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 .
Election/Restrictions
Applicant’s election with traverse of Group I (Claims 1, 3, 7, 10, and 16; drawn to a modified U1 snRNA) in the reply filed on March 31, 2025, is acknowledged.
Claims 19-21, 27, 31, 39-40, 42-43, 51-52, 57-59, 61, and 63-64 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention (Groups II-IV), there being no allowable generic or linking claim.
DETAILED ACTION
The amended claims filed on August 14, 2026, have been acknowledged. Claims 2, 4-6, 8-9. 11-15, 17-18, 22-26, 28-30, 32-38, 41, 44-50, 53-56, 60, and 62 were cancelled. Claims 1 and 16 were amended. In light of the Applicant’s elected invention, claims 19-27, 31, 39-40, 42-43, 51-52, 57-59, 61, and 63-64 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Claims 1, 3, 7, 10, and 16 are pending and examined on the merits.
Priority
The applicant claims foreign priority from GB1910518.8 filed on July 23, 2019. Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55, received January 22, 2022. Claims 1, 3, 7, 10, and 16 find support in foreign application GB1910518.8 filed on July 23, 2019.
Information Disclosure Statement
The information disclosure statement (IDS) filed on August 14, 2026, has been considered.
Claim Rejections - 35 USC § 112
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.
Claims 1, 3, 7, 10, and 16 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. This is a new rejection that is substantially similar to a previous rejection of record made in response to Applicant’s amendments to claim 1. Any aspect of Applicant’s traversal that is relevant to the rejection as newly written is addressed below.
Claim 1 recites the following claim language, “A modified U1A snRNA, wherein said modified U1A snRNA comprises a heterologous sequence of 10-25 nucleotides and an Sm protein binding site, wherein the heterologous sequence is located within the native splice donor annealing sequence of U1A snRNA, and wherein the heterologous sequence comprises at least 10 nucleotides of complementarity to a target sequence within the packaging region of a lentiviral vector genome sequence, wherein the target sequence is located in the PBS element, stem loop (SL) 1 element, SL2 element, SL3W element, SL4 element, gag sequence, or an overlapping region thereof of the packaging region, wherein binding of the modified U1A snRNA to the packaging region is capable of increasing lentiviral vector titer during lentiviral vector production relative to lentiviral vector production in the absence of the modified U1A snRNA; and wherein the lentiviral vector is derived from a human lentivirus.”
The broadest reasonable interpretation is that any modified U1A snRNA comprising an Sm protein binding site with a 10-25 nucleotide heterologous sequence located within the native splice donor annealing sequence with at least 10 nucleotides of complementarity to a target sequence within the packaging region of any human lentiviral vector genome sequence (including additional mutations in other regions of the U1A snRNA sequence) is capable of increasing lentiviral vector titer during any lentiviral vector production method relative to any lentiviral vector production method in the absence of the modified U1A snRNA. As applicant has not specified the relative production method, the broadest reasonable interpretation is that any lentiviral vector production method in the absence of the modified U1A snRNA can be used as a comparison point. The specification discloses a multitude of modified U1A snRNAs that fall under the structural limitations of claim 1 but fail to accomplish the functional limitation of claim 1. Therefore, the functional limitation of claim 1 is not characteristic of the whole structural genus as recited in claim 1.
Under the written description guidelines (see MPEP 2163) the Examiner is directed to determine whether one skilled in the art would recognize that the Applicant was in possession of the claimed invention as a whole at the time of filing. The following considerations are critical to this determination.
To satisfy the written description requirement, a patent specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. See, e.g., Moba, B.V. v. Diamond Automation, Inc., 325 F.3d 1306, 1319, 66 USPQ2d 1429, 1438 (Fed. Cir. 2003); Vas-Cath, Inc. v. Mahurkar, 935 F.2d at 1563, 19 USPQ2d at 1116. An original claim may lack written description support when (1) the claim defines the invention in functional language specifying a desired result but the disclosure fails to sufficiently identify how the function is performed or the result is achieved or (2) a broad genus claim is presented but the disclosure only describes a narrow species with no evidence that the genus is contemplated. See Ariad Pharms., Inc. v. Eli Lilly & Co., 598 F.3d 1336, 1349-50 (Fed. Cir. 2010) (en banc). The written description requirement is not necessarily met when the claim language appears in ipsis verbis in the specification. "Even if a claim is supported by the specification, the language of the specification, to the extent possible, must describe the claimed invention so that one skilled in the art can recognize what is claimed. The appearance of mere indistinct words in a specification or a claim, even an original claim, does not necessarily satisfy that requirement." Enzo Biochem, Inc. v. Gen-Probe, Inc., 323 F.3d 956, 968, 63 USPQ2d 1609, 1616 (Fed. Cir. 2002).
