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 .
Applicant’s response dated 3/19/2026 is acknowledged. No amendments to the claims were submitted with the response dated 3/19/2026. Claims 1-2, 4-5, 11-16, 30, 32-33, 35, 41, 92, 96, 107, 119, and 122-126, of record 8/1/25, are pending and subject to prosecution.
RESPONSE TO ARGUMENTS
Re: the 103 rejection of claims 1-2, 4-5, 11-16, 30 and 92 are obvious over Wright, further in view of Genbank Accession No. NM_024312, and Gray.
In the reply dated 3/19/2026, Applicant reiterates previously presented arguments. Applicant reiterates that the Examiner has not established a prima facie case of obviousness over the pending claims and has relied on improper hindsight based on Applicant's disclosure. Applicant points to the primary reference Wright, and argues, again, that the rejection was “essentially” based on 2 paragraphs of Wright. Applicant repeats arguments arguing paragraph [014] of Wright “provides a laundry list of genes associated with essentially every genetic disease” and paragraph [026] of Wright “provides a list of all the AAV capsid serotypes that were known as of the filing date of Wright.” Applicant argues that there is no single passage in Wright that expressly discloses the specific combination of the claimed gene and the claimed AAV virus, and there is no motivation to select such a combination. Applicant further argues that the rejection appears to be based on obviousness to try rationale.
The Examiner notes that each of these arguments were previously presented, and found unpersuasive and addressed in the Non-final Action mailed 11/19/2025. The Examiner notes the Non-final Action mailed 11/19/2025 provided at least the following, copy and pasted herein for applicant’s convenience (from page 3, sections 10 – page 11, section 35):
Applicant traverses the 103 rejection over the pending claims as obvious over Wright, and alleges that the Examiner’s position is “essentially based on two paragraphs in Wright,” wherein Applicant argues that the Examiner’s rejection is based on paragraph [14] of Wright which “provides a laundry list of genes associated with essentially every genetic disease” and paragraph [26] of Wright, provides “a list of all the AAV capsid serotypes that were known as of the filing date of Wright” (Pages 10-11 of the Reply).
The Examiner does not agree with Applicant’s synopsis of the rejection of record, nor with Applicant’s synopsis of Wright’s teachings. Applicant’s argument that the disclosure of [14] of Wright allegedly “provides a laundry list of genes associated with essentially every genetic disease” and the disclosure of [26] allegedly provides “a list of all the AAV capsid serotypes that were known as of the filing date of Wright” is made in an attempt to support Applicant’s argument that Wright is a non-limiting, infinite disclosure, is unfounded and not supported by any evidence. As of March 2013, more than 7,000 genetic disorders had been identified, and more than 3,600 of the genetic disorders identified had been associated with a specific genetic defect (page 603, in Brunham, 2013). Thus, paragraph [14] of Wright does not provide a list of genes associated with “essentially every genetic disease” as asserted by Applicant. In addition, paragraph [26] delineates “representative” serotypes of AAV1-AAV11, Rh74, and Rh10 serotypes; however, there is no evidence that these serotypes are “all the AAV capsid serotypes known at the time of filing” as alleged. Asokan, 2012 discloses AAV1-AAV2, AAV3a/3b, AAV4-AAV12, AAV2-AAV3 hybrid, AAVrh32.33, AAVhu.37 and AAVrh.8 serotypes were known (Table 1, page 702). Drouin, 2013 discloses AAV1-AAV13 serotypes were known (page 3).
Regardless, the rejection of record was not so narrowly based on a two paragraph (14] and [26] disclosure of Wright as alleged. As demonstrated previously and in the rejection above, the Examiner cited numerous paragraphs within Wright to support the finding of obviousness, citing to disclosures relating to AAV capsids, which include AAV8 (paragraphs [0026], [0045]-[0046], [0049]), and identified wherein Wright includes GNPTAB as an optional encoded heterologous transgene in paragraphs [0014] and [0059].
Applicant argues that Wright includes GNPTAB and AAV8 on “laundry lists” of options known in the art (Reply at 10-12). Focusing on Wright’s working embodiments, Applicant suggests that the fact that Wright did not reduce the claimed invention to practice demonstrates nonobviousness. Patents, however, are prior art for all they contain and what they would have reasonably suggested to the person of ordinary skill in the art as of the effective filing date of the invention. MPEP 2123. Applicant appears to take the position that the prior art must point the person of ordinary skill in the art to a particular option within the prior art in order to fairly suggest it, but such a “blaze marks” requirement is not the test for obviousness. The obviousness test is flexible and relies upon the background knowledge, understanding, and judgment of the skilled artisan. See MPEP 2141.
