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 .
This action is in response to the papers filed on April 03, 2026.
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 04/03/2026 has been entered.
Claims 1-2, 8, 10, 17, 20-21, 23, 48, 50, 52, 55, 59 and 67 are currently pending. Claims 1, 10, 23, 48, 50, 55 and 57 have been amended, no claims are newly added and claim 51 is canceled by Applicant’s amendments filed on 03/28/2026. Claims 1 and 48 are independent claims.
Election/Restrictions
In response to the restriction requirement filed on 7/29/2024, Applicant's election with traverse of the following species in the reply filed on 11/25/2024 is acknowledged:
Capsid protein sequence: SEQ ID NO: 2 (claim 1)
Transgene sequence: SEQ ID NO: 7 (claim 10)
rAAV gene therapy vector sequence: SEQ ID NO: 10 (claim 23)
Target organ: Heart (claim 59)
Effect upon administration: LAMP2B protein expression (claim 59)
Therefore, claims 1-2, 8, 10, 17, 20-21, 23, 48, 50, 52, 55, 59 and 67 are pending in the application and examined on the merits. Claims 1 and 48 are independent claims.
Priority
The present application is a 35 U.S.C. 371 national stage filing of International Application No. PCT/US2020/017987, filed February, 12 2020
Applicant’s claim for the benefit of a prior-filed parent provisional applications 62/934,928, filed 11/13/2019, and 62/804,521 filed 02/12/2019 under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) is acknowledged.
Thus, the earliest possible priority for the instant application is February 12, 2019.
Response to arguments
Withdrawn objections/ Rejections in response to Applicants’ arguments or amendments
Claim Rejections - 35 USC § 112(a) Written Description
The rejection of claims 1-2, 8, 10, 17, 20-21, 23, 25-30, 33, 37, 48-52, 55 and 59 and claim 67 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112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement is withdrawn.
Applicant’s arguments and amendments filed 03/28/2026 have been considered and are persuasive. Particularly, the amendments to claim 1, 10, and 23 have narrowed the scope of the invention to the specific SEQ ID NOs with 100% identity.
Maintained objections/ Rejections in response to Applicants’ arguments or amendments
Claim Rejections - 35 USC § 103
Claims 1-2, 8, 17, 21, 48, 50, 52, 55, 59 and 67 remain rejected under 35 U.S.C. 103 as being unpatentable over Adler et al. (WO2017/127565; previously cited) in view of Mendell (WO2013/078316; IDS Reference) as evidenced by RNG (20250204_142835_us-17-430-107-1.rng; Search Result within Application), RAI (20250204_142842_us-17-430-107-2.rai; Search Result within Application), Lang (2019, NATURE COMMUNICATIONS 10:3415), and Jackson Lab (Body Weight Information for C57BL/6J; accessed 10/31/2022).
This rejection has been modified as necessitated by Applicant’s arguments and amendments filed 09/22/2025.
Regarding claims 1, 48, 55, and 67, Adler teaches an rAAV vector comprising an AAV capsid protein and LAMP-2 flanked by ITRs for the purpose of treating Danon disease (Abstract, para. 0030, Figure 1). The AAV vector serotype is selected from AAV1-AAV11 and AAVrh10 (para. 0066). This vector is in a pharmaceutical composition comprising pharmaceutically acceptable carriers, diluents or excipients such as saline solutions (para. 0081-0082). Adler further teaches that Danon disease is a skeletal and cardiac muscle disorder (para. 0006). Moreover, the subject to be treated can be any mammal at any stage of development such as a human through intravenous injection of the polynucleotide of the vector encoding LAMP2 (para. 0057, 0061, 0066, 0081, 0088, Claim 1, 20, Example 9).
Regarding the claimed range of dosages and amounts, Adler teaches administering the gene therapy vector at a dose of 5x1011 , 1x1012, and 2x1012 gc/mouse (Example 3, 5, 9). As genome copies (gc) are viral particles with the target genome and is known in the art according to Lang that AAV vectors have gc/ml equal to vg/ml (p. 8, AAV vectors), it is interpreted that a dose of 2x1012 gc would therefore have 2x1012 vg. As evidenced by Jackson Lab, male mice at 6 months weigh about 36 grams (C57/BL/6J; 24 weeks). Therefore, it would be determined that the dosages would be 5x1011 vg/36g to 2x1012 vg/36g = 1.3 x 1013 to 5.6 x 1013 vg/kg which overlaps the claimed range.
