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 04/29/2026. Claims 2-6, 8-10, 12-13, 16-22, 26, 28-30, 32-42, 45-48 and 50 are currently pending.
Any rejection or objection not reiterated herein has been overcome by amendment. Applicant' s amendments and arguments have been thoroughly reviewed, but are not persuasive to place the claims in condition for allowance for the reasons that follow.
Claim Objections
Claim 50 is objected to because of the following informalities: there is no period at the end of the claim. Appropriate correction is required.
Claim Rejections - 35 USC § 103 – Response to Arguments
In the remarks filed 04/29/2026, on page 13, Applicant argues that, “Bhattacharyya states that "...TGF-a-induced lung fibrosis and CCl4-induced hepatic fibrosis appeared to be exacerbated, rather than attenuated, in mice lacking Egr-1 raising the possibility that Egr-1 in fact has a more context-dependent role in fibrogenesis, possibly determined by the initiating nature of injury and cell type where it is active." Therefore, although Bhattacharyya reports elevated Egr-1 in IPF lungs, it calls into question if its suppression would be linked to any anti-fibrotic therapeutic effect. This would have discouraged the skilled person from extrapolating the kidney-based findings of Xu to lung fibrosis therapy.”. This argument has been fully considered and is persuasive. The rejection of claims 17-19, 22, 26, 28 and 48 under 35 USC 103 has been withdrawn.
In response to applicant's arguments against Xu individually (p. 12), one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
Claim Rejections - 35 USC § 112(a) – Scope of Enablement
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 12-13, 16 and 30 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for:
methods of using the claimed miRNA mimetics comprising SEQ ID NOs: 15, 17, 18, 19, and combinations thereof for treatment of PF-ILD, IPF, connective tissue disease (CTD)-associated ILD, rheumatoid arthritis ILD, chronic fibrosing hypersensitivity pneumonitis (HP), idiopathic non-specific interstitial pneumonia (iNSIP), unclassifiable idiopathic interstitial pneumonia (IIP), environmental/occupational lung disease, systemic sclerosis ILD
methods of using SEQ ID NO: 17 to treat Egr1-induced renal fibrosis
The specification does not reasonably provide enablement for:
treating any of the claimed disorders using an RNA that inhibits the function of one or more miRNAs selected from the group consisting of miRNAs of SEQ ID NOs: 1-14, 16, and 34-36
The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
Factors to be considered in determining whether a disclosure meets the enablement requirement of 35 U.S.C. 112, first paragraph, have been described by the court in In re Wands, 8 USPQ2d 1400 (CA FC 1988). Wands states at page 1404,
“Factors to be considered in determining whether a disclosure would require undue experimentation have been summarized by the board in Ex part Forman. They include (1) the quantity of experimentation necessary, (2) the amount of direction or guidance presented, (3) the presence or absence of working examples, (4) the nature of the invention, (5) the state of the prior art, (6) the relative skill of those in the art, (7) the predictability or unpredictability of the art, and (8) the breadth of the claims.”
The nature of the invention
Claims 12 and 13 are drawn to the method of claim 26, wherein the viral vector comprises a transgene that codes for both one or more miRNAs selected from the group consisting of SEQ ID NOs: 15, 17, 18 and 19, and for an RNA that inhibits the function of one or more miRNAs selected from the group consisting of the miRNAs of SEQ ID NOs: 1-14, 16, and 34-36. These claims differ only insofar as claim 12 recites wherein the packaged nucleic acid comprises one or more expression cassettes, whereas claim 13 specifically recites a first and second expression cassette, with the inhibitory RNA comprised within the second cassette. Claim 16 depends from claim 12 but does not further limit the claimed inhibitors. Claim 30 recites the same inhibitors as above, and depends from claim 26. Amended claim 26 recites a method of treating a disease selected from PF-ILD, IPF, connective tissue disease (CTD)-associated ILD, rheumatoid arthritis ILD, chronic fibrosing hypersensitivity pneumonitis (HP), idiopathic non-specific interstitial pneumonia (iNSIP), unclassifiable idiopathic interstitial pneumonia (IIP), environmental/occupational lung disease, and systemic sclerosis ILD. The invention is the class of invention that the CAFC has characterized as “the unpredictable arts such as chemistry and biology”. Mycogen Plant Sci., Inc. v. Monsanto Co., 243 F. 3d 1316 (Fed. Cir. 2001).
The breadth of the claims
Claims 12-13 and 16 are drawn to the method of claim 26 comprising administration of an expression cassette coding any RNA that inhibits the function of any one or more of the miRNAs selected from SEQ ID NOs: 1-14, 16, and 34-36.
The broadest reasonable interpretation of “any RNA that inhibits the function” encompasses any RNA oligonucleotide which either directly (e.g., through direct binding of the miRNA) or indirectly (e.g., through binding its mRNA target or preventing its transcription) inhibits the function of a miRNA.
Beavers (Beavers et al. miRNA Inhibition in Tissue Engineering and Regenerative Medicine. Adv Drug Deliv Rev. 2015 July 1; 88: 123–137.) review various microRNA inhibitors, including:
Anti-miR oligonucleotides which bind and inhibit the activity of the mature miRNA guide strand (§Artificial miRNA inhibitors §§Anti-miRNA oligonucleotides)
Anti-mIRs which bind and inhibit the activity of the pri- or pre-miRNA
“Blockmirs” which bind to the miRNA’s target mRNA and block miRNA binding sites
Tang (Tang et al. microRNA inhibitors: Natural and artificial sequestration of microRNA. Cancer Letters 407 (2017) 139e147.) also describes several types of competing endogenous miRNA inhibitors (ceRNAs) such as pseudogene RNAs, lncRNAs, viralRNAs, circRNAs and mRNAs (§The advent of the ceRNA hypothesis and its mechanism).
