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 .
Claim Status
1. Claims 1, 5-6, 8-12, 14-15, and 21-26 are pending and under examination on the merits.
Claims 2-4, 7, 13, and 16-20 are cancelled.
Information Disclosure Statement
2. The Office reiterates that the listing of references in the specification (see pp. 107-112) is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered.
Response to Arguments – Claim Objections
3. Applicant’s amendments filed March 03, 2026 have overcome the objections of record. However, said amendments have introduced new grounds for objection.
Claim Objections
4. Claims 1, 5-6, 8-12, and 14-15 are objected to because of the following:
Claim 1, ln. 7 contains a typographical error. It is recommended, “KTI 1 polypeptide” be amended to “KTI1 polypeptide”, if appropriate.
Regarding the recitation of “the KTI 1 polypeptide” in ln. 7; no “KTI1 polypeptide” is recited prior to this recitation. If Applicant intends to recite a KTI1 polypeptide encoded by the modified KTI1 gene of ln. 6, it is suggested Applicant amend “the KTI 1 polypeptide” to “the KTI1 polypeptide encoded therein” to further clarify the antecedent basis of the recitation.
Dependent claims are included.
Appropriate correction is required.
Response to Arguments – Claim Rejections - 35 USC § 112(b)
5. Applicant’s arguments and amendments filed March 03, 2026 have overcome the rejections of record.
Response to Arguments – Claim Rejections - 35 USC § 112(d)
6. Applicant’s arguments and amendments filed March 03, 2026 have overcome the rejections of record.
Response to Arguments – Claim Rejections - 35 USC § 103
7. Applicant’s amendments filed March 03, 2026 have been carefully considered, but they are not persuasive and do not overcome the rejections of record.
In traversing the rejection, Applicant argues primarily that Gillman does not disclose, teach, or suggest defined C-terminal deletions in KTI1 (pp. 02-08), Gillman does not teach or suggest retaining or producing a truncated KTI1 polypeptide (p. 04), NM_00125776.3 does not teach or suggest the claimed KTI1 deletion (pp. 04-05), the cited art does not teach or suggest replacing a null KTI1 allele with a defined C-terminal deletion or that they would be equivalents (pp. 05-06), the cited art does not establish prima facie equivalence between the claimed KTI1 deletion and Gilmman’s KTI1 mutation (p. 06), and the cited art does not provide a motivation or reasonable expectation of success for the claimed KTI1 modification (p. 06).
Applicant’s argument has been carefully considered but is not persuasive. Though Gillman is silent with regard to 60bp deletions within the KTI1 gene, wherein said deletion results in a protein with a truncated C-terminus, Applicant has provided no evidence or assertion that such a deletion and/or polypeptide would provide any surprising or unexpected results in comparison to the kti1 loss-of-function mutation taught by Gillman. In fact, Applicant’s own disclosure describes introducing a 60bp deletion within the 3’ half of the KTI1 gene as knocking out the gene[0245-0246] and indicates that said knockout results in a loss of trypsin inhibitor activity[0258], which is identical to the phenotype disclosed in the kti1 loss-of-function mutant taught by Gillman (see rejection of claims under 35 U.S.C. 103, below). Though Applicant appears to argue that the claimed invention is nonobvious in view of the cited art because the claimed invention results in the production of a truncated protein, Applicant has provided no evidence or assertion that such a protein results in any surprising or unexpected results in comparison to kti1 null alleles known in the art. See MPEP 2183. Thus, the claims remain unpatentable over Gillman et al. (Journal of Agricultural and Food Chemistry. 2015; 63(5):1352-1359 (previously cited)), in view of NCBI Reference Sequence: NM_001250776.3 (NCBI. 2017 (previously cited)), and further in view of NCBI Reference Sequence: NM_001251682.2 (NCBI. 12 Mar 2022 (previously cited)).
Claim Rejections - 35 USC § 103
8. 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.
9. Claims 1, 5-6, 8-12, 14-15 and 21-26 are rejected under 35 U.S.C. 103 as being unpatentable over Gillman et al. (Journal of Agricultural and Food Chemistry. 2015; 63(5):1352-1359 (previously cited)), in view of NCBI Reference Sequence: NM_001250776.3 (NCBI. 2017 (previously cited)), and further in view of NCBI Reference Sequence: NM_001251682.2 (NCBI. 12 Mar 2022 (previously cited)) and Applicant’s admitted state of the art.
Regarding claim 1, Gillman teaches the role in trypsin inhibitor genes in limiting the digestibility of raw soybeans (Abstract); that heating the soybean inactivates the inhibitors, is costly, and reduces the nutritional value of the soybeans (Abstract); and an engineered soybean plant comprising two mutant KTI genes thereby reducing or eliminating the expression of, amount of, and/or activity of the two or more mutant KTI genes and/or gene products as compared to a wild-type or conventionally cultivated soybean/soybean plant therefrom, wherein the two or more mutant KTI genes comprises a mutant KTI1 gene and a mutant KTI3 gene each comprising a frameshift mutation which truncates and lowers protein amount and/or activity of the genes and/or products encoded therein (Abstract; p. 1353, left column, first full paragraph; p. 1353, left column, “Population Development”; p. 1354, left column, “Determination of Molecular Genetic Basis for Reduced KTi Levels in PI 68679.”; p. 1354, Figure 1 and Figure 2).
