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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on January 15, 2026, has been entered.
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Claims 19-27, 31, 39-40, 42-43, 51-52, 57-59, 61, and 63-64 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention (Groups II-IV), there being no allowable generic or linking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 January 15, 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, 3, 7, 10, 16, 20-21, and 31 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 In light of the Applicant’s elected invention, claims 19-27, 31, 39-40, 42-43, 51-52, 57-59, 61, and 63-64 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim.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.
Declaration under 37 CFR 1.132
The declaration under 37 CFR 1.132 filed by Dr. Daniel Farley on January 15, 2026, has been considered but is insufficient to overcome the rejections of instant claims based upon 35 U.S.C 103 as set forth in the current Office action for the following reasons:
The Farley declaration argues that claim 1 overcomes the 112a rejection by identifying key structural features (U1A snRNAs and Sm protein binding site) that are important for achieving the claimed function. The Farley declaration cites to data from Examples 2 and 7 to show that the above cited features are enough to teach a person skilled in the art the structural elements and identifying characteristics of the modified snRNAs that correlate to the claimed function (page 1, paragraph 2-page 3, paragraph 2).
Applicant's arguments have been fully considered but they are not persuasive.
Although Applicant has amended the claims to identify two structural features that are important to achieving the claimed function and the declaration has cited to data in the specification that show these features are important to achieving the claimed function, these are not the only structural features that are important.
Figure 14 and Example 7 identify that mutations in the PBS to Gag regions 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, mutations in 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, mutations in the Gag region only showed vector production in experiment 2 while experiment 1 showed no viral vector production. 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.
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 37 and example 22 identifies that a 9 nt heterologous sequence with 9 nt of complementarity to region 305 (SL2) failed to increase viral titer of a CD19 CAR lentivirus.
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.
Figure 40 and Example 24 identify that non-human primate lentiviral vector EIAV does not show improved viral titer when using a modified U1A snRNA targeting region 212 (PBS region) of EIAV with either a CMV or EF1a promoter and region 228 with a CMV promoter.
Figure 41 and Example 25 identify that non-human primate lentiviral vector SIVagm does not show improved viral titer when using a modified U1A snRNA targeting regions 219, 234, 313, and 353 of SIV.
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.
As identified above, there are a multitude of structural characteristics that are necessary to achieve the claimed function. Each of these structural components are important to achieving the claimed function and modifications to any one of these components can prevent the U1A snRNA from being capable of performing the claimed function. Therefore, although the amendments and cited data clarify some of the structural components, they do not clarify all of the structural components that are important for achieving the claimed function.
In view of the foregoing, when all of the evidence is considered, the totality of the rebuttal evidence fails to outweigh the evidence for the 112a written description rejection.
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 9-25 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 9 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, and 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.” The broadest reasonable interpretation is that any modified U1A snRNA comprising an Sm protein binding site with a 9-25 nucleotide heterologous sequence located within the native splice donor annealing sequence with at least 9 nucleotides of complementarity to a target sequence within the packaging region of any 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 relative to any lentiviral vector production in the absence of the modified U1A snRNA. 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
In regard to claim 1 encompassing a genus of modified U1A snRNA comprising an Sm protein binding site with a 9-25 nucleotide heterologous sequence located within the native splice donor annealing sequence with at least 9 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, 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 mutations in the PBS to Gag regions 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, mutations in 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, mutations in the Gag region only showed vector production in experiment 2 while experiment 1 showed no viral vector production. 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.
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 37 and example 22 identifies that a 9 nt heterologous sequence with 9 nt of complementarity to region 305 (SL2) failed to increase viral titer of a CD19 CAR lentivirus.
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.
Figure 40 and Example 24 identify that non-human primate lentiviral vector EIAV does not show improved viral titer when using a modified U1A snRNA targeting region 212 (PBS region) of EIAV with either a CMV or EF1a promoter and region 228 with a CMV promoter.
Figure 41 and Example 25 identify that non-human primate lentiviral vector SIVagm does not show improved viral titer when using a modified U1A snRNA targeting regions 219, 234, 313, and 353 of SIV.
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 9-25 nucleotide heterologous sequence located within the native splice donor annealing sequence with at least 9 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.
Disclosure of structure
The Applicant has provided limited examples of a genus of modified U1A snRNA comprising an Sm protein binding site with a 9-25 nucleotide heterologous sequence located within the native splice donor annealing sequence with at least 9 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. Furthermore, Applicant has provided a multitude of modified U1A snRNA that have the structural characteristics of the genus but fail to perform the claimed functional language.
Sufficient relevant identifying characteristics
The breadth of the claims encompass a genus of modified U1A snRNA comprising an Sm protein binding site with a 9-25 nucleotide heterologous sequence located within the native splice donor annealing sequence with at least 9 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 9-25 nucleotide heterologous sequence located within the native splice donor annealing sequence with at least 9 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. Although the making of modified U1 snRNAs was known in the art, according to the claimed genus of modified U1 snRNAs.
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).
Regarding claim 1, 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 9-25 nucleotide heterologous sequence located within the native splice donor annealing sequence with at least 9 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 example 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 January 15, 2026, are acknowledged.
Applicant argues the amendments to claim 1 overcome the 112a rejection by identifying key structural features (U1A snRNAs and Sm protein binding site) that are important for achieving the claimed function (page 6, paragraph 5-page7, paragraph 4).
Applicant's arguments have been fully considered but they are not persuasive.
Although Applicant has amended the claims to identify two structural features that are important to achieving the claimed function, these are not the only structural features that are important. As identified in the rejection above, there are a multitude of structural characteristics that are necessary to achieve the claimed function, such as 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. As identified in the cited figures from the instant specification in the rejection above, each of these structural components are important to achieving the claimed function and modifications to any one of these components can prevent the U1A snRNA from being capable of performing the claimed function. Therefore, although the amendments clarify some of the structural components, they do not clarify all of the structural components that are important for achieving the claimed function.
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-page11, 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 6, 2025, are acknowledged.
Applicant argues that the ‘004 application has a later filing date than the instant application. Therefore, should the present application otherwise be in condition for allowance before the ‘004 application is granted, a terminal disclaimer should not be required for allowance of the present application (7, paragraph 5-page 8, paragraph 1).
Applicant's arguments have been fully considered but they are not persuasive.
As the instant application is not in condition for allowance, the arguments are not persuasive and the rejection is maintained.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to KEENAN A BATES whose telephone number is (571)270-0727. The examiner can normally be reached M-F 7:30-5:00.
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/KEENAN A BATES/Examiner, Art Unit 1631
/PETER PARAS JR/Supervisory Patent Examiner, Art Unit 1632
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