DETAILED ACTIONNotice 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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 1/14/26 has been entered.
Application Status and Election
Claims 1-11 are pending. No claims are amended or added.
Examination on the merits commences on claims 1-11.
Applicants are informed that the rejections and/or objections of the previous Office action not stated below have been withdrawn from consideration in view of the Applicant' s arguments and/or amendments. 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 Rejections - 35 USC § 103 - MAINTAINED
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claim(s) 1-3 is/are rejected under 35 U.S.C. 103 as being unpatentable over Zhao of record (Zhao, Mian, et al. "SNHG12 promotes angiogenesis following ischemic stroke via regulating miR-150/VEGF pathway." Neuroscience 390 (2018): 231-240, published October 15 2018), as evidenced by Canugovi of record (Canugovi, Chandrika, et al. "The role of DNA repair in brain related disease pathology." DNA repair 12.8 (2013): 578-587.) and Li (Li, Peiying, et al. "Mechanistic insight into DNA damage and repair in ischemic stroke: exploiting the base excision repair pathway as a model of neuroprotection." Antioxidants & redox signaling 14.10 (2011): 1905-1918.), in view of Deveza of Record (Deveza, Lorenzo, Jeffrey Choi, and Fan Yang. "Therapeutic angiogenesis for treating cardiovascular diseases." Theranostics 2.8 (2012): 801.)
Regarding claim 1, Zhao teaches methods related to treating ischemic stroke. Zhao teaches over 80% of stroke is ischemic where ischemia results from the lack of blood flow with oxygen and nutrients (pg 231 col1 para1). Zhao teaches that in response to insufficient blood supply, the body undergoes angiogenesis as natural processes to restore blood flow and that angiogenesis is essential for the repair of cerebral ischemia. Zhao teaches the promotion of angiogenesis is widely recognized as a promising therapeutic strategy for ischemic stroke (pg 231 col1 para1). Zhao further teaches Small nucleolar RNA host gene 12 (SNHG12) is a novel lncRNA identified to be up-regulated in several cancer cells and plays important roles in cancer cell proliferation and migration (pg 232 col 1 para 2). Zhao teaches in a method of treating ischemic stroke vascular disease where overexpression of long non-coding RNA SNHG12 improved the recovery of neurological function, reduced infarct volume and miR-150 expression, and increased vascular density and VEGF expression in the infarct border zone of MCAO mice (abstract and Fig. 6). Zhao teaches overexpression of lncRNA SNHG12 attenuates ischemic stroke that is related to miR-150/VEGF signaling in vivo (pg 237 col 1 para 1). Zhao further teaches SNHG12 promotes angiogenesis following ischemic stroke via miR-150/VEGF pathway, which clarifies the mechanism of angiogenesis after ischemic stroke and provides a target for the treatment stroke (abstract and Fig. 1,2).
Zhao is silent as to the relationship of stroke and failure of a DNA repair response. However, Canugovi discloses the role of DNA repair in brain related disease pathology including stroke (title, pg 578 col 1 para 1). Canugovi establishes stroke as a disease state associated with inadequate DNA repair response for avoiding oxidative neuronal damage (abstract, pg 579 col 2 para 1). Canugovi teaches the brain has a decreased ratio of anti-oxidant to pro-oxidant enzymes where this imbalance amplifies the level of oxidative damage within brain cells, which increases the demand on DNA repair activity, which in turn requires additional energy, creating a perpetual state of oxidative stress (pg 578 col 2 para 1). Canugovi teaches that ischemic stroke causes loss of blood flow from blood clotting which causes lack of oxygen supply and other nutrients leading to surrounding tissue damage where the neurological damage in ischemic stroke is caused by the acute burst of ROS during reperfusion (pg 579 col 2 para 1). Canugovi teaches oxidative DNA damage in neurons with BER glycosylase-deficient mouse models that are being used to explore the role of BER neurodegenerative diseases including stroke (pg 578 col 2 para 2).
Li further teaches “Stroke” implicated as a disease associated with malfunction of DNA repair response given loss of DNA repair exacerbates neuronal loss after ischemic stroke indicating the importance of DNA integrity in neuronal viability (pg 1907 col 1 para 3)
Zhao does not specifically teach wherein the treated disease is atherosclerosis.