Accordingly, to satisfy the written description requirement, the specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. Vas-Cath, Inc. v. Mahurkar, 935 F.2d 1555, 1562-63, 19 USPQ2d 1111 (Fed. Cir. 1991). See also MPEP 2163.
Actual Reduction to Practice and Disclosure of Structure
In regard to the genus of modified U1A snRNA of claim 1, the specification provides limited examples of modified U1A snRNA capable of performing the claimed functional language and a multitude of modified U1A snRNA that fail to perform the claimed functional language.
Figure 14 and Example 7 identify that U1 snRNAs with 15 nucleotides of complementarity targeted to the PBS to Gag regions of MSD-mutated lentiviral vectors predominantly only exhibited increased lentiviral vector production compared to lentiviral vector production in the absence of the modified U1A snRNA in one of the two experimental groups that is dependent on the region mutated. For example, U1 snRNAs with 15 nucleotides of complementarity targeted to the PBS to SL3ψ region primarily only showed increased vector production in experiment 2 while experiment 1 typically showed no viral vector production. On the contrary, U1 snRNAs with 15 nucleotides of complementarity targeted to in the Gag region only showed vector production in experiment 2 while experiment 1 showed no viral vector production. Only U1 snRNAs with 15 nucleotides of complementarity targeted to position 226 (in the PBS region) and 305 (in the SL2 region) showed lentiviral production in both conditions and U1 snRNAs targeted to position 226 showed reduced viral titers compared to the standard. It’s is not clear what the difference is between experiment 1 and experiment 2 but as both experiments show no vector production depending on mutation site, Figure 14 shows there are experimental protocols that fail to exhibit the required function. Furthermore, Figure 14 shows that multiple mutations in the PBS and Gag regions exhibit reduced viral vector production compared to the standard lentiviral vector production in the absence of the modified U1A snRNA. Although these modifications show increased viral titers compared to the MSD control (the second set of bar graphs), Applicant has included the standard genome production method and both are considered reasonable comparison points for assessing improved lentiviral vector production.
Figure 15 and example 8 identify that only specific promoter and SL2 mutant lentiviral vector genome combinations increase lentiviral vector production compared to the standard lentiviral vector titer in the absence of the modified U1A snRNA.
Figure 27 discloses that the concentrations of plasmids p256U1, pVSVG, and pGenome are important to increasing lentiviral vector titer as 0.15 p256 U1, 0.02 pVSVG, and 0.5 and 1.5 pGenome failed to increase the titer compared to controls without the U1A snRNA.
Figure 38 and example 22 identified that modifying the first two nucleotides of the heterologous sequence to Gt while maintaining 13 nucleotides of complementarity reduced viral titer compared to the absence of the modified U1A snRNA. A separate construct, 256-13-gT (i.e. the same dinucleotide variant) maintained increased viral vector titer but with a different targeting sequence
Therefore, the sequence of the U1A snRNA, the promoter and lentiviral vector genome, the concentration of the U1A snRNA and other components, the target region, the transgene expressed by the lentiviral vector, and the sequence of the heterologous sequence located within the native splice donor annealing sequence are all important to the function and modifications to any one of these components can prevent the U1A snRNA from being capable of performing the claimed function.