Gillman is silent to the sequences of KTI1 and KTI3 and to a deletion of at least 60bp with a region of the KTI1 gene encoding the C-terminal portion of the KTI1 polypeptide.
NCBI Reference Sequence: NM_001250776.3 teaches a KTI1 gene comprising an upstream in-frame stop codon (p. 01, “misc_feature”).
NCBI Reference Sequence: NM_001251682.2 teaches a soybean KTI3 sequence identical to Applicant’s SEQ ID NO:3, from which Applicant’s SEQ ID NOs:6-9 and 49 are obtained[0250].
The level of ordinary skill in the plant biotechnology arts is high as evidenced by Gillman. In view of the teachings of Gillman, NCBI Reference Sequence: NM_001250776.3, and NCBI Reference Sequence: NM_001251682.2 it would have been prima facie obvious for one of ordinary skill in the art to engineer a soybean plant comprising loss-of-function mutations in the KTI1 and KTI3 gene sequences. One of ordinary skill in the art would have been motivated to do so because Gillman teaches that soybean accession PI 157740 comprises a frameshift mutation in its KTI3 gene and demonstrates a 40% reduction in trypsin inhibitor activity and an increase in raw digestibility (p. 1353, left column, first full paragraph); soybean accession PI 68679 comprises a frameshift mutation in its KTI1 gene and demonstrates a reduction in both KTI1 and KTI3 protein content (p. 1354, left column, second full paragraph; p. 1354, Figure 1 and Figure 2); and soybean plants comprising both KTI1 and KTI3 frameshift mutations show a greater decrease in trypsin inhibitor activity than plants comprising either mutation alone (p. 1355, “Trypsin and Chymotrypsin Activities in Seed of Mutant Lines.”). Though Gillman is silent to a deletion of at least 60bp with a region of the KTI1 gene encoding the C-terminal portion of the KTI1 polypeptide, such a KTI1 polypeptide comprising a C-terminal truncation provides no surprising or unexpected effect or result in comparison to the kti1 loss-of-function allele taught by Gillman. Applicant has provided no evidence or assertion that such a deletion and/or polypeptide would provide any surprising or unexpected results in comparison to the kti1 loss-of-function mutation taught by Gillman. The mutation in the KTI1 gene in Gillman resulted in a truncated transcript being expressed and a reduced trypsin inhibitor activity in the plant. It was therefore obvious to those of ordinary skill in the prior art that abolishing KTI1 protein activity by causing deletions in the KTI1 gene coding region, including in the region encoding the C-terminal portion, would also result in expression of a truncated transcript and reduced trypsin inhibitor activity in the plant as well. Absent any evidence and assertion to the contrary, the claimed kti1 loss-of-function alleles are prima facie equivalent to the kti1 loss-of-function allele taught by Gillman. Furthermore, methods for introducing mutations into a targeted gene are both routine and well-known in the art as discussed by Applicant[0153]. Given the global economic importance of soybeans, one of ordinary skill in the art would be motivated to develop soybean with increased raw digestibility to reduce the production costs and increase the nutritional value of food and feed products made from soybean. Accordingly, one of ordinary skill in the art would have been motivated to produce the claimed invention with a reasonable expectation of success and without any surprising results.
Regarding claim 5, the teachings of Gillman are as discussed above. Applicant’s SEQ ID NO:5 comprises a kti1 loss-of-function allele resulting in a truncated KTI1 polypeptide that lacks trypsin inhibitor activity[0258]. Applicant has provided no evidence supporting any surprising or unexpected function, activity, or benefit of such a truncated polypeptide; furthermore, Applicant indicates the allele encoding the truncated polypeptide is simply a loss-of-function mutation[0245-0246]. Accordingly, a kti1 loss-of-function allele comprising SEQ ID NO:5 would provide no surprising or unexpected results when compared to the teachings of Gillman in view of NCBI Reference Sequence: NM_001250776.3.
Regarding claim 6, the teachings of Gillman are as discussed above. Applicant’s SEQ ID NOs:6-9 and 49 comprise kti3 loss-of-function alleles. Applicant has provided no evidence supporting any surprising or unexpected function, activity, or benefit of the truncated polypeptide. Accordingly, a kti3 loss-of-function allele comprising SEQ ID NOs:6-9 or 49 would provide no surprising or unexpected results in view of the teachings of Gillman.
Regarding claim 8, in addition to the teachings discussed above, Gillman teaches crossing KTI1- soybean lines with KTI3- soybean lines (p. 1353, left column, “Population Development”). Because the F1 offspring of the above crossings will comprise a copy of each KTI allele inherited from either parent, Gillman teaches an engineered soybean/soybean plant wherein the soybean/soybean plant is heterozygous for two or more mutant KTI genes.