In addition, Applicant suggests that the selection of AAV8 would have required improper hindsight. 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). In the instant case, Wright discloses AAV particles, including AAV8 paragraphs [0004]-[0005], [0021], [0026], [0038]-[0039], [0045]-[0049]), can encode a heterologous peptide, including N-acetylglucosamine-1-phosphate transferase (GNPTAB) (paragraphs [0014] and [0059]).
Applicant argues the Examiner is improperly selecting species from two lists where there is no indication that the particular species can be combined; that there is no motivation to select AAV8 from the genus of AAV serotypes disclosed, or GNPTAB from the genus of transgenes disclosed to meet the requirements of MPEP 2144.08; that Wright does not teach a “finite number” of identified predictable solutions, and that the art was unpredictable (Reply at pages 13-14).
With regard to Applicant’s assertion that the Examiner is improperly selecting species from two lists where there is no indication that a particular species can be combined is not persuasive. There is no disclosure in Wright wherein any specified transgene is limited to a specific AAV capsid, or wherein a specific AAV capsid is limited to encode only a specific transgene. Rather, Wright discloses the rAAV particles therein can encode a heterologous polynucleotide sequence (paragraphs [0004]-[0005]), and that the heterologous polynucleotide sequence can encode a therapeutic protein, that is N-acetylglucosamine-1-phosphate transferase (paragraphs [0014], [0059]). The Examiner further notes that Applicant has not proffered any evidence supporting the idea that Wright either teaches or suggests only certain transgenes are capable of be encoded and expressed from certain AAV serotypes, nor any other evidence supporting such an idea from the prior art.
With regard to Applicant’s argument that there is no motivation to select AAV8 from the genus of AAV serotypes disclosed, or GNPTAB from the genus of transgenes disclosed to meet the requirements of MPEP 2144.08, the Examiner cannot agree. The Examiner addressed Applicant’s concerns regarding MPEP2144.08 in the Final Rejection of 10/01/2024, the Examiner argued the combination of AAV8 and GNPTAB was obvious at least because:
“each protein listed within Wright as being capable of being encoded in an AAV vector is functionally equivalent to the other, and each AAV capsid listed within Wright as capable of generating AAV particles is functionally equivalent to the others” (page 16, section 56) and requirements of MPEP2144.08 were met, in light of the claimed composition, “Each protein listed within Wright as being capable of being encoded in an AAV vector is functionally equivalent to the others. Each AAV capsid listed within Wright as capable of generating AAV particles is functionally equivalent to the others. The packaging constraints of AAV vectors was known, and Grey identified use of mini-promoters was a way to aid in achieving packaging of larger transgenes into viral vectors. Furthermore, Wright’s lists are each a finite number of identified, predictable solutions to an art-recognized need to generate AAV particles, and the person of ordinary skill in the art could have pursued each combination with a reasonable expectation of success because Wright provides specific guidance for doing so. It would therefore indeed have been obvious to make each of the AAV capsids suggested by Wright. See MPEP 2143(I)(E) (obvious to try finite number of identified, predictable solutions with reasonable expectation of success)” (page 18, section 60, Final Rejection of 10/01/2024).
Thus, the Obvious To Try Rationale was only one argument within a larger section citing how the requirements of MPEP2144.08 were met by Wright and/or the cited art.
Applicant argues that the obvious to try rationale is not met because Wright does not teach a “finite number” of identified predictable solutions, that the Examiner did not articulate why there would be a reasonable expectation of success, and that combining every AAV serotype with every gene of Wright is not a finite number of predictable solutions. Applicant’s attempt to show Wright’s passages at paragraphs [14] and [26] is not-limiting examples of therapeutic transgenes and AAV capsids, it not persuasive for the reasons stated above, in light of the teachings of Brunham, 2013, Asokan, 2012 and Drouin, 2013. Thus, as iterated above, each protein listed within Wright as being capable of being encoded in an AAV vector is functionally equivalent to the others. Each AAV capsid listed within Wright as capable of generating AAV particles is functionally equivalent to the others. The packaging constraints of AAV vectors was known, and Grey identified use of mini-promoters was a way to aid in achieving packaging of larger transgenes into viral vectors. Furthermore, Wright’s lists are each a finite number of identified, predictable solutions to an art-recognized need to generate AAV particles, and the person of ordinary skill in the art could have pursued each combination with a reasonable expectation of success because Wright provides specific guidance for doing so.