Accordingly, Applicant demonstrated a limited reduction to practice of modified U1A snRNAs comprising an Sm protein binding site with a 10-25 nucleotide heterologous sequence located within the native splice donor annealing sequence with at least 10 nucleotides of complementarity to a target sequence within the packaging region of a lentiviral vector genome sequence (including additional mutations in other regions of the U1A snRNA sequence) is capable of increasing lentiviral vector titer during lentiviral vector production relative to lentiviral vector production in the absence of the modified U1A snRNA, nor did Applicant adequately set forth in terms of distinguishing identifying characteristics as evidenced by other descriptions of the invention that are sufficiently detailed to show that Applicant was in possession of the claimed genus of modified U1 snRNAs.
Sufficient relevant identifying characteristics
The breadth of the claims encompass a genus of modified U1A snRNA comprising an Sm protein binding site with a 10-25 nucleotide heterologous sequence located within the native splice donor annealing sequence with at least 10 nucleotides of complementarity to a target sequence within the packaging region of a lentiviral vector genome sequence (including additional mutations in other regions of the U1A snRNA sequence) is capable of increasing lentiviral vector titer during lentiviral vector production relative to lentiviral vector production in the absence of the modified U1A snRNA, yet the present specification provides limited guidance and descriptions regarding which modifications would result in a U1A snRNA comprising an Sm protein binding site with a 10-25 nucleotide heterologous sequence located within the native splice donor annealing sequence with at least 10 nucleotides of complementarity to a target sequence within the packaging region of a lentiviral vector genome sequence capable of increasing lentiviral vector titer during lentiviral vector production relative to lentiviral vector production in the absence of the modified U1A snRNA, therefore the skilled artisan would not know what rational approach to take to make the genus of modified U1A snRNAs with the claimed function as the function is not characteristic of the entire genus. Therefore, it is incumbent on the applicant to provide this nexus between structure and function, in order to be given credit for possession of the claimed genus of modified U1A snRNAs.
An applicant may show that an invention is complete by disclosure of sufficiently detailed, relevant identifying characteristics which provide evidence that applicant was in possession of the claimed invention, i.e., complete or partial structure, other physical and/or chemical properties, functional characteristics when coupled with a known or disclosed correlation between function and structure, or some combination of such characteristics. Enzo Biochem, 323 F.3d at 964, 63 USPQ2d at 1613.
STATE OF THE ART & QUANTITY OF EXPERIMENTATION
The method of making the claimed invention is not well established. However, methods of making of modified U1 snRNAs were known in the art.
The following describes the state of the art with respect to modified U1 snRNAs that impact lentiviral vector titer. The prior art teaches a modified U1 snRNA that reduce viral titer of HIV, as identified by Mandal et al. (Journal of Virology 84: 12790-12800. 2010; art of record), Lawrence et al. (J. Mol. Biol. 326: 529–542. 2003; art of record), Ferri et al. (Molecular Therapy—Nucleic Acids 5: 1-12. 2016; art of record) and United States Patent No. 9932364 (Gatignol; art of record).
Mandal teaches a modified snRNA comprising a mutated 11 nucleotide sequence of the native splice donor annealing site with the sequence of 5’-UCUCUCCUCUG-3’ (U1T5) (the specification of the instant application identifies the native splice donor annealing sequence as 5’-ACUUACCUG-3’ (page 28, paragraph 5) and Mandal teaches that the modified U1 snRNA sequence is mutated based on the WT U1 sequence which is 5’-AUACUUACCUG-3’ (Figure 1)). Although Mandal teaches that their U1T5 mutated snRNA sequence targets region 5814-5825 of the HIV-1 genome (a lentiviral vector), Lawrence evidences that the SL4 region of the HIV-1 genome (Figure 1) comprises eight complimentary sequences with the modified U1T5 sequence. Mandal teaches that their modified snRNPs reduce HIV-1 replication and this could be used in patients to inhibit virus replication (abstract).
Ferri teaches that U1snRNAs are useful for the stable expression of antisense molecules and other therapeutic RNAs. Eight nucleotides at the single-stranded 5’ terminus of U1 (i.e. the native splice donor annealing sequence) can be replaced by unrelated sequences with up to 50 nucleotides, without affecting either stability or the ability to assemble into snRNP particles (page 2, paragraph 4).