However, Deveza teaches treatment modalities for cardiovascular disease classified into coronary artery disease, cerebrovascular disease, peripheral arterial disease, and atherosclerosis (pg 801 col 2 para 2). Deveza teaches cardiovascular disease is generally characterized by narrowing or occlusion of the blood supply of these vascular beds, and is most commonly caused by atherosclerosis (pg 801 col 2 para 2). Deveza teaches treatment options for cardiovascular disease aim to re-establish blood flow through the affected vascular beds (pg 801 col 2 para 2) by stimulating angiogenesis (pg 802 col 1 para 3).
It would have been obvious to one skilled in the art before the effective filing date of the claimed invention to have applied Zhao’s method of delivering lncRNA SNHG12 which promotes angiogenesis in the treatment of stroke to also be delivered to a subject to treat atherosclerosis. It would have merely amounted to a simple combination of prior art elements according to known methods to yield predictable results. The skilled artisan would have had a reasonable expectation that the VEGF angiogenesis promoting lncRNA SNHG12 to treat ischemic stroke could also be effectively applied to treat subjects to with atherosclerosis because the disease processes are significantly related given that 1) Deveza teaches atherosclerosis as a form of cardiovascular disease involving blockage of blood supply which can be treated by angiogenesis of new blood vessels, 2) Canugovi describes ischemic stroke by loss of blood flow from blood clotting which causes lack of blood supply and other nutrients leading to surrounding tissue damage, 3) Li teaches stroke as a disease associated with malfunction of DNA repair response and 4) because Zhao’s lncRNA SNHG12 composition promotes angiogenesis to treat ischemic stroke, a condition in which atherosclerotic blockage plays a significant role. The skilled artisan would therefore be motivated to employ Zhao’s lncRNA SNHG12 constructs to promote new blood flow angiogenesis in the treatment of atherosclerosis vascular disease who have similarly occluded vasculature by atherosclerotic blocking lesions and who would benefit from increased blood flow. Regarding claim 2, Zhao teaches overexpression of lncRNA SNHG12 attenuates ischemic stroke that is related to miR-150/VEGF signaling in vivo (pg 237 col 1 para 1), i.e. the composition comprising all or part of the SNHG12 long-coding RNA.
Regarding claim 3, Zhao teaches LNC SNHG12 delivered to MCAO mouse models via intracerebroventricular injection of SNHG12 lentivirus expression vector (pg 233 col 1 para 3).
Claim(s) 1, 4, and 6 is/are rejected under 35 U.S.C. 103 as being unpatentable over Zhao of record (Zhao, Mian, et al. "SNHG12 promotes angiogenesis following ischemic stroke via regulating miR-150/VEGF pathway." Neuroscience 390 (2018): 231-240, published October 15 2018), claim 1 as evidenced by Canugovi of record (Canugovi, Chandrika, et al. "The role of DNA repair in brain related disease pathology." DNA repair 12.8 (2013): 578-587.) and Li (Li, Peiying, et al. "Mechanistic insight into DNA damage and repair in ischemic stroke: exploiting the base excision repair pathway as a model of neuroprotection." Antioxidants & redox signaling 14.10 (2011): 1905-1918.), in view of Deveza of record (Deveza, Lorenzo, Jeffrey Choi, and Fan Yang. "Therapeutic angiogenesis for treating cardiovascular diseases." Theranostics 2.8 (2012): 801.), as applied to claim 1, and in further view of in view of GenBank1 of record (GenBank1, Homo sapiens small nucleolar RNA host gene 12 (SNHG12), transcript variant 5, long non-coding RNA https://www.ncbi.nlm.nih.gov/nuccore/1171452140?sat=46&satkey=116101966, revision Sept 10 2017, retrieved July 13 2024, printed as pages 1/1-1/3.)
The teachings of Zhao and Canugovi and Li and Deveza as applied above for claim 1 are incorporated here.
Regarding claims 4 and 6, Zhao does not teach the sequence of the lncRNA SNHG12 employed in the method of treating stroke in mice.
GenBank1 teaches long non-coding RNA for homo sapiens small nucleolar RNA host gene 12 (SNHG12) with 96.9% sequence match to Applicant’s SEQ ID NO: 1.
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It would have been obvious to one skilled in the art before the effective filing date of the claimed invention for Zhao to have used the lncRNA SNHG12 sequence of Genbank1. It would have merely amounted to a simple substitution of prior art elements according to known methods to yield predictable results. The skilled artisan would have had a reasonable expectation that the sequence disclosed by GenBank1 would similarly influence stroke symptoms of the mouse endothelium cells because GenBank1 teaches the sequence of lncRNA SNHG12 and Zhao teaches using an expression vector coding for lncRNA SNHG12. The skilled artisan would be motivated to employ the lncRNA sequence taught by GenBank1 in Zhao’s method in order to investigate further treatment potential for lncRNA SNHG12 for subjects with stroke and also applied to treat subjects with atherosclerosis, given the §103 rejection rationale above applied to claim 1.