The Examiner maintains that the prior rejections of record are proper with regard to MPEP 2144.08, but are expanded herein to further articulate the analysis:
In addition, Wright discloses the species therein are equivalents: at paragraph [0153] Wright states, “All of the features disclosed herein may be combined in any combination. Each feature disclosed in the specification may be replaced by an alternative feature serving a same, equivalent, or similar purpose. Thus, unless expressly stated otherwise, disclosed features ( e.g., a recombinant vector ( e.g., AAV) plasmid, vector genome, or recombinant virus particle ( e.g., AAV)) are an example of a genus of equivalent or similar features.”
Further when considering the selection of species from a genus,
MPEP2144.08 II(A)(4)a (Consider the Size of the Genus).
Consider the size of the prior art genus, bearing in mind that size alone cannot support an obviousness rejection. There is no absolute correlation between the size of the prior art genus and a conclusion of obviousness. See, e.g., Baird, 16 F.3d at 383, 29 USPQ2d at 1552. Thus, the mere fact that a prior art genus contains a small number of members does not create a per se rule of obviousness. Even where the genus contains a small number of members, the disclosed genus may not possess a recognizable class of compounds with common properties.
Applicant’s argument that the alleged size of the genus of transgenes and AAV serotypes disclosed by Wright undermines the selection of GNPTAB and AAV8 is not persuasive. The size of the genus is does not undermine the obviousness of a species, particularly when the disclosed genus contains a recognizable class of compounds with common properties. In the instant case, GNPTAB is listed among a genus of therapeutic peptides that are suitable for being encoding in the AAV vectors therein. AAV8 is listed among a genus of AAV capsids that are suitable for encoding the heterologous transgenes therein.
MPEP2144.08 II(A)(4)b (Consider the Express Teachings).
If the prior art reference expressly teaches a particular reason to select the claimed species or subgenus, Office personnel should point out the express disclosure and explain why it would have been obvious to one of ordinary skill in the art to select the claimed invention. An express teaching may be based on a statement in the prior art reference such as an art recognized equivalence.
As disclosed in the rejection, Wright discloses the heterologous peptides encoded on the vector include N-acetylglucosamine- 1-phosphate transferase for treating lysosomal storage disease (paragraphs [0014], [0059]).
In addition, Wright discloses the species therein are equivalents: at paragraph [0153] Wright states, “All of the features disclosed herein may be combined in any combination. Each feature disclosed in the specification may be replaced by an alternative feature serving a same, equivalent, or similar purpose. Thus, unless expressly stated otherwise, disclosed features ( e.g., a recombinant vector ( e.g., AAV) plasmid, vector genome, or recombinant virus particle ( e.g., AAV)) are an example of a genus of equivalent or similar features.”
Applicant’s argument that even if a skilled artisan combined every AAV serotype with every gene of Wright, while a myriad of different rAAV particles would be made, but the myriad of particles is not a finite number of predictable solutions is not persuasive. Wright particularly enumerates a specific list of transgenes and a specific list of AAV particles for delivering them. GNPTAB is listed among a genus of therapeutic peptides that are suitable for being encoding in the AAV vectors therein. AAV8 is listed among a genus of AAV capsids that are suitable for encoding the heterologous transgenes therein. There is no disclosure in Wright wherein any specified transgene is limited to a specific AAV capsid, or wherein a specific AAV capsid is limited to encode only a specific transgene. Nor has Applicant proffered any evidence supporting the idea that only certain transgenes are capable of be encoded and expressed from certain AAV serotypes.
The fact that the art was aware of numerous permutations of transgenes and delivery particles, however, does not compel a conclusion that the list is infinite. Wright is explicit about the options for transgenes and for the AAV particles, and as of the claims’ effective filing date, the person of ordinary skill in the art would have understood that all of those combinations would have been equally obvious. It cannot be the case that as the art becomes aware of more operable options, it simultaneously becomes more unpredictable.