Gatignol teaches that they developed antisense nucleic acid molecules, such as shRNAs and siRNAs (antisense molecules), targeting the Gag region of HIV-1 to inhibit HIV-1 replication (abstract). Gatignol teaches that the region of full complementarity between the antisense molecule and the target sequence (i.e. Gag) can be about 14 nucleotides in length (column 12, lines 4-25). Gatignol teaches that ribozymes (e.g. SOFA-HDV-Rz1498) and shRNA (e.g. shRNA1498 a 22 nucleotide sequence) targeting Gag can be used in combination to additively inhibit HIV-1 production (Example 5).
As such, the prior art is focused on using modified U1 snRNPs that inhibit the titer of HIV (a lentiviral vector).
Applicant has claimed a genus of modified U1A snRNA comprising an Sm protein binding site with a 10-25 nucleotide heterologous sequence located within the native splice donor annealing sequence with at least 10 nucleotides of complementarity to a target sequence within the packaging region of a lentiviral vector genome sequence (including additional mutations in other regions of the U1A snRNA sequence) is capable of increasing lentiviral vector titer during lentiviral vector production relative to lentiviral vector production in the absence of the modified U1A snRNA, yet the specification has disclosed a limited number of modified U1A snRNPs capable of performing this function, has set forth limited distinguishing identifying characteristics as evidenced by other descriptions of the invention that are not sufficiently detailed to show that Applicant was in possession of the claimed genus of modified U1A snRNAs. Furthermore, the state of the art indicated no modified U1 snRNAs that are capable of increasing titer, only those capable of decreasing the viral titer. The claims are much broader to the examples found in the specification and art and would require undue experimentation to determine whether modified U1A snRNAs within the structural limitations have the claimed function, and one of skill in the art would neither expect nor predict the claimed function beyond those described in the specification that have the claimed function.
CONCLUSION
Therefore, the Examiner concludes that there is insufficient written description of the instantly claimed genus of modified U1A snRNAs. Specifically, there is limited description of the structure-function relationship between the claimed genus of modified U1A snRNAs, and the Examiner further concludes a skilled artisan would find the specification inadequately describes the claimed genus of modified U1A snRNAs.
Response to Arguments
The Applicant's arguments filed August 14, 2026, are acknowledged.
Applicant argues that the evidence provided in the Office action does not support the written description rejection. The written description inquiry asks whether the Specification reasonably conveys to a person of ordinary skill that the Inventors were in possession of the claimed invention at the filing date. It does not require that every disclosed embodiment within a claimed genus exhibit identical performance or that every experimental variable affecting performance be identified.
Applicant argues that claim 1 requires (i) at least 10 nucleotides of complementarity between the heterologous sequence and a target sequence and (ii) a lentiviral vector derived from a human lentivirus. These features align the claims with the embodiments consistently demonstrating the recited increase in lentiviral vector titer, and remove categories of embodiments upon which portions of the rejection rely.
Applicant argues that the results from Figure 38 and Example 22 have been taken out of context. Example 22 was not designed to determine the minimum structural limitations required by the invention. Rather, it investigated whether the highly conserved 5' dinucleotide of endogenous U1 snRNA-which is known to influence cap-binding complex recruitment during normal splicing-was also important for the newly discovered mechanism underlying lentiviral vector titer enhancement.
To answer that question, the inventors generated an extensive panel of modified U1 snRNAs differing only in the identity of the first two nucleotides, while maintaining essentially identical targeting characteristics. Specifically, each construct maintained 13 contiguous base pairs with the target sequence and a predicted melting temperature of approximately 46°C. The Specification reports that all tested dinucleotide variants except 256_13_Gt increased vector titers, with most exhibiting enhancement comparable to the control construct. However, the Specification immediately explains that the isolated behavior of 256_13_Gt does not establish a general structural requirement because another construct, 256_13_gT, containing the same dinucleotide, nevertheless increased vector titer. Accordingly, the Inventors concluded that "there may not necessarily be dinucleotides to avoid."
Rather than identifying an unclaimed structural limitation of the claimed genus, the Inventors concluded that the conserved U1 dinucleotide is not determinative of the claimed functional effect. The existence of one anomalous construct within an otherwise successful screening experiment does not establish that the inventors lacked possession of the claimed genus.