Zhao (Zhao et al. Sequence-specific inhibition of microRNA via CRISPR/CRISPRi system. Sci Rep 4, 3943 (2014).) describe using the CRISPR interference system to prevent the expression of miRNAs, thereby inhibiting them. Zhao also teaches inhibition of miRNA targets via CRISPR knockdown. (§Abstract).
Therefore, based on the information available in the prior art, the genus of any RNA that inhibits the function of an miRNA encompasses all of the species described by Beavers, Tang and Zhao.
It is also relevant to note that the claims are not limited to any particular subject or delivery to any particular tissue in that subject. Therefore, the claims encompass the administration of the miRNAs and their inhibitors to any subject of any age, to any tissue.
The unpredictability of the art and the state of the prior art
The state of the prior art shows that the genus of RNAs which inhibit miRNA is broad and exhibits significant structural and functional variability and unpredictability.
Regarding RNA inhibitors of miRNA:
As discussed above, the claims encompass several types of RNA inhibitors of miRNA, which vary both structurally and functionally. Per Tang, these include naturally occurring RNAs such as pseudogene RNAs, lncRNAs, viralRNAs, circRNAs and mRNAs. All of these different kinds of RNAs, termed “competing endogenous RNAs (ceRNA)” (p. 140), “…can sequestrate miRNA and act as ceRNA. However, their activity is influenced and regulated by multiple factors, including the relative abundance of ceRNA, miRNA and target mRNA; the stability of ceRNA; and the subcellular localization of ceRNA/miRNA.” (p. 142 §Factors that influence ceRNA activity). This points to a significant degree of complexity, variability and unpredictability within the system of ceRNAs and their interactions with their target miRNAs and each other. In particular, Tang notes that, “the function and regulatory mechanisms of circRNAs remain elusive” (p. 141).
Regarding the miRNAs:
While the scope of the claimed miRNAs and their RNA inhibitors is limited, the scope of their functions is broad, encompassing treatment of any fibroproliferative disorder in any subject or tissue.
The state of the art prior to the filing date of the instantly claimed invention shows that the expression and function of miRNAs vary widely among organs, tissues and species, as evidenced by Ha et al. (Biochim Biophys Acta. 2008 Nov;1779(11):735-42) and Banzhaf-Strathmann and Edbauer (Cell Commun Signal 12, 30 (2014)). Ha discloses that, as of 2008, thousands of miRNAs had been identified in animals and plants (with the majority found in animals), and estimates indicate that 1-5% of the transcribed genes in animals contain miRNAs (p. 2).
The above evidences that the scope of all miRNAs in animals is vast. Within that scope, Ha further discloses that many miRNAs are species- and/or tissue-specific, and that the expression patterns of animal miRNAs is varied and thus, difficult to predict even when the miRNA sequences are conserved among species: Conserved miRNAs do not necessarily exhibit the same expression levels or patterns in different species or at different stages within a species, even though the sequences of mature miRNAs are generally conserved in the animal kingdom. [abstract]
Major miRNA renovations occurred at the emergence of vertebrates and placental mammals. Many miRNAs, such as miR-126 and miR-206, are expressed in vertebrate-specific organs. Moreover, ∼42% of the 800 primate miRNAs are primate-specific and are absent in other mammals…477 new miRNA genes in the brains of humans and chimpanzee. Among all small RNAs cloned, 75% were known human and primate miRNAs, 14% were conserved in vertebrates, 10% were primate-specific, and 1% were human specific. [p. 3]
Although sequence conservation of miRNAs and target genes may suggest conservation of expression patterns and functions, this assumption does not hold true for many conserved miRNAs. By comparing expression patterns of ∼100 miRNAs that are conserved in sequences in fish, chicken, and mouse, Ason et al. (2006) indicated that the timing and location of miRNA expression is not strictly conserved [107]. Several conserved miRNAs such as miR-454a, miR-145, and miR-205 clearly displayed spatial expression differences between two closely related species, medaka and zebrafish. It is conceivable that the spatial and temporal regulation of conserved miRNAs may also play an important role in shaping developmental and physiological changes during animal evolution. [p. 4]
Therefore, Ha shows that there is a high level of variability in and unpredictability of miRNA expression through the full scope of animal subjects.
When we narrow the scope even to a single miRNA in a single species, Banzhaf-Strathmann and Edbauer provide an example wherein the expression of said miRNA varies by tissue:
One miRNA that has gained special interest in the field of cancer research is miRNA- 125b (miR-125b). MiR-125b is a ubiquitously expressed miRNA that is aberrantly expressed in a great variety of tumors. In some tumor types, e.g. colon cancer and hematopoietic tumors, miR-125b is upregulated and displays oncogenic potential, as it induces cell growth and proliferation, while blocking the apoptotic machinery. In contrast, in other tumor entities, e.g. mammary tumors and hepatocellular carcinoma, miR-125b is heavily downregulated. This downregulation is accompanied by de-repression of cellular proliferation and anti-apoptotic programs, contributing to malignant transformation. The reasons for these opposing roles are poorly understood. [abstract].