Claim(s) 1, 7 and 11 is/are rejected under 35 U.S.C. 103 as being unpatentable over Zhao of record (Zhao, Mian, et al. "SNHG12 promotes angiogenesis following ischemic stroke via regulating miR-150/VEGF pathway." Neuroscience 390 (2018): 231-240, published October 15 2018), as evidenced by Canugovi of record (Canugovi, Chandrika, et al. "The role of DNA repair in brain related disease pathology." DNA repair 12.8 (2013): 578-587.) and Li (Li, Peiying, et al. "Mechanistic insight into DNA damage and repair in ischemic stroke: exploiting the base excision repair pathway as a model of neuroprotection." Antioxidants & redox signaling 14.10 (2011): 1905-1918.), in view of Deveza of record (Deveza, Lorenzo, Jeffrey Choi, and Fan Yang. "Therapeutic angiogenesis for treating cardiovascular diseases." Theranostics 2.8 (2012): 801.), as applied to claim 1, and in further view of Xie of record (Xie, Hongzhi, et al. "Inhibition of intimal hyperplasia via local delivery of vascular endothelial growth factor cDNA nanoparticles in a rabbit model of restenosis induced by abdominal aorta balloon injury." Experimental and therapeutic medicine 10.1 (2015): 55-61.) and Jufri of record (Jufri, Nurul F., et al. "Mechanical stretch: physiological and pathological implications for human vascular endothelial cells." Vascular cell 7 (2015): 1-12.)
Regarding claims 7 and 11, the teachings of Zhao and Canugovi and Li and Deveza as applied above for claim 1 are incorporated here. Briefly, Zhao teaches overexpression of lncRNA SNHG12 attenuates ischemic stroke that is related to miR-150/VEGF signaling in vivo (pg 237 col 1 para 1). Zhao teaches LNC SNHG12 delivered to MCAO mouse models via intracerebroventricular injection (pg 233 col 1 para 3).
Zhao does not teach administration of compositions delivered arterially and to the tunica intima of a subject. Zhao is also silent as to the relationship of stroke and failure of a DNA repair response. However, Canugovi teaches stroke as a disease state associated with a malfunction in DNA repair response (abstract).
Xie teaches local delivery of VEGF gene delivering nanoparticles reduced intimal thickening and cell proliferation following abdominal aorta balloon injury in a rabbit model, demonstrating the efficacy of this therapy against restenosis arterial injury (abstract). Xie teaches a perfusion balloon, GENIE Catheter, as a new local drug delivery catheter designed to deliver various liquid therapeutic agents into arteries (pg 57 col 2 para 1). Xie teaches the delivery method for the sustained delivery of VEGF is an appropriate and efficient method of promoting reendothelialization following arterial injury (pg 60 col 2 para 2).
Jufri teaches the tunica intima is the innermost layer of the vascular wall that contains the endothelium (endothelial cell (EC) layers) that provides a smooth surface for blood flow (pg 1 col 1 para 1). It would have been obvious to one skilled in the art before the effective filing date of the claimed invention to have modified Zhao’s delivery method of lncRNA SNHG12 for treating stroke to utilize the perfusion balloon catheter of Xie for local arterial delivery of lncRNA to the tunica intima of a subjects vessels. It would have merely amounted to a simple substitution of prior art elements according to known methods to yield predictable results. The skilled artisan would have had a reasonable expectation that Zhao’s lncRNA SNHG12 delivery method could be enhanced by local balloon catheter arterial delivery because Xie demonstrated the effectiveness of delivering agents to treat vascular injury by using the perfusion balloon catheter delivery method. It would have been predictable that Zhao’s nucleic acid compositions would be delivered to the tunica intima of the subjects vascular wall because Jufri teaches the tunica intima as the innermost layer of the vascular wall thus exposed to arterial delivery and because Xie teaches the subjects intima is directly influenced by the balloon catheter delivery method. The skilled artisan would be motivated to employ Xie’s direct local arterial delivery method to deliver Zhao’s lncRNA SNHG12 to enhance angiogenesis effects of lncRNA SNHG12 in a subject with stroke vascular disease and also applied to treat subjects with atherosclerosis, given the §103 rejection rationale above applied to claim 1.