Furthermore, Applicant argues that the Office Action relies on experiments involving plasmid dosage, promoter selection, production systems, and other operational variables to assert that Applicant has demonstrated "a limited reduction to practice." These are not structural characteristics of the claimed modified U1A snRNA.
For example, Figure 27 concerns the amount of plasmid introduced during transient transfection. Optimization of plasmid ratios is a routine aspect of transient lentiviral vector production and concerns the manner in which the invention is practiced, not the structure of the claimed modified U1A snRNA itself. The fact that different transfection conditions produce different viral titers does not establish that the Inventors lacked possession of the claimed RNA molecule. Similarly, the Office Action cites differences in promoters, vector backbones, and production systems. These variables describe experimental context rather than structural limitations of the claimed invention. Written description does not require Applicant to demonstrate identical performance under every conceivable production condition (page 7, paragraph 1-page 8, paragraph 6).
Applicant's arguments have been fully considered but they are not persuasive.
Although Applicant has amended the claims to overcome some of the issues raised in the previous written description rejection, these amendments do not overcome all of the identified issues associated with the written description rejection, as identified in the rejection above.
Regarding Applicant’s arguments about Figure 38 and Example 22, although the 256-13-gT variant was successful in increasing the viral titer, this doesn’t overcome the issue with 256-13-Gt as, although the dinucleotide sequence is the same, the overall sequences of the 2 variants are not the same and have different targeting sequences. As such, this suggests that one of ordinary skill in the art would have to undergo trial and error with a limited ability to predict whether the chosen sequence would be successful to determine which U1 snRNAs have the stated function. As identified by the Applicant, the results from 256_13_Gt does not establish a general structural requirement because another construct, 256_13_gT, containing the same dinucleotide, increased vector titer.
Regarding Applicant’s arguments about operational variables affecting the claimed function, Applicant is correct that the structure of the U1 snRNA does not change based on the change in the different operational variables (e.g. plasmid dosage and promoter selection). However, these operational variable are directly tied to whether the U1 snRNA has the claimed function or not. Therefore, the claimed function can be modified based on a multitude of operational variables, as outlined in the rejection above, that changes whether the U1 snRNA performs the function or not even as the structure of the U1 snRNA has not changed. As such, these operational variables are considered integral to the claimed function of the U1 snRNA.
Therefore, Applicant’s arguments are considered unpersuasive.
Applicant further argues that Figure 14 likewise does not demonstrate a lack of
possession of the claimed genus. In particular, the Office Action appears to interpret the absence of a data bar for certain constructs in Experiments 1 and 2 as indicating that those constructs produced no viral vector. However, Figure 14 does not identify the absence of a depicted bar as representing a measured titer of zero rather than that certain constructs were not tested in one of the two experiments.
Moreover, as shown in Figure 14, the Standard and MSD-2KO lentiviral vector systems have different baseline titers, such that the magnitude of U1-dependent titer enhancement should be assessed relative to the appropriate control within each experimental system rather than by comparing absolute titers across the two systems. Accordingly, Figure 14 does not establish, as suggested in the Office Action, that the depicted modified U1A snRNAs failed to exhibit the claimed function under particular experimental protocols (page 9, paragraph 1-paragraph 4).
Applicant's arguments have been fully considered but they are not persuasive.
Regarding Applicant’s arguments about the absence of data bars for certain experiments, Applicant argues that interpreting the lack of error bars corresponds to a measured titer of zero is incorrect and that it should be, instead, read to mean that certain constructs were not tested in one of the two experiments. However, Applicant has not cited to part of the Specification to back up their interpretation of the claims. Although there may be more than one interpretation of the lack of error bars, it is reasonable to interpret it to mean that zero titer was produced as most of the examined U1 snRNAs were examined in both experiments including some within the region with increased viral titers. As there is no information within the Specification regarding the differences between Experiments 1 and 2 (if there are any) and that some U1 snRNAs were not tested in both experimental groups, it is reasonable to conclude that no bar graphs represents a zero viral titer in those experiments.