Therefore, Banzhaf-Strathmann and Edbauer evidence further unpredictability of miRNA expression within the full scope of any sample type even when it relates to one miRNA in one species.
Regarding SEQ ID NOs: 1-14, 16, and 34-36, the miRNA targets for the recited RNAs that inhibit their function, even within this smaller genus there is a significant amount of variability and unpredictability. For example, Chai (Chai et al. miR-146b expression is upregulated in the lung of pulmonary fibrosis mice. Int J Clin Exp Pathol 2016;9(2):464-472.) found that expression of miR-146b (SEQ ID NO: 16; see Fig. 5 of the specification and note the same sequence in Figure 5 of Chai) increased significantly in pulmonary fibrosis (p. 469) and that it may inhibit foxO3 expression to facilitate pulmonary fibrosis (p. 471, Conclusion). However, in their conclusion (p. 471) they caution that:
Although miRNAs have the potential in the therapy of diseases, it has a long way to go before anti-fibrotic therapy is conducted targeting miR-146b. In the inflammation related to interstitial lung diseases, which inflammation related signaling pathway is mainly regulated by miR-146 and the clinical significance of this pathway are largely unclear. In addition, whether increased miR-146 expression in the inflammation may further induce fibrosis and whether inhibition of miR-146 expression may deteriorate inflammation are still needed to be elucidated. There is evidence showing that the miRNA expressing profile is different between fibrotic tissues, which might be helpful for the prediction of fibrosis in different tissues. Currently, most studies on miR-146 are observational, and more studies are required before the application of miR-146 as a target in the therapy of PF.
What this indicates is that even within the genus of the recited miRNAs intended for inhibition, there is considerable variability and unpredictability regarding their role in fibroproliferative disorders, with that role largely unexplored and, insofar as it has been explored, unclear.
Guidance in the specification and working examples
The specification discloses that in both human lung fibroblasts and a mouse model of pulmonary fibrosis, administration of various combinations of miRNA mimics of miR-181a, miR-181b, miR-212-p, miR10a, and miR-212-3p demonstrated anti-inflammatory, anti-proliferative and anti-fibrotic effects. The specification does not disclose the same effects in any other model of fibrosis in any other organ system. The specification also does not disclose any working examples of RNA inhibition of miRNAs comprising SEQ ID NOs: 11-14, 16, or 34-36 to treat the recited diseases.
The quantity of experimentation
To use the invention as claimed, at a minimum, the skilled artisan would need to:
Test the full scope of all artificial RNA inhibitors of miRNA to determine if they are able to inhibit the miRNAs comprising SEQ ID NOs: 11-14, 16, or 34-36 and are also able to treat the recited disorders.
Discover the full scope of all naturally occurring ceRNAs which may inhibit miRNAs comprising SEQ ID NOs: 11-14, 16, or 34-36 and test those throughout the scope of disorders described above.
Conclusion
Taking into consideration the factors outlined above, including the nature of the invention, the breadth of the claims, the state of the art, the guidance provided by the specification, and the amount of experimentation required, it is the conclusion that an undue amount experimentation would be required to make and use the invention as claimed.
Response to Arguments
Applicant's arguments filed 04/29/2026 have been fully considered but they are not persuasive. On page 14, Applicant argues that, “Accordingly, once the sequence of the relevant miRNA is provided, these detailed instructions enable the skilled person, without undue burden, to design a corresponding inhibitory RNA.”. Applicant further points out that Figures 8B and 8C describe anti-miRs and sponges. Respectfully, this is not persuasive because the claims do not only require the design of miRNA inhibitors, but also require that inhibition of those targets treat the recited disorders. However, the specification provides no working examples of said method, only working examples of methods comprising administration of miRNA mimics of miR-212-5p, 181a-5p, 181b-5p, and 10a in the context of animal models of pulmonary fibrosis. As discussed above, there is significant variability and unpredictability in the effects of individual miRNAs and the inhibition thereof. This would have made it difficult for the ordinary artisan to predict, with a reasonable expectation of success, that inhibition of the recited miRNAs would result in the claimed treatment outcomes. This unpredictability is also evidenced by the specification: on pages 39-40, Applicants disclose that five miRNAs were tested, including a mix of miRNAs that were both downregulated and upregulated in a model of pulmonary fibrosis (i.e., miR-212-5p and miR-212-3p, which were up-regulated, and miR-181a-5p, 181b-5p and 10a-5p, which were down-regulated; see Fig. 5). Of the five, four (all but miR-212-3p) resulted in a significant reduction of TGFB-induced mRNA expression of IL6 (p.39). This suggests that it is difficult to predict, from transcriptomic data alone and without trial and error experimentation, which miRNA mimics or inhibitors would have been effective at treating the claimed disorders.
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.
Note: This rejection has been modified in light of the amendments to claims 28-30, 32-42 and 45-48, which are now drawn to a method, not to a product.
Claim 2-6, 8-10, 17-22, 26, 28-30, 32-42, 45-48 and 50 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 10-15, 28, 34 and 44-45 of copending Application No. 18251562 in view of Bofill-De Ros (Guidelines for the optimal design of miRNA-based shRNAs. Methods. 2016 July 1; 103: 157–166.).