MPEP 2144.05 states, “In the case where the claimed ranges "overlap or lie inside ranges disclosed by the prior art" a prima facie case of obviousness exists. In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976); In re Woodruff, 919 F.2d 1575, 16 USPQ2d 1934 (Fed. Cir. 1990) (The prior art taught carbon monoxide concentrations of "about 1-5%" while the claim was limited to "more than 5%." The court held that "about 1-5%" allowed for concentrations slightly above 5% thus the ranges overlapped.); In re Geisler, 116 F.3d 1465, 1469-71, 43 USPQ2d 1362, 1365-66 (Fed. Cir. 1997) (Claim reciting thickness of a protective layer as falling within a range of "50 to 100 Angstroms" considered prima facie obvious in view of prior art reference teaching that "for suitable protection, the thickness of the protective layer should be not less than about 10 nm [i.e., 100 Angstroms]." The court stated that "by stating that ‘suitable protection’ is provided if the protective layer is ‘about’ 100 Angstroms thick, [the prior art reference] directly teaches the use of a thickness within [applicant’s] claimed range."). See also In re Bergen, 120 F.2d 329, 332, 49 USPQ 749, 751-52 (CCPA 1941) (The court found that the overlapping endpoint of the prior art and claimed range was sufficient to support an obviousness rejection, particularly when there was no showing of criticality of the claimed range).”
However, Adler does not teach an AAVrh.74 capsid protein sequence encoded by SEQ ID NO: 1.
Mendell teaches utilizing an rh.74 AAV capsid protein encoded by their SEQ ID NO: 1 which has a 100% identity to the present application’s SEQ ID NO: 1 (RNG; Result #1) in their method of delivering a gene to the muscle of a subject (para. 0017). Mendell teaches methods of transducing a target cell such as skeletal muscle, smooth muscle or cardiac muscle cells with an rAAV encoding a therapeutic gene of interest (para. 0033). Previous studies have shown that AAVrh.74 delivered through circulation is vastly superior to AAV1 and superior to AAV6 in transducing skeletal muscle (para. 0076). Mendell reduces to practice that transgenes are expressed with broad distribution throughout the major muscles of the lower limb when utilizing the AAVrh.74 capsid encoded by the nucleotide sequence of SEQ ID NO: 1 (para. 0097, 0017, Claim 1). Mendell further teaches that the amino acid sequence for this SEQ ID NO: 1 capsid is SEQ ID NO: 2 which has a 100% identity to SEQ ID NO: 2 of the present application (RAI, Result #5; Mendell, para. 0017)
Based on such teachings, it would have been obvious to one of ordinary skill in the art to deliver a LAMP2 transgene for the treatment of Danon Disease via substituting the AAV capsid protein in Adler for the AAVrh.74 capsid protein encoded by SEQ ID NO: 1 or SEQ ID NO: 2 as taught by Mendell with a reasonable expectation of success. An artisan would be motivated to utilize an AAVrh.74 protein capsid in the treatment of Danon disease as Adler teaches that Danon disease is a skeletal muscle and cardiac muscle disorder (para. 0006) and previous studies have shown that AAVrh.74 delivered through circulation is vastly superior to AAV1 and superior to AAV6 in transducing skeletal muscle (Mendell; para. 0076). Therefore, an artisan would be motivated to utilize a known superior capsid protein.
Regarding claim 2, the combination of Adler and Mendell make obvious the pharmaceutical composition of claim 1. Moreover, Adler teaches one or more LAMP2 isoforms (LAMP-2A, LAMP-2B, LAMP-2C) located within the AAV construct (para. 0031, Figure 1B, 1G, 1O).
Regarding claim 8, the combination of Adler and Mendell make obvious the pharmaceutical composition of claim 1. Moreover, Adler teaches that their vector has ITRs for 3’ and 5’ from AAV2 and that the AAV expression vector need not necessarily be identical or derived from the same AAV serotype (para. 0068, 0099)
Regarding claim 17, the combination of Adler and Mendell make obvious the pharmaceutical composition of claim 1. Moreover, Adler’s construct does not have a start codon 5’ to the transgene’s start codon, as Adler shows the LAMP2 coding region transgene has one isoform of LAMP2 and the only element upstream from the LAMP2 isoform is the ITR and promoter sequence (Figure 1A).
Regarding claim 21, the combination of Adler and Mendell make obvious the pharmaceutical composition of claim 1. Moreover, Adler teaches that one construct containing a cardiac-specific promoter such as, but not limited to, the cardiac troponin T2 promoter and this constructure is used to express the transgene only in cardiac tissue to avoid hepatic expression (i.e. expression in liver tissue) (para. 0036, Figure 1E).
