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 .
Status of Application/Amendments/Claims
Applicant’s response filed on 6/9/2026 has been considered. Claims 16 and 21 have been amended. Claims 34-42 have been newly added. Claims 25-33 have been canceled. Claims 16-25 and 34-42 are pending. Claims 17-20, 23-25 and 35-42 are currently withdrawn from further consideration pursuant to 37 CFR 1.142 (b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Claim 16, 21-22 and 34 are the subject of the present Official action. The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Priority
Applicant’s claim for the benefit of a prior-filed application JP 2020-179947 and 371 of PCT/JP2021/039717 filed on 10/27/2020 and 10/27/2021, respectively, under 35 U.S.C 119(e) or under 35 U.S.C 120, 121 or 365(c) is acknowledged.
Accordingly, the effective priority date of the instant application is granted as 10/27/2020.
Withdrawn Claim Rejections
The 35 U.S.C. 103 rejection of claims 16, 21-22 and 25 over Mykles in view of Munkley as evidenced by Cell signaling technology has been withdrawn and reapplied in modified form to address applicants claim amendments which describes the inhibition of a mTOR pathway growth related gene.
Reply to Applicants Arguments
Although the rejection is newly applied in modified form, some of applicant’s arguments are relevant and are addressed below.
Applicant argues that the Examiner has confused TSC2A and TSC, since TSC2A is an isoform of TSC2 which acts to promote cell proliferation and is the opposite function to that of TSC2. Applicant argues that it cannot be said to suggest that inhibiting the expression of TSC2a or TSC2 would promote the growth of the body of a Decapod.
This argument has been fully considered, however, Mykles identifies TSC1/2 as known inhibitors of mTOR and cellular growth in crustaceans and states that “signaling pathways that stimulate cellular growth such as…inhibition of TSC1/2” (Mykles, pg 5 col 2 and Table 2). Furthermore, in the obviousness rejection, the Examiner expressly describes “TSC2” and not “TSC2a” in the statement of obviousness, which is repeated here. It would have been prima facie obvious to one of ordinary skill in the art to inhibit the function of TSC2 using a siRNA as described by Munkley in the methods for controlling crustacean molting and growth described by Mykles. It would have been a matter of combining prior art elements according to known methods to yield predictable results since Munkley provides a mechanism for selectively inhibiting TSC2 using siRNAs to activate cell growth.
Applicant further argues that the study of Munkley was conducted in human cultured cells which cannot be generalized to decapods since they are phylogenetically distinct and have diverged over millions of years.
This argument has been fully considered, however, Caban shows that “TSC1 and TSC2 are widely expressed across cell types and organ systems and there is high interspecies sequence conservation of these genes and proteins from Drosophila to humans” (Canba, pg 3 col 1). Thus, TSC2 is a highly conserved gene and one would have a reasonable expectation of success given that there are numerous commercial suppliers for siRNAs targeting TSC2 which offers a selective approach towards mTOR upregulation as a mechanism to promote crustacean growth.
Claim Interpretation
With respect to the “optionally” language recited in claim 16, it is emphasized that claim scope is not limited by claim language that suggests or makes optional but does not require steps to be performed, or by claim language that does not limit a claim to a particular structure, see MPEP 2111.04.
Furthermore, applicant has elected TSC2 as the single specific combination of growth-related genes.
New 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 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.
Claims 16, 21-22 and 34 are rejected under modified form under 35 U.S.C. 103 as being unpatentable over Mykles et al. "Hormonal control of the crustacean molting gland: Insights from transcriptomics and proteomics." General and Comparative Endocrinology 294 (2020): 113493 (hereinafter Mykles, reference of record) in view of Munkley et al. "A novel androgen-regulated isoform of the TSC2 tumour suppressor gene increases cell proliferation." Oncotarget 5.1 (2013): 131 (hereinafter Munkley, reference of record) as evidenced by Cell signaling technology. SignalSilence. Way Back Machine. 11/21/2015 and Caban et al. "Genetics of tuberous sclerosis complex: implications for clinical practice." The application of clinical genetics (2016): 1-8 (hereinafter Caban). This is a new rejection necessitated by amendment of the claims in the responses filed 6/9/2026.
Claims 16 and 21-22: Mykles describes the hormonal controls of crustacean molting and growth by examining the mechanisms of mTOR signaling (Mykles, abstract and Fig 1). Mykles discloses experiments using rapamycine to down-regulate mTOR signaling genes (Mykles, abstract and Fig 1). Mykles identifies TSC1/2 as known inhibitors of mTOR and cellular growth in crustaceans and states that “signaling pathways that stimulate cellular growth such as…inhibition of TSC1/2” (Mykles, pg 5 col 2 and Table 2). Although Mykles discloses TSC2 as a growth-related gene which inhibits mTOR signaling and thus acts to limit crustacean molting and growth, Mykles does not expressly disclose a method for inhibiting the function of TSC2 via RNA interference to promote crustacean growth.
Claims 16 and 21-22: Similar to Mykles, Munkley describes TSC2 as an important tumor suppressor gene which complexes with TSC1 to block the ability of Rheb GTPase to activate mTOR (Munkley, abstract, mechanism of action provided below as in Fig 4). Although Munkley describes this mechanism in mammalian cells, Caban shows that “TSC1 and TSC2 are widely expressed across cell types and organ systems and there is high interspecies sequence conservation of these genes and proteins from Drosophila to humans” (Canba, pg 3 col 1).
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Claim 34: Munkley discloses several approaches to knockdown TSC2 using siRNAs (Ambion S14437). Munkley was able to successfully inhibit TSC2 using siRNAs to activate cell growth (Munkley, pg 136). Furthermore, numerous other commercial providers like cell signaling technology supply siRNAs targeting TSC2 as evidenced by SignalSilence.
It would have been prima facie obvious to one of ordinary skill in the art to inhibit the function of TSC2 using a siRNA as described by Munkley in the methods for controlling crustacean molting and growth described by Mykles. It would have been a matter of combining prior art elements according to known methods to yield predictable results since Munkley provides a mechanism for selectively inhibiting TSC2 using siRNAs to activate cell growth. In particular, one of ordinary skill would be motivated to knockdown the highly conserved TSC2 and increase mTOR to accelerate growth and molting in decapod crustaceans for improved aquaculture. One would have a reasonable expectation of success given that there are numerous commercial suppliers for siRNAs targeting TSC2 which offers a selective approach towards mTOR upregulation. Accordingly, in the absence of evidence to the contrary, one of ordinary skill in the art would have considered the claimed invention to have been prima facie obvious to at the time the invention was made.
Conclusion
No claims 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 extension fee 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.
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Alexander Nicol
Patent Examiner
Art Unit 1634
/ALEXANDER W NICOL/Examiner, Art Unit 1634
/FEREYDOUN G SAJJADI/Supervisory Patent Examiner, Art Unit 1699
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