This is a provisional nonstatutory double patenting rejection because the copending claims have not been patented.
The instant and copending claims are related as follows:
Instant claim
Copending claim
26. Method of treating a disease selected from the group consisting of PF-ILD, IPF, connective tissue disease (CTD)-associated ILD, rheumatoid arthritis ILD, chronic fibrosing hypersensitivity pneumonitis (HP), idiopathic non-specific interstitial pneumonia (iNSIP), unclassifiable idiopathic interstitial pneumonia (IIP), environmental/occupational lung disease, and systemic sclerosis ILD, the method comprising administering to a patient in need thereof a therapeutically active amount of viral vector comprising: a capsid and a packaged nucleic acid, wherein the packaged nucleic acid codes for one or more miRNAs, wherein at least one of the one or more miRNAs comprises the miRNA of Seq ID No. 15, Seq ID No. 17, or Seq ID No. 19.
48. Method of treating a disease selected from the group consisting of PF-ILD, IPF, connective tissue disease (CTD)-associated ILD, rheumatoid arthritis ILD, chronic fibrosing hypersensitivity pneumonitis (HP), idiopathic non-specific interstitial pneumonia (iNSIP), unclassifiable idiopathic interstitial pneumonia (IIP), environmental/occupational lung disease, systemic sclerosis ILD, sarcoidosis, and fibrosarcoma, the method comprising administering to a patient in need thereof a therapeutically active amount of a pharmaceutical composition comprising (i) a miRNA mimetic of a miRNA having the sequence of Seq ID No. 15, or (ii) a miRNA mimetic of a miRNA having the sequence of Seq ID No. 17, or (iii) a miRNA mimetic of a miRNA having the sequence of Seq ID No. 18, or (iv) a miRNA mimetic of a miRNA having the sequence of Seq ID No. 19, and apharmaceutical-acceptable carrier or diluent.
1. A method of treating or preventing a disease selected from the group consisting of ILD, PF-ILD, IPF, connective tissue disease (CTD)-associated ILD, rheumatoid arthritis ILD, chronic fibrosing hypersensitivity pneumonitis (HP), idiopathic non-specific interstitial pneumonia (iNSIP), unclassifiable idiopathic interstitial pneumonia (IIP), environmental/occupational lung disease, pulmonary hypertension (PH), fibrotic silicosis, systemic sclerosis ILD, sarcoidosis, and fibrosarcoma, the method comprising:administering to a patient in need thereof a therapeutically active amount of viral vector,wherein said viral vector comprises a capsid and a packaged nucleic acid, wherein the packaged nucleic acid codes for one or more miRNAs, wherein the one or more miRNAs comprise the miRNA fragment having the sequence of Seq ID No. 99.
2. The method of claim 26, wherein the packaged nucleic acid codes for more than one miRNA, wherein said miRNAs comprise the miRNA of Seq ID No. 15 and the miRNA of Seq ID No. 19 and a miRNA of Seq ID No. 18.
3. The method of claim 26, wherein the packaged nucleic acid codes for more than one miRNA, wherein said miRNAs comprise the miRNA of Seq ID No. 15 and the miRNA of Seq ID No. 17 and a miRNA of Seq ID No. 18.
4. The method of claim 26, wherein the packaged nucleic acid codes for more than one miRNA, wherein said miRNAs comprise the miRNA of Seq ID No. 15 and the miRNA of Seq ID No. 17 and the miRNA of Seq ID No. 19.
5. The method of claim 26, wherein the packaged nucleic acid codes for more than one miRNA, wherein said miRNAs comprise the miRNA of Seq ID No. 15 and the miRNA of Seq ID No. 17.
6. The method of claim 26, wherein the packaged nucleic acid codes for more than one miRNA, wherein said miRNAs comprise the miRNA of Seq ID No. 15 and the miRNA of Seq ID No. 19.
8. The method of claim 26 wherein the packaged nucleic acid codes for more than one miRNA, wherein said miRNAs comprise the miRNA of Seq ID No. 19 and the miRNA of Seq ID No. 17.
9. The method of claim 26 wherein the packaged nucleic acid codes for more than one miRNA, wherein said miRNAs comprise the miRNA of Seq ID No. 19 and a miRNA of Seq ID No. 18.
10. The method of claim 26 wherein the packaged nucleic acid codes for a miRNA having the sequence of Seq ID No. 19, and for a miRNA having the sequence of Seq ID No. 18 and for a miRNA having the sequence of Seq ID No. 17.
28. The method of claim 26, said viral vector comprising a genome that codes for one or more miRNAs selected from the group comprising the miRNA of Seq ID No. 15, the miRNA of Seq ID No. 17, and the miRNA of Seq ID No. 19.
29. The method of claim 28, wherein said vector genome codes for a miRNA having the sequence of Seq ID No. 15 and for a miRNA having the sequence of Seq ID No. 17 and optionally for a miRNA having the sequence of Seq ID No. 19.
30. The method of claim 28, wherein said vector genome further codes for an RNA that inhibits the function of one or more miRNAs selected form the group consisting of the miRNAs of Seq ID Nos. 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 16, 34, 35 and 36.
40. The method of claim 32, wherein the method further comprises the administration of a mimetic of a miRNA having the sequence of Seq ID No. 18 and a mimetic of a miRNA having the sequence of Seq ID No. 19.