At page 13, Applicant argues that at the time of filing gene therapy was unpredictable, contrary to assertions allegedly made by the Examiner without any evidence. Applicant also points to Lee, and argues that Lee examined 18 different AAV serotypes for delivery and expression of particular therapeutic payloads to bone, and only three AAV8, AAV9 and AAV-DJ were able to effectively transduce bone, and that AAV8 showed the highest payload expression in the tibia.
It is not clear whether Applicant is using Lee as evidence that gene therapy in general was unpredictable at the time of filing? Or gene therapy to bone? Also, the Examiner does not agree that Lee demonstrates AAV8 has advantages over any other AAV variant, except in one particular instance.
The AAV8 vector expressing Cre under the Sp7 promoter was able to systemically transduce
osteoblasts at high efficiency, leading to a permanent recombination event marked by tdTomato expression. This vector has numerous applications in preclinical modeling of genetic disease and can be applied to conditional (floxed) mouse models to create bone-specific knockout. The vector could also be applied locally to create knockout fractures, analogous to a previously published adenovirus model. Page 103.
Lee administers AAV8 vectors 1) directly into bone, 2) systemically and also transduces human fetal osteoblasts in culture. And, Lee shows that the efficiency of transduction changes between method of administering the vector, and setting. Of the 18 variants administered directly to fracture, Lee shows 3 transduced cells in the callus with “high efficiency” AAV-DJ, AAV8 and AAV9. For systemic delivery, Lee only tests 3 variants: AAV2, AAV8 and AAV-DJ, not all 18. Lee does test all 18 in vitro, on human fetal osteoblasts in culture, and shows 7 of 18 transduced osteoblasts, and of the highest expression levels were AAV5, AAV-DJ and AAV2. And, Lee makes a point to say “AAV-DJ was the only variant that showed high efficiency in the murine fracture model and cultured osteoblasts.”
Lee also articulates that AAV8 was chosen for the systemic administration studies over AAV-DJ, but admits, the lower efficiency may have been due to lower vector dose, but unlike for AAV8, they did not increase the dosage. Lee also states that AAV-DJ has higher transduction efficiency inhuman osteoblasts that AAV8.
Applicant also alleges the Examiner has failed to take into account unexpected results arising from the claimed invention, which Applicant argues are fully commensurate with the experimental results provided in the application as filed. Pages 5-6 of the Reply dated 3/19/26 state:
Applicant further reemphasizes that that the specification as filed does show unexpected results. The studies described in the specification provide the first successful examples of using gene therapy to deliver the GNPTAB gene and to treat mucolipidosis type II (ML II) or mucolipidosis type III (ML III). The results shown in the application as filed show for the first time an increase in bone mineral density and content following rAAV treatment. Post-filing references including Exhibit B, provided in the prior response, recognize that Applicant's discovery is a breakthrough in developing gene therapy for targeting bone, and hence finds application in treating bone disorders such as ML II. There is no art identified by the Examiner that suggested that AAV8 could effectively target bone and be used as a therapy targeting bone. The Examiner provides no rationale as to why a skilled person would have expected an AAV8-capsid serotype to effectively transduce bone, deliver a therapeutic payload and have a profound effect on bone density and bone mass, as described in the specification, particularly when there was no teaching of an AAV8 capsid in the prior art shown to deliver payloads to bones. Furthermore, there is no reason why a skilled person would have expected that the claimed rAAV particles can attenuate bone loss via inhibition of IL-6 production.
Again, the Examiner cannot agree, and notes the Examiner provided the analysis of the purported unexpected results in the Non-final Action mailed 11/19/2025 (page 11, section 32- page 13, section 40):
Applicant has not articulated how this information is relevant to the pending claims or the citation to Ko. Ko does not test any other AAV capsid other than AAV8. Given the inconsistency of transduction of AAV vector capsids shown in Lee, depending on mode of administration, etc, and that Ko does not test any other capsid, the examiner is not persuaded that the exhibits provided by Applicant show either unpredictability or an unexpected result.
Applicant alleges that methods of treating ML II are relevant to the claimed invention, which is an adenoviral particle (Reply at pages 8-10, 12-13). Applicant argues that the previous response of the Examiner to point out that the instant claims were to a product, and not a method, implies “that the method of treatment could not be potentially patentable over Wright, but the product is allegedly not patentable (Reply, page 12-13).