Regarding claim 9, in addition to the teachings discussed above, Gillman teaches an engineered soybean/soybean plant wherein the soybean/soybean plant is homozygous for two or more mutant KTI genes (p. 1354, right column, “Proteomic Investigations of Mutant Lines Bearing KTi- Mutations.”).
Regarding claim 10, in addition to the teachings discussed above, Gillman teaches a soybean/soybean plant wherein the plant lacks any KTI protein (p. 1354, right column, “Proteomic Investigations of Mutant Lines Bearing KTi- Mutations.”; p. 1355, Figure 4). Therefore, Gillman teaches a soybean/soybean plant wherein the expression of, amount of, and/or activity of the one or more modified KTI genes and/or gene products is reduced 0.1-1000-fold or more.
Regarding claim 11, in addition to the teachings discussed above, Gillman teaches a soybean/soybean plant wherein the plant has reduced trypsin inhibitor amount and/or activity as compared to a control (Abstract; p. 1354, right column, “Proteomic Investigations of Mutant Lines Bearing KTi- Mutations.; p. 1355, Figure 4).
Regarding claim 12, in addition to the teachings discussed above, Gillman teaches a method of growing, harvesting, or otherwise cultivating an engineered soybean/soybean plant (p. 133, left column, “Population Development”).
Regarding claim 14, in addition to the teachings discussed above, Gillman suggests a feed/food product comprising a soybean/soybean plant comprising reduced trypsin inhibitor activity (Abstract; p. 1352, left column, first and second full paragraphs; p. 1358, left column, first full paragraph).
Regarding claim 15, in addition to the teachings discussed above, Gillman suggests feeding a feed/food product comprising a soybean/soybean plant comprising reduced trypsin inhibitor activity to a human or non-human animal (Abstract; p. 1352, left column, first and second full paragraphs; p. 1358, left column, first full paragraph).
Regarding claim 21, in addition to the teachings discussed above, Gillman teaches a soybean plant comprising a mutant KTI3 gene thereby reducing or eliminating the expression of, amount of, and/or activity of the mutant KTI3 genes and/or gene products as compared to a wild-type or conventionally cultivated soybean/soybean plant therefrom, wherein the mutant KTI3 gene comprises a frameshift mutation which truncates and lowers protein amount and/or activity of the gene and/or product encoded therein (Abstract; p. 1353, left column, first full paragraph; p. 1353, left column, “Population Development”; p. 1354, left column, “Determination of Molecular Genetic Basis for Reduced KTi Levels in PI 68679.”; p. 1354, Figure 1 and Figure 2).
Regarding claim 22, in addition to the teachings discussed above, Gillman also teaches soybean plant comprising a mutant KTI1 gene and a mutant KTI3 gene (Abstract; p. 1353, left column, first full paragraph; p. 1353, left column, “Population Development”; p. 1354, left column, “Determination of Molecular Genetic Basis for Reduced KTi Levels in PI 68679.”; p. 1354, Figure 1 and Figure 2).
Regarding claim 23, as discussed above in the rejection of claim 8 under 35 U.S.C. 103, Gillman teaches an engineered soybean/soybean plant wherein the soybean/soybean plant is heterozygous for a mutant KTI3 gene (p. 1353, left column, “Population Development”).
Regarding claim 24, in addition to the teachings discussed above, Gillman teaches a soybean/soybean plant comprising a frameshift mutation in KTI3 that results in a 40% reduction in trypsin inhibitor activity and a soybean/soybean plant wherein the plant lacks any KTI protein (p. 1353, left column, first full paragraph; p. 1354, right column, “Proteomic Investigations of Mutant Lines Bearing KTi- Mutations.”; p. 1355, Figure 4). Therefore, Gillman teaches a soybean/soybean plant wherein the expression of, amount of, and/or activity of KTI3 and/or its gene products is reduced 0.1-1000-fold or more.
Regarding claim 25, in addition to the teachings discussed above, Gillman teaches a soybean/soybean plant wherein the plant has reduced trypsin inhibitor amount and/or activity as compared to a control (Abstract; p. 1354, right column, “Proteomic Investigations of Mutant Lines Bearing KTi- Mutations.; p. 1355, Figure 4).
Regarding claim 26, in addition to the teachings discussed above, Gillman suggests a feed/food product comprising a soybean/soybean plant comprising reduced trypsin inhibitor activity (Abstract; p. 1352, left column, first and second full paragraphs; p. 1358, left column, first full paragraph).
Accordingly, one of ordinary skill in the art would have been motivated to produce the claimed invention with a reasonable expectation of success and without any surprising results.
Conclusion
10. No claim is 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.
Examiner’s Contact Information
11. Any inquiry concerning this communication or earlier communications from the examiner should be directed to DEQUANTARIUS J SPEED whose telephone number is (703)756-4779. The examiner can normally be reached M-F; 9AM-5PM ET.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Amjad Abraham can be reached on (571)-270-7058. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/DEQUANTARIUS JAVON SPEED/Junior Examiner, Art Unit 1663
/Amjad Abraham/SPE, Art Unit 1663
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