41. The method of claim 32, wherein the method further comprises the administration of a mimetic of a miRNA having the sequence of Seq ID No. 17 and a mimetic of a miRNA having the sequence of Seq ID No. 18.
28. A method of prevention and/or treatment of a fibroproliferative disorder, said method comprising administering to a patient in need thereof a miRNA mimetic of miRNA-212-5p, wherein the miRNA mimetic is or contains an oligomer of nucleotides that consist of the sequence of Seq ID No. 99…wherein said prevention and/or treatment further comprises the administration of a mimetic of a miRNA having the sequence of Seq ID No. 17 and/or a mimetic of a miRNA having the sequence of Seq ID No. 19.
34. A method according to claim 28, wherein said prevention and/or treatment further comprises the administration of a mimetic of a miRNA having the sequence of Seq ID No. 18.
17. The method of claim 26, wherein the vector is a recombinant AAV vector.
18. The method of claim 26, wherein the vector is a recombinant AAV vector having the AAV-2 serotype.
19. The method of claim 26, wherein the capsid comprises a first protein that comprises the sequence of Seq ID No. 29 or 30.
20. ,The method of claim 26, wherein the capsid comprises a first protein that is 80% identical to a second protein having the sequence of Seq ID No. 82, whereas one or more gaps in the alignment between the first protein and the second are allowed.
21. The method of claim 26, wherein the capsid comprises a first protein that is 95% identical to a second protein of Seq ID No. 82, whereas a gap in the alignment between the first protein and the second protein is counted as a mismatch.
22. The method of claim 26, wherein the vector is a recombinant AAV vector having the AAV5 or the AAV6.2 serotype, and wherein the capsid of the recombinant AAV6.2 vector preferably comprises a capsid protein having the sequence of Seq ID No. 82.
50. The method of claim 22,wherein the capsid of the recombinant AAV6.2 vector comprises a capsid protein having the sequence of SEQ ID NO: 82.
10. The method of claim 26, wherein the vector is a recombinant AAV vector.
11. The method of claim 26, wherein the vector is a recombinant AAV vector having the AAV-2 serotype.
12. The method of claim 26, wherein the capsid comprises a first protein that comprises the sequence of Seq ID No. 29 or 30.
13. ,The method of claim 26, wherein the capsid comprises a first protein that is 80% identical to a second protein having the sequence of Seq ID No. 82, whereas one or more gaps in the alignment between the first protein and the second are allowed.
14. The method of claim 26, wherein the capsid comprises a first protein that is 95% identical to a second protein of Seq ID No. 82, whereas a gap in the alignment between the first protein and the second protein is counted as a mismatch.
15. The method of claim 26, wherein the vector is a recombinant AAV vector having the AAV5 or the AAV6.2 serotype, and wherein the capsid of the recombinant AAV6.2 vector preferably comprises a capsid protein having the sequence of Seq ID No. 82.
32. A miRNA mimetic for use in a method of prevention and/or treatment of a fibroproliferative disorder, wherein miRNA comprises the sequence of Seq ID No. 15.
34. A miRNA mimetic for use in a method according to claim 32, wherein said prevention and/or treatment further comprises the administration of a mimetic of a miRNA having the sequence of Seq ID No. 19 or a mimetic of a miRNA having the sequence of Seq ID No. 18, or a mimetic of a miRNA having the sequence of Seq ID No. 17.
35. A miRNA mimetic for use in a method according to claim 32, wherein said prevention and/or treatment further comprises the administration of a mimetic of a miRNA having the sequence of Seq ID No. 17.
37. A miRNA mimetic for use in a method according to claim 32, wherein said prevention and/or treatment further comprises the administration of a mimetic of a miRNA having the sequence of Seq ID No. 19.
39. A miRNA mimetic for use in a method according to claim 32, wherein said prevention and/or treatment further comprises the administration of a mimetic of a miRNA having the sequence of Seq ID No. 17 and a mimetic of a miRNA having the sequence of Seq ID No. 19.
42. A miRNA mimetic for use in a method according to claim 32, wherein the fibroproliferative disorder is IPF or PF-ILD.
38. Pharmaceutical composition comprising (i) a miRNA mimetic of a miRNA fragment having the sequence of Seq ID No. 99 and (ii) a miRNA mimetic of a miRNA having the sequence of Seq ID No. 17 and/or a mimetic of the miRNA having the sequence of Seq ID No. 19, and a pharmaceutical-acceptable carrier or diluent.
33. A miRNA mimetic of miRNA 212-5p for use in a method according to claim 32, wherein the miRNA mimetic is an oligomer of nucleotides that consist of the sequence of Seq ID No. 15, with the following proviso:- the oligomer optionally comprises nucleotides with chemical modifications leading to non- naturally occurring nucleotides that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 15;- the oligomer optionally comprises nucleotide analogues that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 15;- the oligomer is optionally lipid conjugated to facilitate drug delivery.
36. A miRNA mimetic for use in a method according to claim 32, wherein said prevention and/or treatment further comprises the administration of a miRNA mimetic of miRNA 181 a-5p, and wherein the miRNA mimetic is an oligomer of nucleotides that consists of the sequence of Seq ID No. 17, with the following proviso:- the oligomer optionally comprises nucleotides with chemical modifications leading to non- naturally occurring nucleotides that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 17;- the oligomer optionally comprises nucleotide analogues that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 17;- the oligomer is optionally lipid conjugated to facilitate drug delivery.