Claim(s) 1, 2, 8 and 9 is/are rejected under 35 U.S.C. 103 as being unpatentable over Zhao of record (Zhao, Mian, et al. "SNHG12 promotes angiogenesis following ischemic stroke via regulating miR-150/VEGF pathway." Neuroscience 390 (2018): 231-240, published October 15 2018), as evidenced by Canugovi of record (Canugovi, Chandrika, et al. "The role of DNA repair in brain related disease pathology." DNA repair 12.8 (2013): 578-587.) and Li (Li, Peiying, et al. "Mechanistic insight into DNA damage and repair in ischemic stroke: exploiting the base excision repair pathway as a model of neuroprotection." Antioxidants & redox signaling 14.10 (2011): 1905-1918.) in view of Deveza of record (Deveza, Lorenzo, Jeffrey Choi, and Fan Yang. "Therapeutic angiogenesis for treating cardiovascular diseases." Theranostics 2.8 (2012): 801.), as applied to claim 1, and in further view of Cummins of record (Cummins, Lendell L., et al. "Characterization of fully 2′-modified oligoribonucleotide hetero-and homoduplex hybridization and nuclease sensitivity." Nucleic acids research 23.11 (1995): 2019-2024.)
Regarding claims 8 and 9, the teachings of Zhao and Canugovi and Li and Deveza as applied above for claims 1 and 2 are incorporated here.
Zhao does not teach 2’-O-methyl chemical modifications of the nucleic acid constructs with enhanced nuclease stability.
Cummins teaches 2’-O-methyl modified nucleic acid constructs demonstrate enhanced nuclease stability (pg 2024 col 1 para 2).
It would have been obvious to one skilled in the art before the effective filing date of the claimed invention for Zhao to have used the lncRNA SNHG12 constructs which includes 2’-O-methyl chemical modifications. It would have merely amounted to a simple combination of prior art elements according to known methods to yield predictable results. The skilled artisan would have had a reasonable expectation that the lncRNA SNHG12 construct disclosed by Zhao when chemically modified with 2’-O-methyl would have increased utility because Cummins teaches 2’-O-methyl modified nucleic acid constructs demonstrate enhanced nuclease stability. The skilled artisan would be motivated to employ 2’-O-methyl modification of the lncRNA SNHG12 construct in order to improve the lncRNA SNHG12 influence upon subjects with stroke and also applied to treat subjects with atherosclerosis, given the §103 rejection rationale above applied to claim 1.
Claim(s) 1, 2, 8, 9, and 10 is/are rejected under 35 U.S.C. 103 as being unpatentable over Zhao of record (Zhao, Mian, et al. "SNHG12 promotes angiogenesis following ischemic stroke via regulating miR-150/VEGF pathway." Neuroscience 390 (2018): 231-240, published October 15 2018), as evidenced by Canugovi of record (Canugovi, Chandrika, et al. "The role of DNA repair in brain related disease pathology." DNA repair 12.8 (2013): 578-587.) and Li (Li, Peiying, et al. "Mechanistic insight into DNA damage and repair in ischemic stroke: exploiting the base excision repair pathway as a model of neuroprotection." Antioxidants & redox signaling 14.10 (2011): 1905-1918.), in view of Deveza of record (Deveza, Lorenzo, Jeffrey Choi, and Fan Yang. "Therapeutic angiogenesis for treating cardiovascular diseases." Theranostics 2.8 (2012): 801.), as applied to claim 1 and 2, and Cummins of record (Cummins, Lendell L., et al. "Characterization of fully 2′-modified oligoribonucleotide hetero-and homoduplex hybridization and nuclease sensitivity." Nucleic acids research 23.11 (1995): 2019-2024.) as applied to claims 8 and 9, and in further view of Hoke of record (Hoke, Glenn D., et al. "Effects of phosphorothioate capping on antisense oligonucleotide stability, hybridization and antiviral efficacy versus herpes simplex virus infection." Nucleic acids research 19.20 (1991): 5743-5748.)
Regarding claim 10, the teachings of Zhao, Canugovi, Li, and Deveza applied above for claims 1 and 2 and the teachings of Cummins applied above to claims 8 and 9 are incorporated here.
Zhao does not teach 5’ cap chemical modifications of the nucleic acid constructs with enhanced nuclease stability.