To be clear, there has been no statement by the Examiner that evidence/results seen from an unclaimed method of use or unclaimed functional result of using the claimed product cannot be used as evidence to support the patentability of a claimed product. Applicant appears to have misconstrued the Examiner’s position about the analysis of product claims compared to that of method claims (Reply at pages 14-15). It is not the case that these two claim types receive different analyses. The question is only whether the method limitations or functional results alleged to be relevant are in fact invoked by the product as Applicants have chosen to claim it. If the claimed structures of the product are shown to be directly responsible for the alleged affect seen with use, such a composition could be patentable. Here, the only structural requirements in claim 1 are for an AAV particle comprising single stranded AAV vector comprising a GNPTAB gene operably linked a generic promoter, and an AAV8 capsid. Such a virus is obvious for the reasons of record.
Applicant’s arguments that the claimed virus is not obvious because of unexpected results, such as the particles be capable of transducing bone or that they treat ML II disorder remain unpersuasive. Indeed, evidence of an unexpected property may not be sufficient regardless of the scope of the showing. Usually, a showing of unexpected results is sufficient to overcome a prima facie case of obviousness. See, e.g., In re Albrecht, 514 F.2d 1389, 1396, 185 USPQ 585, 590 (CCPA 1975). However, where the claims are not limited to a particular use, and where the prior art provides other motivation to select a particular species or subgenus, a showing of a new use alone may not be sufficient to confer patentability. See Dillon, 919 F.2d at 692, 16 USPQ2d at 1900-01. MPEP2145. emphasis added.
And
Mere recognition of latent properties in the prior art does not render nonobvious an otherwise known invention. In re Wiseman, 596 F.2d 1019, 201 USPQ 658 (CCPA 1979). MPEP2145II:
Again, however, the claims are not drawn to a method of treating ML II or to a particle that can treat ML II or even to an adenovirus that can transduce bone tissue. Further, Applicant’s evidence of Lee shows that AAV8 is not the only AAV vector to transduce bone. And, as iterated above, KO does not compare the use of AAV8 to any other AAV capsid.
Any experimental showing, however, must be commensurate in scope with the claimed invention. Applicant has removed the requirement in claim 1 for a particular promoter system that was used in the working examples and in the post-filing Exhibits A and B to achieve this outcome.
Applicant appears to have misconstrued the Examiner’s position about the analysis of product claims compared to that of method claims (Reply at pages 14-15). It is not the case that these two claim types receive different analyses. The question is only whether the method limitations alleged to be relevant are in fact invoked by the product as Applicants have chosen to claim it. If the claimed structures of the product are shown to be directly responsible for the alleged affect seen with use, such a composition could be patentable. Here, the only structural requirements are for an AAV vector with GNPTAB driven by a generic promoter, all within an AAV8 capsid. Such a virus is obvious for the reasons of record. Again, there is no claimed requirement that the particles be capable of transducing bone or that they treat ML II disorder.
Applicant contends that claim 1 is “quite narrow in scope” (Reply at page 15), but the analysis does not hinge on claim breadth, but rather on whether a showing is commensurate in scope with the claims. Here, Applicant has removed the requirement in claim 1 for any specific promoter, so evidence showing a special property of vectors driven by a particular promoter is necessarily not sufficient to address the full scope of claim 1.
Applicant further alleges the claimed invention results in unexpected results in gene therapy treatment of ML II. However, considering Ko does not test any other capsid, and Lee, provided by Applicant, shows other capsids can transduce bone, the examiner is not persuaded.
Thus, each of Applicant’s arguments have been fully addressed on record, and remain unpersuasive. However, Applicant does not address any points previously articulated by the Examiner, including at least:
Contrary to Applicant’s argument, Wright’s paragraph [14] does not provide “a laundry list of genes associated with essentially every genetic disease” in light of Brunham, 2013. As of March 2013, more than 7,000 genetic disorders had been identified, and more than 3,600 of the genetic disorders identified had been associated with a specific genetic defect (page 603, in Brunham, 2013).
Contrary to Applicant’s argument, Wright’s paragraph [14] does not provide “all the AAV capsid serotypes known at the time of filing” in light of Asokan, 2012, and Drouin, 2013: Asokan, 2012 discloses AAV1-AAV2, AAV3a/3b, AAV4-AAV12, AAV2-AAV3 hybrid, AAVrh32.33, AAVhu.37 and AAVrh.8 serotypes were known (Table 1, page 702). Drouin, 2013 discloses AAV1-AAV13 serotypes were known (page 3).