44. Pharmaceutical composition according to claim 38, comprising (a) a miRNA mimetic of miRNA 212-5p, wherein the miRNA mimetic is or contains an oligomer of nucleotides that consists of the sequence of Seq ID No. 99, with the following proviso:- the oligomer optionally comprises nucleotides with chemical modifications leading to non-naturally occurring nucleotides that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of SEQ ID No. 99; - the oligomer optionally comprises nucleotide analogues that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of SEQ ID No. 99; - the oligomer is optionally lipid conjugated to facilitate drug delivery; and (b) a miRNA mimetic of miRNA 181 a-5p, wherein the miRNA mimetic is or contains an oligomer of nucleotides that consists of the sequence of Seq ID No. 17 or Seq ID No.100, with the following proviso: - the oligomer optionally comprises nucleotides with chemical modifications leading to non-naturally occurring nucleotides that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 17 or SEQ ID No. 100; - the oligomer optionally comprises nucleotide analogues that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 17 or SEQ ID No. 100, - the oligomer is optionally lipid conjugated to facilitate drug delivery
38. A miRNA mimetic for use in a method according to claim 32, wherein said prevention and/or treatment further comprises the administration of a miRNA mimetic of miRNA 181b-5p, and wherein the miRNA mimetic is an oligomer of nucleotides that consists of the sequence of Seq ID No. 19, with the following proviso:- the oligomer optionally comprises nucleotides with chemical modifications leading to non- naturally occurring nucleotides that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 19;- the oligomer optionally comprises nucleotide analogues that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 19;- the oligomer is optionally lipid conjugated to facilitate drug delivery.
45. Pharmaceutical composition according to claim 38, comprising (a) a miRNA mimetic of miRNA 212-5p, wherein the miRNA mimetic is or contains an oligomer of nucleotides that consist of the sequence of Seq ID No. 99, with the following proviso:- the oligomer optionally comprises nucleotides with chemical modifications leading to non-naturally occurring nucleotides that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of SEQ ID No. 99; - the oligomer optionally comprises nucleotide analogues that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of SEQ ID No. 99; - the oligomer is optionally lipid conjugated to facilitate drug delivery; and (b) a miRNA mimetic of miRNA 181b-5p, wherein the miRNA mimetic is or contains an oligomer of nucleotides that consist of the sequence of Seq ID No. 19 or Seq ID No.101, with the following proviso: - the oligomer optionally comprises nucleotides with chemical modifications leading to non-naturally occurring nucleotides that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 19 or SEQ ID No 101; - the oligomer optionally comprises nucleotide analogues that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 19 or SEQ ID No 101, - the oligomer is optionally lipid conjugated to facilitate drug delivery; and (c) a pharmaceutical-acceptable carrier or diluent.
Please note that SEQ ID NOs: 15, 17, 18 and 19 are used to denote the same nucleotide sequences in both applications. Please see the attached OA appendix for the alignments.
Regarding instant claim 26 and copending claim 1, SEQ ID NO: 99 is the same sequence as SEQ ID NO: 15 except for a single mismatch at the 3’ end. Bofill-De Ros provides a teaching, suggestion or motivation to introduce a mismatch between the terminal 3’ positions of a miRNA guide strand and its target, because this would enhance RISC performance and thus silencing:
While extensive complementarity in both the 5′ and the middle regions of guide strand are crucial for Ago2 mediated cleavage, base pairing at the 3′ end is not required. In fact, mismatches at position 18, 19, 20, 21 promote dislocation and thereby turnover rate of Ago2, enhancing RISC performance towards highly abundant targets.
Please note that Bofill De-Ros provides this guidance in the context of a 21 nt strand (Fig. 4A), such that a mismatch at position 21 is a mismatch at the 3’-terminal position. This is equivalent to the present situation, in which SEQ ID NO: 99 has a mismatch at the 3’-terminal position.
It would have been prima facie obvious to a person having ordinary skill in the art before the effective filing date of the claimed invention to have modified the miRNA guide sequence of 18251562 to introduce a 3’ mismatch and thereby enhance the silencing effect, as taught by Bofil-De Ros.
Regarding the copending claims limited only to compositions comprising the recited oligonucleotides, the copending specification discloses that the composition comprising any one of or a combination or subcombination of SEQ ID NOs: 99 (miR212-5p), 17 (181a-5p), and/or 19 (181b-5p) may be used in methods of treating pulmonary fibrosis (p. 82 ln 6-9, ln 14-21). Thus the invention as a whole was prima facie obvious. See MPEP 804.II.B.
Claim 4-6, 8, 17-22, 26, 32, 34-36, 42, 48 and 50 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 10-15, 28, 33, 37, and 43-44 of copending Application No. 18251597.
This is a provisional nonstatutory double patenting rejection because the copending claims have not been patented.
The instant and copending claims are related as shown below:
Instant claim
Copending claim
26. Method of treating a disease selected from the group consisting of PF-ILD, IPF, connective tissue disease (CTD)-associated ILD, rheumatoid arthritis ILD, chronic fibrosing hypersensitivity pneumonitis (HP), idiopathic non-specific interstitial pneumonia (iNSIP), unclassifiable idiopathic interstitial pneumonia (IIP), environmental/occupational lung disease, systemic sclerosis ILD, sarcoidosis, and fibrosarcoma, the method comprising administering to a patient in need thereof a therapeutically active amount of viral vector comprising: a capsid and a packaged nucleic acid, wherein the packaged nucleic acid codes for one or more miRNAs, wherein at least one of the one or more miRNAs comprises the miRNA of Seq ID No. 15, Seq ID No. 17, or Seq ID No. 19.