Hoke teaches phosphodiester 5’ terminal cap modified nucleic acid constructs demonstrate enhanced nuclease stability (pg 5743 col 2 para 1).
It would have been obvious to one skilled in the art before the effective filing date of the claimed invention for Zhao to have used the lncRNA SNHG12 constructs which includes 5’ terminal cap chemical modifications. It would have merely amounted to a simple combination of prior art elements according to known methods to yield predictable results. The skilled artisan would have had a reasonable expectation that the lncRNA SNHG12 construct disclosed by Zhao when chemically modified with 5’ terminal cap would have increased utility because Hoke teaches 5’ terminal cap modified nucleic acid constructs demonstrate enhanced nuclease stability. The skilled artisan would be motivated to employ 5’ terminal cap modification of the lncRNA SNHG12 construct in order to improve the lncRNA SNHG12 influence upon subjects with stroke, and also applied to treat subjects with atherosclerosis, given the §103 rejection rationale above applied to claim 1.
Allowable Subject Matter
Claim 5 is objected to for depending from rejected claim 1. Examiner suggests incorporating the limitations of claim 5 into independent claim 1.
Regarding claim 5, after a thorough search of the related prior art, Applicant’s SEQ ID NO: 1 and 2 are not found to match any sequences such that it would be obvious that the nucleic acid sequence of claim 1 comprises exactly SEQ ID NO: 1 or 2. The closest prior art is GenBank1 which teaches long non-coding RNA for homo sapiens small nucleolar RNA host gene 12 (SNHG12) with 96.9% sequence match to Applicant’s SEQ ID NO: 1.
Response to Arguments
Examiner notes that the claims remain unamended and Applicant’s arguments resemble previous arguments from the Remarks filed 5/6/25 in response to the Non-Final rejection filed 2/7/25. Applicants argue (Remarks pg 1) that the cited references, alone or in combination, fail to teach each and every element of the present claims and that there is insufficient motivation described to combine the reference teachings according to the claimed invention. Applicants argue (Remarks pg 1) that Canugovi fails to teach stroke as a disease associated with a malfunction in DNA repair response and that Canugovi describes stroke as a neurodegenerative disease and not related to atherosclerosis. Applicants argue (Remarks pg 4) the potential dual role of angiogenesis treatment of atherosclerosis to undermine the predictability of therapeutic angiogenesis for atherosclerosis treatment.
Applicant’s arguments have been thoroughly reviewed and found unpersuasive for the following reasons:
Canugovi clearly establishes stroke related to oxidative damage which overwhelms the inadequate BER repair activity leading to neuronal deficit (pg 579 col 2 para 1). Examiner notes that just because Canugovi describes stroke as a type of neurodegenerative disease, this does not preclude stroke as being also a type of cardiovascular disease and as such highly related in therapeutic strategy to atherosclerosis treatment, as the Deveza of record reference teaches in the above 103 rejection. Examiner notes as a further example, “Stroke” is implicated as a disease associated with malfunction of DNA repair response by Li et. al., who teaches loss of DNA repair exacerbates neuronal loss after ischemic stroke indicating the importance of DNA integrity in neuronal viability (pg 1907 col 1 para 3; Li, Peiying, et al. "Mechanistic insight into DNA damage and repair in ischemic stroke: exploiting the base excision repair pathway as a model of neuroprotection." Antioxidants & redox signaling 14.10 (2011): 1905-1918.).
Applicants argue (Remarks pg 3) that “Stroke” is classically characterized as a neurological deficit attributed to an acute focal injury of the central nervous system (CNS) by a vascular cause,” while atherosclerosis "is a chronic immunoinflammatory, fibroproliferative disease of large and medium-sized arteries.” Applicants argue that Zhao relates to a method of treating stroke, a disease with a completely different etiology from atherosclerosis. These arguments have been thoroughly reviewed and found unpersuasive. Examiner notes that Zhao’s teachings focus specifically on ischemic stroke which is a vascular related condition and not “stroke” in general as Applicants refer to as merely a CNS disease.
