 2025
Response Filed
Jan 27, 2026
Final Rejection — §103 (current)

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Prosecution Projections

5-6
Expected OA Rounds
55%
Grant Probability
99%
With Interview (+67.0%)
3y 5m
Median Time to Grant
High
PTA Risk
Based on 202 resolved cases by this examiner. Grant probability derived from career allow rate.

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