Regarding claim 50, the combination of Adler and Mendell make obvious the pharmaceutical composition of claim 1 and the method of claim 48 utilizing the pharmaceutical composition intravenously. Moreover, Adler demonstrates examples of administering the vectors to LAMP-2 KO mice which model Danon disease (Example 2-3). Furthermore, Adler discloses that the target subject/patient is one at risk of Danon disease as other disorders of autophagy such as heart failure, or on which currently has Danon disease (para. 0057, 0059).
Regarding claim 52, the combination of Adler and Mendell make obvious the pharmaceutical composition of claim 1 and the method of claim 48 utilizing the pharmaceutical composition intravenously. Moreover, Adler demonstrates examples of administering the vectors to LAMP-2 KO mice (i.e. reduced or non-detectable endogenous LAMP-2 expression) (Example 2-3).
Regarding claim 59, the combination of Adler and Mendell make obvious the pharmaceutical composition of claim 1 and the method of claim 48 utilizing the pharmaceutical composition intravenously. Moreover, Adler teaches the administration of the gene therapy vector encoding LAMP2B causes dose dependent increase in mRNA expression and protein expression in heart tissue (para. 103-104, Example 3, Figure 5 and 6).
Therefore, the invention would have been prima facie obvious to one of ordinary skill in the art at the time of the effective filing date.
Claim 20 is rejected under 35 U.S.C. 103 as being unpatentable over Adler et al. (supra) in view of Mendell (supra) as evidenced by RNG (supra), RAI (supra), Lang (supra) and Jackson Lab (supra) as applied to claim 1 above, and in further view of Li (Mol Hum Reprod. 2009 Aug 3;15(12):779–788) and Minshull (US Patent No. 11,713,468) as evidenced by RNI (20250204_142836_us-17-430-107-26.rni; Sequence Search Result within Application)
This rejection has been modified as necessitated by Applicant’s arguments and amendments filed 09/22/2025.
As discussed above, Adler and Mendell make obvious a rAAV gene therapy vector comprising an AAV capsid protein and LAMP-2 flanked by ITRs for the purpose of treating Danon disease wherein the rh.74 AAV capsid is encoded by SEQ ID NO: 1.
Regarding claim 20, Adler teaches that expression cassette comprises operably linked in the 5' to 3' direction, a first inverse terminal repeat, an enhancer/promoter region, the polynucleotide encoding one or more isoforms of LAMP-2, a 3' untranslated region including a polyadenylation signal, and a second inverse terminal repeat (Claim 8). Adler’s construct does not have a start codon 5’ to the transgene’s start codon, as Adler shows the LAMP2 coding region transgene has one isoform of LAMP2 and the only element upstream from the LAMP2 isoform is the ITR and promoter sequence (Figure 1A).
However, Adler nor Mendell teaches that the polyadenylation sequence is a full length polyA sequence and does not teach that a consensus optimal Kozak sequence is also present within the construct.
The present application discloses a consensus optimal Kozak sequence as SEQ ID NO: 20 (GCCGCCACCATGG) and full length polyadenylation signal is SEQ ID NO: 26
Li teaches that the “perfect Kozak sequence (gccgccaccatgg)” was engineered to ensure the correct and efficient initiation of translation of expression constructs via ribosomes by Kozak in 1986-87 (p. 782, 2nd column).
Minshull teaches a polyadenylation signal encoded by SEQ ID NO: 212 utilized within polynucleotide vector for high expression of heterologous genes (Abstract; Column 35, lines 39-49). As evidenced by the RNI file for SEQ ID NO: 26, Minshull’s SEQ ID NO: 212 is the same as the present application’s SEQ ID NO: 26.
It would have been obvious to one of ordinary skill in the art to modify the rh.74 AAV construct taught by Adler and Mendell by substituting the polyadenylation signal already present in Adler for Minshull’s polyadenylation signal (the same sequence as present application’s full length polyadenylation signal) and additionally include a Kozak sequence inside the construct as taught by Li et al. with a reasonable expectation of success. An artisan would be motivated to include a Kozak sequence, particularly an optimal consensus Kozak sequence, in the AAV vector as Li teaches said sequence is known in the art to ensure correct translation of expression constructs (p. 782, 2nd column). Regarding the polyadenylation signal, one would be substituting known art recognized equivalent polyadenylation signals for the purpose of expressing a target gene within a construct (See MPEP 2144.06)
Therefore, the invention would have been prima facie obvious to one of ordinary skill in the art at the time of the effective filing date.
In response to Applicant’s arguments and amendments regarding the 103 rejections,
Applicant’s arguments and amendments filed 03/28/2026 have been considered. However, they are not persuasive.