48. Method of treating a disease selected from the group consisting of PF-ILD, IPF, connective tissue disease (CTD)-associated ILD, rheumatoid arthritis ILD, chronic fibrosing hypersensitivity pneumonitis (HP), idiopathic non-specific interstitial pneumonia (iNSIP), unclassifiable idiopathic interstitial pneumonia (IIP), environmental/occupational lung disease, systemic sclerosis ILD, sarcoidosis, and fibrosarcoma, the method comprising administering to a patient in need thereof a therapeutically active amount of a pharmaceutical composition comprising (i) a miRNA mimetic of a miRNA having the sequence of Seq ID No. 15, or (ii) a miRNA mimetic of a miRNA having the sequence of Seq ID No. 17, or (iii) a miRNA mimetic of a miRNA having the sequence of Seq ID No. 18, or (iv) a miRNA mimetic of a miRNA having the sequence of Seq ID No. 19, and apharmaceutical-acceptable carrier or diluent.
28. A method of prevention and/or treatment of a fibroproliferative disorder by administering an miRNA …wherein said prevention and/or treatment further comprises the administration of a mimetic of a miRNA having the sequence of Seq ID No. 15 and/or a mimetic of a miRNA having the sequence of Seq ID No. 17.
4. The method of claim 26, wherein the packaged nucleic acid codes for more than one miRNA, wherein said miRNAs comprise the miRNA of Seq ID No. 15 and the miRNA of Seq ID No. 17 and the miRNA of Seq ID No. 19.
5. The method of claim 26, wherein the packaged nucleic acid codes for more than one miRNA, wherein said miRNAs comprise the miRNA of Seq ID No. 15 and the miRNA of Seq ID No. 17.
6. The method of claim 26, wherein the packaged nucleic acid codes for more than one miRNA, wherein said miRNAs comprise the miRNA of Seq ID No. 15 and the miRNA of Seq ID No. 19.
8. The method of claim 26 wherein the packaged nucleic acid codes for more than one miRNA, wherein said miRNAs comprise the miRNA of Seq ID No. 19 and the miRNA of Seq ID No. 17.
28. A method of prevention and/or treatment of a fibroproliferative disorder by administering an miRNA …wherein said prevention and/or treatment further comprises the administration of a mimetic of a miRNA having the sequence of Seq ID No. 15 and/or a mimetic of a miRNA having the sequence of Seq ID No. 17.
33. A method according to claim 28, wherein said prevention and/or treatment further comprises the administration of a mimetic of a miRNA having the sequence of Seq ID No. 19.
26. Method of treating a disease selected from the group consisting of PF-ILD, IPF, connective tissue disease (CTD)-associated ILD, rheumatoid arthritis ILD, chronic fibrosing hypersensitivity pneumonitis (HP), idiopathic non-specific interstitial pneumonia (iNSIP), unclassifiable idiopathic interstitial pneumonia (IIP), environmental/occupational lung disease, systemic sclerosis ILD, sarcoidosis, and fibrosarcoma, the method comprising administering to a patient in need thereof a therapeutically active amount of viral vector comprising: a capsid and a packaged nucleic acid, wherein the packaged nucleic acid codes for one or more miRNAs, wherein at least one of the one or more miRNAs comprises the miRNA of Seq ID No. 15, Seq ID No. 17, or Seq ID No. 19.
17. The method of claim 26, wherein the vector is a recombinant AAV vector.
18. The method of claim 26, wherein the vector is a recombinant AAV vector having the AAV-2 serotype.
19. The method of claim 26, wherein the capsid comprises a first protein that comprises the sequence of Seq ID No. 29 or 30.
20. ,The method of claim 26, wherein the capsid comprises a first protein that is 80% identical to a second protein having the sequence of Seq ID No. 82, whereas one or more gaps in the alignment between the first protein and the second are allowed.
21. The method of claim 26, wherein the capsid comprises a first protein that is 95% identical to a second protein of Seq ID No. 82, whereas a gap in the alignment between the first protein and the second protein is counted as a mismatch.
22. The method of claim 26, wherein the vector is a recombinant AAV vector having the AAV5 or the AAV6.2 serotype, and wherein the capsid of the recombinant AAV6.2 vector preferably comprises a capsid protein having the sequence of Seq ID No. 82
50. The method of claim 22,wherein the capsid of the recombinant AAV6.2 vector comprises a capsid protein having the sequence of SEQ ID NO: 82..
1. Viral vector comprising: a capsid and a packaged nucleic acid, wherein the packaged nucleic acid codes for two or more miRNAs, wherein the two or more miRNAs comprise…the miRNA of Seq ID No. 15…or…miRNA of Seq ID No. 17
10. Viral vector according to claim 1, wherein the vector is a recombinant AAV vector.
11. Viral vector according to claim 1, wherein the vector is a recombinant AAV vector having the AAV-2 serotype.
12. Viral vector according to claim 1, wherein the capsid comprises a first protein that comprises the sequence of Seq ID No. 29 or 30.
