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 .
Application Status
This action is written in response to applicant’s correspondence received 29 July 2026. Claims 1, 3-4, 6-9, 18, 20-23, 33-40, 43, and 46 are currently pending. Claims 1, 3-4, 6-9, 18, and 37-40 are withdrawn from prosecution as being drawn to non-elected subject matter. Accordingly, claims 20-23, 33-36, 43, and 46 are examined herein. The restriction requirement mailed 11 December 2025 is still deemed proper. Applicant's elected Group II with traverse in the reply filed 10 March 2026.
Any rejection or objection not reiterated herein has been overcome by amendment.
Applicant' s amendments have been thoroughly reviewed, but are not persuasive to place the
claims in condition for allowance for the reasons that follow. Because the newly recited rejection under 35 USC 112(b) was not necessitated by amendment, this action is NON-FINAL.
Claim Rejections - 35 USC § 112
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.
Claims 20-23, 33-36, 43, and 46 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.
Regarding claim 20, the claim recites the limitations "the respective wild type exon nucleotide sequence" in lines 13-14 of the claim, “the 5’ exon sequence” in line 15 of the claim, and “the 3’ exon sequence” in line 16 of the claim. There is insufficient antecedent basis for these limitation in the claim. It is unclear if the claimed “5’ exon sequence” and “3’ exon sequence” are the same or different exonic sequences when compared to the previously claimed “5’ exon nucleotide sequence” and the previously claimed “3’ exon nucleotide sequence”. It is also unclear if the claimed “wild type exon nucleotide sequence” is referring to the previously claimed “5’ exon nucleotide sequence” and the previously claimed “3’ exon nucleotide sequence”.
Additionally, it is unclear if the claimed 5’ and 3’ exon nucleotide sequences in part (iii) are limited to the claimed SEQ ID NOs: 5-6 or if they are not because there is a mutational wherein clause that relates to the claimed exon nucleotide sequences. It is unclear if the exon itself is to be limited to the claimed sequences (i.e., the 5’ and 3’ exon nucleotide sequences are intended to consist of the claimed SEQ ID NOs) or if the 5’ and 3’ exon nucleotide sequences may just comprise the claimed SEQ ID NOs within any position of the polynucleotide, so long as they are 5’ and 3’ from the self-splicing intron. It is unclear if the claimed “5’ exon sequence” and the claimed “3’ exon sequence” in lines 15-16 of the claim are intended to limit the claimed “5’ exon nucleotide sequence” and the claimed “3’ exon nucleotide sequence” or if the phrases are referring to different sequences within the exonic nucleotide sequences.
Regarding claims 22-23, 33-36, 43, and 46, as the claims are ultimately dependent on claim 20 and do not rectify the outstanding 35 USC 112(b) rejection above, the claims are also rejected under 35 USC 112(b).
Closest Prior Art
Regarding claim 20, the closest prior art is Thompson ( "Group I aptazymes as genetic regulatory switches." BMC biotechnology 2.1 (2002): 21) and Pichler ("Folding problems of the 5′ splice site containing the P1 stem of the group I thymidylate synthase intron: substrate binding inhibition in vitro and mis-splicing in vivo." Journal of Biological Chemistry 277.20 (2002): 17987-17993).
Regarding claim 20, Thompson is drawn towards a study concerned with the control of gene expression through the use of self-splicing introns (Abstract). Regarding the isolated polynucleotide, Thompson teaches the use of a plasmid construct (i.e., a polynucleotide) that was transformed into cells (i.e., the plasmid is isolated polynucleotides prior to the transformation (page 10, column 2, paragraph 5), the construct comprising a polynucleotide sequence encoding (ii) a thymidylate synthase gene (i.e. a polynucleotide sequence encoding an ROI), wherein (b) the polynucleotide sequence is interrupted by an intron that is self-splicing (i.e., the self-splicing intron is located within the polynucleotide portion encoding the ROI) (page 5, column 1, last paragraph), and whose splicing activity is under the control of an aptamer, wherein the aptamer has binding affinity for theophylline (i.e. an inducer) (see Figure 2). Regarding part (i), Thompson teaches that upon induction with theophylline, the cells were able to express the thymidylate synthase gene following the self-splicing of the inserted intron and grow in media (pg. 5, column 1, last paragraph to column 2, first paragraph). Regarding part (iii), Thompson teaches that the intron interrupts the thymidylate synthase gene (page 5, column 1, last paragraph).
Pichler is drawn towards a study concerned with the mutational analysis of splice sites of a thymidylate synthase gene (pg. 17987; see Abstract). Pichler teaches that a P1 motif upstream of the splice site of the thymidylate synthase gene can be mutated to either stabilize or destabilize the splice site in order to induce more splicing activity in both cases, while P2 motif mutations were not tolerated (pg. 17990-17991). Pichler also teaches that the wildtype P1 sequence is suboptimal for inducing splicing activity within the thymidylate synthase gene (pg. 17991). Thus, Pichler provides evidence that some base pairs upstream of the thymidylate synthase gene are tolerant to mutations.
However, neither Thompson nor Pichler teach or suggest that the 5’ exon sequence is TTBYBDGGT or that the 3’ exon sequence is CTH as currently claimed (see Claim 20).
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to KYLE T REGA whose telephone number is (571)272-2073. The examiner can normally be reached Mon-Fri, 9AM-5PM (EDT/EST).
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/KYLE T REGA/Examiner, Art Unit 1636
/NEIL P HAMMELL/Supervisory Patent Examiner, Art Unit 1636