Applicant argues that the amendments overcome the previously set forth rejection as not all new limitations are rejected.
The Examiner has modified the previous rejection without adding any new secondary references, only evidentiary references, to address all claim limitations set forth by the amendments.
Applicant argues that the combination of references do not provide for a AAVrh.74 capsid vector provided at the claimed dosage of 1 x 1013 vg/kg to about 3 x 1014 vg/kg administered to a human. Particularly, Applicant argues that Adler and Mendell do not provide any teaching or guidance related to dosage or concentration of the AAVrh74 construct being utilized at the claimed dosage of about 1 x 1013 vg/kg to about 3 x 1014 vg/kg in humans presented in the amended claims. Applicant argues only dosages of 2 x 102 or 6 x 1012 vg/kg in mice and non-human primates are utilized and that there is no motivation to combine as that rationale that AAVrh.74 is known to be superior than other types of AAV capsids does not provide any reasonable expectation of success.
The examiner disagrees. Adler provides dosage and concentration of the rAAV vector as set forth in the previous rejection is reiterated. Regarding the claimed range of dosages and amounts, Adler teaches administering the gene therapy vector at a dose of 5x1011 , 1x1012, and 2x1012 gc/mouse (Example 3, 5, 9). As genome copies (gc) are viral particles with the target genome, it is interpreted that a dose of 2x1012 gc would therefore have 2x1012 vg. As evidenced by Jackson Lab, male mice at 6 months weigh about 36 grams (C57/BL/6J; 24 weeks). Therefore, it would be determined that the dosages would be 5x1011 vg/36g to 2x1012 vg/36g = 1.3 x 1013 to 5.6 x 1013 vg/kg which overlaps the claimed range. Moreover, Adler discloses that humans are recipients of this therapeutic vector as stated above. Mendell is a secondary reference to Adler which provides for the specific capsid. As Adler teaches that Danon disease is a cardiac and skeletal muscle disease and that AAV vectors are utilized in their invention, there is motivation to combine an AAV capsid known for its superiority over other AAV capsids in skeletal muscle. Mendell provides teachings on the utilization of the capsid for the same purpose as Adler and therefore there is teaching and suggestion to combine.
In response to applicant's arguments against the references individually, 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). Moreover, Mendell is utilized to demonstrate that AAVrh.74 vectors in previous studies have shown that AAVrh.74 delivered through circulation is vastly superior to AAV1 and superior to AAV6 in transducing skeletal muscle (Mendell; para. 0076). The test for obviousness is not whether the features of a secondary reference may be bodily incorporated into the structure of the primary reference; nor is it that the claimed invention must be expressly suggested in any one or all of the references. Rather, the test is what the combined teachings of the references would have suggested to those of ordinary skill in the art. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981). Mendell modifies the reference of Adler, which already demonstrates the appropriate dosage as calculated above. Mendell provides teaching, suggestion and motivation to utilize an AAVrh.74 capsid identical to the one encoded by the present application’s SEQ ID NO: 2 within constructs taught by Adler.
Applicant further reiterates the arguments which describe AAVrh74 vectors at the time of the invention also teach away from the specific vector concentrations and dosage of the amended claims. Applicant provides a table summarizing the findings of Xu in order to detail the significantly higher effective dosages and their therapeutic results (p. 12 of Applicant’s Remarks). Regarding this table, Applicant states that the dosage within the range of their claimed invention teaches away from its usage as only “increased glycosylation” in less than 20% of cardiomyocytes.
While Xu does state this, Xu additionally admits that the dosage is calculated via the supercoiled standard and not the linear and Applicant has detailed that in Table 1. Dose 3 would be within the range of the claimed invention at about 4.6 x 1013 and dose 4 and 5 are either at the low end of the claimed range or less than the claimed range via the linear standard comparison measurement. Dose 3 shows a significant elevation in the target mRNA (Figure 1E of Xu). Furthermore, the instant claims any astounding levels of efficacy: all that is required under 103 is what KSR has told us. For example, clam 59 merely requires that “administration of the rAAV gene therapy vector causes LAMP2B mRNA expression in one or more of heart, muscle, and liver”. Applicants have not provided any evidence that Xu’s Dose 3 which increases “glycosylation ...only in a minority of cardiomyocytes (less than 20%)” should not be reasonably expected to causes of LAMP2B mRNA in heart. Furthermore, Applicant’s argument is not found to be persuasive in arguing a teaching away as the dosages within the range of the claimed invention still are effective in their significant elevation of the target mRNA.