Furthermore, regarding Applicant’s statement that certain constructs were not tested with the implication being that this is the correct interpretation of Figure 14, this is considered arguments of counsel as no evidence is provided to support their conclusion. Arguments of counsel cannot take the place of factually supported objective evidence in the record. See In re Schulze, 346 F.2d 500, 602, 145 USPQ 716, 718 (CCPA 1965), In re Huang, 100 F.3d 135, 139-40, 40 USPQ2d 1685, 1689 (Fed. Cir. 1996); In re De Blauwe, 736 F.2d 699, 705, 222 USPQ 191, 196 (Fed. Cir. 1984). Thus, Attorney statements regarding the correct interpretation of Figure 14, are not evidence without a supporting declaration.
Regarding Applicant’s arguments about which control is appropriate for comparing vector titer, it is worth reiterating, as identified in the rejection above, that Applicant has not specified the relative production method. As such, the broadest reasonable interpretation is that any lentiviral vector production method in the absence of the modified U1A snRNA can be used as a comparison point. Although the U1 snRNAs with a MSD genome modification show increased viral titers compared to the MSD control (the second set of bar graphs), Applicant has included the standard genome production method as part of the graph. This shows that the lentiviral vector production method using a standard genome is a logical comparison as Applicant has included it as part of Figure 14 for direct comparison. Therefore, the lentiviral production method using the standard and MSD genomes are considered reasonable comparison points for assessing improved lentiviral vector production.
As such, Applicant’s arguments are considered unpersuasive.
Maintained Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1, 3, 7, 10, and 16 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 5 of copending Application No. 17/925,004.
‘004 claims a method of increasing viral vector titre in a viral vector production system comprising a genus of modified U1 snRNA that bind to a nucleotide sequence within the packaging region of the lentiviral vector genome. ‘004 does not further claim structural features such as how the snRNA is modified to target the packaging region.
However, MPEP 804(II)(B)(1) states that those portions of the specification which provide support for the reference claims may also be examined and considered when addressing the issue of whether a claim in the application defines an obvious variation of an invention claimed in the reference patent or application (as distinguished from an obvious variation of the subject matter disclosed in the reference patent or application). The court pointed out that "this use of the disclosure is not in contravention of the cases forbidding its use as prior art, nor is it applying the patent as a reference under 35 U.S.C. 103, since only the disclosure of the invention claimed in the patent may be examined." In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014), the court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Sun Pharm. Indus., Ltd. v. Eli Lilly & Co., 611 F.3d 1381, 95 USPQ2d 1797 (Fed. Cir. 2010); Pfizer, Inc. v. Teva Pharm. USA, Inc., 518 F.3d 1353, 86 USPQ2d 1001 (Fed. Cir. 2008); Geneva Pharmaceuticals Inc. v. GlaxoSmithKline PLC, 349 F3d 1373, 1385-86, 68 USPQ2d 1865, 1875 (Fed. Cir. 2003).
In this regard, the specification of ‘004 discloses that U1_256 (a 15 nucleotide complimentary sequence) was modified to replace the native splice-donor annealing sequence with a sequence that targets the SL1 loop of HIV-1 and this modified U1-snRNA boosted the production of lentiviruses (Example 5 and page 10, line 26-page 11, line 2).
As such, this represents the utility of the modified U1 snRNA in the method of claim 5 of ‘004 and is allowed to be considered for non-statutory double patenting. Therefore, in light of the utility information from the specification of ‘004, claims 1, 3, 7, 10, and 16 are rejected for non-statutory double patenting.
This is a provisional nonstatutory double patenting rejection.
Response to Arguments
Applicant's arguments filed August 14, 2026, are acknowledged.
Applicant argues that claim 5 of the ‘004 application is directed to a production method using a PKC activator rather than to a structurally defined modified U1A snRNA as presently claimed. Therefore, the pending claims are patentably distinct from claim 5 (page 10, paragraph 4-paragraph 8).
Applicant's arguments have been fully considered but they are not persuasive.
Although claim 5 of the ‘004 application includes a PKC activator, this additional component does not change that claim 5 encompasses a modified U1 snRNA that binds to a nucleotide sequence within the packaging region of the lentiviral vector genome sequence and that the U1 snRNA of example 5 would fall within the limitations of the U1 snRNA of the instant claims.
Conclusion
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.
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/KEENAN A BATES/Examiner, Art Unit 1631