However, 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 this case, the reference teachings in combination establish the obviousness rejection. Deveza clearly teaches that cardiovascular disease (CVD) is generally characterized by narrowing or occlusion of the blood supply of vascular beds, and that CVD is most commonly caused by atherosclerosis (pg 801 col 2 para 2), and that VEGF mediated therapeutic angiogenesis is an established treatment modality. “Treatment options for CVD generally aim to re-establish blood flow through the affected vascular beds,”. Zhao of record teaches overexpression of lncRNA SNHG12 attenuates ischemic stroke that is related to miR-150/VEGF signaling in vivo (pg 237 col 1 para 1). Zhao further teaches the promotion of angiogenesis is widely recognized as a therapeutic strategy for ischemic stroke (pg 231 col1 para1). Deveza teaches restoring blood supply is critical for the successful treatment of cardiovascular diseases (abstract) and teaches that cardiovascular disease is most commonly caused by atherosclerosis. Applicants assert that ischemic stroke and atherosclerosis are two completely different diseases, however a person of ordinary skill in the art would predictably conclude it obvious that VEGF angiogenesis promoting lncRNA SNHG12 to treat ischemic stroke could also be effectively applied to treat subjects to with atherosclerosis because the disease processes are significantly related given that 1) Deveza teaches atherosclerosis as a form of cardiovascular disease involving blockage of blood supply which can be treated by angiogenesis of new blood vessels, 2) Canugovi describes ischemic stroke by loss of blood flow from blood clotting which causes lack of blood supply and other nutrients leading to surrounding tissue damage, and 3) because Zhao’s lncRNA SNHG12 composition promotes angiogenesis to treat ischemic stroke, a condition in which atherosclerotic blockage plays a significant role. The skilled artisan would therefore be motivated to employ Zhao’s lncRNA SNHG12 constructs to promote new blood flow angiogenesis in the treatment of atherosclerosis vascular disease who have similarly occluded vasculature by atherosclerotic blocking lesions and who would benefit from increased blood flow.
Applicants further argue the claimed method is based on identification of "lncRNA SNHIG12 in atherosclerotic lesions as a homeostatic regulator of genomic stability by interaction with DNA-PK", a key mediator of DNA damage response (DDR) (Specification page 15, lines 24-26). Applicants further describe the Specification as disclosing knockdown of lncRNA SNHG12 impairs DNA damage repair leading to lesional DNA damage, vascular senescence, and accelerated atherosclerosis independent of effects on lipid-lowering or lesional inflammation and that administration of the lncRNA SNHG12 reduced lesional DNA damage and plaque burden (Specification, page 15, lines 26-30). However, Applicant's argument that the references fail to show these features of the invention, it is noted that the features upon which applicant relies are not recited in the rejected claim(s). Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993).
In summary, Atherosclerosis is the primary cause of ischemic stroke, driven by the buildup of fatty plaques in the carotid or cerebral arteries, which restricts oxygen-rich blood flow to the brain. However, atherosclerosis is diffuse in nature and related to a number of vascular dysfunctions as a result of the accumulation of fatty plaques. Such includes for example: 1)Tissue Hypoxia and Ischemia in Peripheral Artery Disease (PAD); 2) Therapeutic angiogenesis aims to increase blood flow to ischemic limb tissues, reducing pain and preventing amputation; 3) Collateral Vessel Formation (Arteriogenesis); 4) Reduced Exercise Tolerance and Angina in Coronary Artery Disease (CAD); and 5) Re-endothelialization and Endothelial Dysfunction. Given the diffuse nature of atherosclerosis, a treatment that effectively reverses or stops plaque formation in arteries, reduces blood viscosity to prevent thrombosis, or lowers systemic cholesterol, such as therapeutic angiogenesis is treating both the stroke and the underlying vascular disease of atherosclerosis.
Furthermore, the rationale to support a conclusion that the claim would have been obvious is that all the claimed elements were known in the prior art and one skilled in the art could have combined the elements as claimed by known methods with no change in their respective functions, and the combination yielded nothing more than predictable results to one of ordinary skill in the art. KSR, 550 U.S. at 416, 82 USPQ2d at 1395; B/E Aerospace, Inc. v. C&D Zodiac, Inc., 962 F.3d 1373, 1379, 2020 USPQ2d 10706 (Fed. Cir. 2020); Sakraida v. AG Pro, Inc., 425 U.S. 273, 282, 189 USPQ 449, 453 (1976); Anderson’s-Black Rock, Inc. v. Pavement Salvage Co., 396 U.S. 57, 62-63, 163 USPQ 673, 675 (1969); Great Atl. & P. Tea Co. v. Supermarket Equip. Corp., 340 U.S. 147, 152, 87 USPQ 303, 306 (1950).
Conclusion
All claims are rejected.
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/JOHN CHARLES MCKILLOP/Examiner, Art Unit 1637
/EKATERINA POLIAKOVA-GEORGANTAS/Primary Examiner, Art Unit 1637