Moreover, the therapeutic results are for a polynucleotide encoding a gene (GALGT2) which is not the same as the LAMP-2 being delivered in the present invention and is for treating Duchenne muscular dystrophy, not patients with Danon Disease. It is known in the art that different genes have different mechanisms and effectiveness at which they provide therapeutic results. Moreover, even if Mendell teaches the same capsid as the present invention and their dosages demonstrate that at the claimed range the effects are negligible, this indicates that the full scope of the invention may not be enabled to achieve the desired therapeutic effect.
Applicants have not provided any examples of delivering LAMP-2 at the full breadth of the claimed doses and there is no expectation that delivery of the LAMP-2 at the dose of “1 x 1013 vg/kg to about 3 x 1014 vg/kg of the rAAV vector” would be more successful that the combined teachings of Xu and the cited references in view of the unpredictability of delivering different genes
Allowable subject matter has been indicated previously, it is advised the independent claims reflect the allowable subject matter.
New objections/ Rejections in response to Applicants’ arguments or amendments
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(B) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 20 and 21 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which applicant regards as the invention.
Claim 20 which depends on claim 1 recites “in the 5' to 3' direction, a first inverse terminal repeat,… and a second inverse terminal repeat,”. However, claim 1 already requires a 5' ITR and a 3' ITR. Thus, it is unclear if the ITR recited in claim 20 are the same or different ones. As uch the metes and bounds of the claim are indefinite.
Claim 21 is indefinite insofar as it depends on claim 20.
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.
Independent claims 1 and 48 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of copending Application No. 18265421 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because
Application ‘421 teaches the genus to the present application’s species. Application ‘421 teaches a method for treating Danon disease in a subject suffering from or at risk of Danon disease in a mutation in a Lamp2 gene. Moreover, the treatment steps are administering to a subject a capsid and vector genome in an rAAV viron with a polynucleotide encoding preferably LAMPB-2 (Claim 1). This overlaps in scope with the present invention. In addition to Claim 1, claim 2 details the dosage recited in the instant claims and claim 21 reads on the present invention’s administration route. All of these methods utilize the genus of the pharmaceutical composition in the present claims and SEQ ID NO: 1 has a 100% identity to SEQ ID NO: 1 of the present invention (Clam 29).
Thus the claims of the instant application are encompassed by, or overlap in scope significantly with, the claims of 18/265421.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Allowable Subject Matter
With respect to Claim 10, the claims are directed to a codon-optimized nucleic acid sequence encoded by SEQ ID NO: 7 which encodes a LAMP2 gene. For which the nearest sequence search result is 60% identical.
Grote et al (JCat: a novel tool to adapt codon usage of a target gene to its potential expression host, Nucleic Acids Research 33: W526-W531; doi:10.1093/nar/gki376, 2005) is considered relevant prior art for having taught a free, publicly available, online codon optimization tool, JCat.
Similarly, Daniel et al (ATGme: Open-source web application for rare codon identification and custom DNA sequence optimization, BMC Bioinformatics 16: 303, 6 pages, doi.10.1186/s12859-015-0743-5; 2015) is considered relevant prior art for having taught a free, publicly available, online codon optimization tool, ATGme. Daniel et al taught that while other codon optimization tools were previously available to the ordinary artisan, most are no longer available (e.g. pg 2, col. 2).
Heintz et al (U.S. 2014/0196176) is considered relevant prior art for having disclosed that those of ordinary skill in the art previously recognized the scientific and technical concepts that codon optimization allows for maximum protein expression by increasing the translational efficiency of the artisan’s gene of interest, whereby codon optimization is a standard component of custom gene design, and may be readily obtained from commercial service providers [0029].
With respect to Claim 23, SEQ ID NO:10 is a codon-optimized expression cassette comprising a polynucleotide encoding LAMP2 which is free of the prior art. The closest prior art aside from Applicant’s own work is below 50% sequence identity.
The Examiner finds that JCat yields a codon-optimized nucleic acid sequence that is about 69% identical to SEQ ID NO:7.
The Examiner finds that JCat yields a codon-optimized nucleic acid sequence that is about 69% identical to SEQ ID NO:10.
The Examiner does not have access to proprietary or commercial codon-optimization tools with which to compare their results to SEQ ID NO: 7 or 10.
Therefore, it is determined that SEQ ID NO: 7 and 10 within Claims 10 and 23 are free of the prior art.
Conclusion
No claims are allowed.
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/ALEXANDRA F CONNORS/Examiner, Art Unit 1634
/MARIA G LEAVITT/Supervisory Patent Examiner, Art Unit 1634
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