That Ko does not test any other AAV capsid other than AAV8.
MPEP2145: However, where the claims are not limited to a particular use, and where the prior art provides other motivation to select a particular species or subgenus, a showing of a new use alone may not be sufficient to confer patentability. See Dillon, 919 F.2d at 692, 16 USPQ2d at 1900-01. MPEP2145.
The question is only whether the method limitations alleged to be relevant are in fact invoked by the product as Applicants have chosen to claim it. If the claimed structures of the product are shown to be directly responsible for the alleged affect seen with use, such a composition could be patentable. Here, the only structural requirements are for an AAV vector with GNPTAB driven by a generic promoter, all within an AAV8 capsid. Such a virus is obvious for the reasons of record. Again, there is no claimed requirement that the particles be capable of transducing bone or that they treat ML II disorder.
With regard to applicant’s arguments regarding the claimed particles can attenuate bone loss via inhibition of IL-6 production, 1) the functional result is not claimed, and 2) there is no evidence that such a response is limited to AAV8 particles encoding the transgene, rather than a different AAV (or other carrier even) would not be capable of resulting in the same response.
Further, the Examiner points out, again, the rejections of record are 103 obviousness rejections, wherein Wright was applied in combination with Genbank Accession No. NM_024312, and Gray; or Wright, Genbank Accession No. NM_024312, and Gray as evidenced by Niwa. In the Reply dated 08/01/2025, as well as that of 3/19/2026, Applicant provides arguments against Wright, but none against the additionally cited art (i.e., with Genbank Accession No. NM_024312, and Gray or Gray as evidenced by Niwa). 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).
The rejections of record are maintained.
CLAIMS
Claim 1 is directed to an rAAV particle comprising a vector encoding a phosphotransferase operably linked to a promoter element wherein the rAAV particle comprises an AAV8 capsid. The 8/1/25 amendment removes the requirement in claim 1 that the promoter is the CMV enhancer/CBA promoter; this limitation is found in new dependent claim 126. Claims 1 and 126 are provided below:
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Claim 122 is directed to an AAV particle comprising a vector encoding a phosphotransferase operably linked to a “CAG promoter” element, wherein the CAG promoter element comprises a truncation, wherein the particle comprises an AAV8 capsid.
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Regarding claim 126, the instant specification teaches:
SEQ ID NO:1 is the human GNPTAB protein sequence and is 1256 amino acids in length. The specification teaches the cDNA encoding the mouse GNPTAB was inserted into an AAV vector [0124]. The specification does not provide either the mouse or the human cDNA sequences. Paragraph [0028] of the published specification teaches the mouse cDNA inserted in the AAV vector is based on Genbank Accession Number NM_001004164.2.
Genbank Accession No. NM_024312.5 discloses the human mRNA for human GNPTAB, wherein the coding sequence comprises nucleotides 285-4053 therein. Thus, the cDNA for human GNPTAB is 3768 nucleotides, absent evidence to the contrary.
Claim Rejections - 35 USC § 103
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claim(s) 1-2, 4-5, 11-16, 30, and 92 remain and new claim 126 is rejected under 35 U.S.C. 103 as being unpatentable over WO2014/144486 to Wright, of record, further in view of Genbank Accession No. NM_024312, earliest priority 1993; 8 pages of record, and Gray et al. Optimizing Promoters for Recombinant Adeno-associated Virus-Mediated Gene Expression in the Peripheral and Central Nervous System Using Self-Complementary Vectors. Human Gene Therapy, 2011. 22:1143-1153, of record, cited on Applicant’s IDS dated 12/07/2018.
With regard to claim 1, Wright discloses recombinant adeno-associated viral particles, comprising rAAV vectors encoding heterologous peptides for therapeutic use, wherein the viral genome comprises “stuffer/filler” sequences in order to improve packaging (Abstract; paragraphs [0034]-[0042], [0058], FIG 1). Wright discloses the AAV vectors are single stranded (paragraph [0042]). Wright discloses the heterologous peptides are flanked by, and operably linked one or more AAV inverted terminal repeats and a promoter/enhancer element, including ubiquitous enhancers from CMA and/or ubiquitous promoters such as chicken beta-actin (paragraphs [0018], [0040], [0084]-[0092], [0104]). Wright teaches the heterologous peptides are operably linked to polyA sequences, including those from SV40 (paragraph [0084]).