13. Viral vector according to claim 1, wherein the capsid comprises a first protein that is 80% identical to a second protein having the sequence of Seq ID No. 82, whereas one or more gaps in the alignment between the first protein and the second are allowed.
14. Viral vector according to claim 1, wherein the capsid comprises a first protein that is 95% identical to a second protein of Seq ID No. 82, whereas a gap in the alignment between the first protein and the second protein is counted as a mismatch.
15. Viral vector according to claim 1, wherein the vector is a recombinant AAV vector having the AAV5 or the AAV6.2 serotype, and wherein the capsid of the recombinant AAV6.2 vector preferably comprises a capsid protein having the sequence of Seq ID No. 82.
32. A miRNA mimetic for use in a method of prevention and/or treatment of a fibroproliferative disorder, wherein miRNA comprises the sequence of Seq ID No. 15.
34. A miRNA mimetic for use in a method according to claim 32, wherein said prevention and/or treatment further comprises the administration of a mimetic of a miRNA having the sequence of Seq ID No. 19 or a mimetic of a miRNA having the sequence of Seq ID No. 18, or a mimetic of a miRNA having the sequence of Seq ID No. 17.
35. A miRNA mimetic for use in a method according to claim 32, wherein said prevention and/or treatment further comprises the administration of a mimetic of a miRNA having the sequence of Seq ID No. 17.
42. A miRNA mimetic for use in a method according to claim 32, wherein the fibroproliferative disorder is IPF or PF-ILD.
1. Viral vector comprising: a capsid and a packaged nucleic acid, wherein the packaged nucleic acid codes for two or more miRNAs, wherein the two or more miRNAs comprise…the miRNA of Seq ID No. 15…or…miRNA of Seq ID No. 17
33. A miRNA mimetic of miRNA 212-5p for use in a method according to claim 32, wherein the miRNA mimetic is an oligomer of nucleotides that consist of the sequence of Seq ID No. 15, with the following proviso:- the oligomer optionally comprises nucleotides with chemical modifications leading to non- naturally occurring nucleotides that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 15;- the oligomer optionally comprises nucleotide analogues that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 15;- the oligomer is optionally lipid conjugated to facilitate drug delivery.
36. A miRNA mimetic for use in a method according to claim 32, wherein said prevention and/or treatment further comprises the administration of a miRNA mimetic of miRNA 181 a-5p, and wherein the miRNA mimetic is an oligomer of nucleotides that consists of the sequence of Seq ID No. 17, with the following proviso:- the oligomer optionally comprises nucleotides with chemical modifications leading to non- naturally occurring nucleotides that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 17;- the oligomer optionally comprises nucleotide analogues that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 17;- the oligomer is optionally lipid conjugated to facilitate drug delivery.
37. Pharmaceutical composition comprising…a miRNA mimetic of a miRNA having the sequence of Seq ID No. 15…or…a miRNA mimetic of a miRNA having the sequence of Seq ID No. 17
43. Pharmaceutical composition according to claim 37, comprising…a miRNA mimetic of miRNA 212-5p, wherein the miRNA mimetic is or contains an oligomer of nucleotides that consists of the sequence of Seq ID No. 15…with the following proviso: - the oligomer optionally comprises nucleotides with chemical modifications leading to non-naturally occurring nucleotides that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 15…the oligomer optionally comprises nucleotide analogues that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 15…the oligomer is optionally lipid conjugated to facilitate drug delivery
44. Pharmaceutical composition according to claim 37 comprising…a miRNA mimetic of miRNA 181 a-5p, wherein the miRNA mimetic is or contains an oligomer of nucleotides that consist of the sequence of Seq ID No. 17…00, with the following proviso: - the oligomer optionally comprises nucleotides with chemical modifications leading to non-naturally occurring nucleotides that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No.17 or Seq ID No. 100; - the oligomer optionally comprises nucleotide analogues that show the base-pairing behavior at the corresponding position (AU and GC) as determined by the sequence of Seq ID No. 17 or Seq ID No. 100, - the oligomer is optionally lipid conjugated to facilitate drug delivery
Please note that, as above, SEQ ID NOs: 15, 17 and 19 are used to denote the same nucleotide sequences in both applications. Please see the attached OA appendix for the alignments.
Regarding the copending claims limited only to compositions comprising the recited oligonucleotides, the copending specification discloses that the composition comprising any one of or a combination or subcombination of SEQ ID NOs: 15 (miR212-5p), 17 (181a-5p), and/or 19 (181b-5p) may be used in methods of treating pulmonary fibrosis (p. 55 ln 6-9, ln 14-21). Thus the invention as a whole was prima facie obvious. See MPEP 804.II.B.
Response to Arguments
Applicant's arguments filed 04/29/2026 have been fully considered but they are not persuasive. Applicant argues that, “later-expiring patents/application were not proper obviousness-type double patenting references” (p. 14-15). Examiner agrees that the co-pending application(s) has/have a later US filing date. However, MPEP 804.I.B.1.(b).(i) makes clear that a provisional double patenting rejection should be made and maintained by the examiner until the rejection has been overcome by amendment or the rejection is the only rejection remaining in an application having the earlier patent term filing date. Because the claims are still rejected under §112(a), the rejection(s) for nonstatutory double patenting is/are maintained.
Conclusion
No claims are allowed at this time.
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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/A.M.Z./Examiner, Art Unit 1636
/BRIAN WHITEMAN/Primary Examiner, Art Unit 1636
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