Wright discloses the stuffer/filler sequences can be included between the two ITRs, or can be positioned outside of the AAV ITR sequences (paragraphs [0007]-[0008]). Wright discloses the stuffer/filler sequences are used to modify the total length of a AAV genome encoding a heterologous peptide such that the combined length of stuffer/filler sequences and heterologous sequences is at, or close to, the natural packing limit of rAAV, which is approximately 4.7 kb (paragraphs [0034]-[0036]). Wright discloses by adjusting the rAAV genomes to be close to the natural packaging limit of AAV reduces the packaging of contaminating DNA impurities (paragraphs [0034]-[0035]). Wright discloses the AAV vector typically accept inserts of DNA having a defined size range from about 4 kb to about 5.2 kb (paragraph [0095]). Wright discloses the nucleic acid encoding the AAV ITRs, the stuffer/filler sequences, promoter/enhancer elements, the heterologous peptide and polyA sequence have a combined length of about 3.0-5.5 kb, or between about 4.0-5.0 kb, or 4.3-4.8kb, when the stuffer/filler sequences are within the AAV ITRs (paragraphs [0010], [0095], and [0114]-[0115]).
Wright discloses the rAAV vectors encoding N-acetylglucosamine-1-phosphate transferase (GNPTAB) are packaged into AAV particles, including AAV8 (paragraphs [0004]-[0005], [0014], [0021], [0026], [0038]-[0039], [0045]-[0049]).
Wright discloses the heterologous peptides encoded on the vector include N-acetylglucosamine-1-phosphate transferase for treating lysosomal storage disease (paragraphs [0014], [0059]).
However, with regard to claim 1, Wright does not disclose wherein the N-acetylglucosamine-1-phosphate transferase protein is comprises an amino acid sequence that is at least about 80% identical to instant SEQ ID NO:1.
Genbank Accession No. NM_024312 discloses the mRNA sequence for human N-acetylglucosamine-1-phosphate transferase, wherein the mature peptide coding nucleotides are from nucleotides 285-4052 therein (3768 base pairs). Alignment of the translation of the peptide disclosed therein with instant SEQ ID NO:1 shows 100% identity.
Gray discloses chimeric CMV enhancer/beta actin promoters are commonly used in gene transfer vectors, operably linked to both therapeutic and reporter genes (page 1144, Table 1). Gray discloses an 800-bp CMV enhancer/beta actin mini-promoter (CBA, comprising an SV40 intron) or an 800-bp CMV enhancer/beta actin mini-promoter (CBh, comprising an MVM intron) function in scAAV vectors (Table 1; FIGs 1, 2, 3, 4). Gray teaches the smaller promoters can be used on vectors with packaging constraints in order to maximize the space for transgenes (Abstract, pages 1143, 1147-1149, 1152).
The cassettes of Gray show the ubiquitous, truncated CMV/CBA promoters are 800 base pairs long (abstract, Table 1). The polyA sequences of Gray are derived from SV40 (226 bp) and BGH (207 bp) see Table 1). Thus, Gray establishes an expression cassette comprising the 800-bp (CBA or CBh) promoter and an approximate 200 bp polyA tail:
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Gray also acknowledges single-stranded AAV vectors have packaging restraints, stating, “AAV has a single-stranded 4.7-kb genome, and after removal of 4.4kb of the viral genome recombinant vectors can be packaged with a similar-sized foreign piece of DNA” (page 1143).
It would have been obvious to combine the disclosure of Wright, on AAV viral particles, including rAAV8 particles, comprising single-stranded AAV vectors encoding therapeutic peptides, including N-acetylglucosamine-1-phosphate transferase (GNPTAB), further with the disclosure of Genbank Accession No. NM_024312 and Gray.
With regard to the claimed requirement wherein the capsid is an AAV8 vector and the transgene is GNPTAB, Wright particularly enumerates a specific list of transgenes and a specific list of AAV particles for delivering them.
If the claimed invention and the structurally similar prior art species share any useful property, that will generally be sufficient to motivate an artisan of ordinary skill to make the claimed species.
See also
MPEP2144.08 II(A)(4)b (Consider the Express Teachings).
If the prior art reference expressly teaches a particular reason to select the claimed species or subgenus, Office personnel should point out the express disclosure and explain why it would have been obvious to one of ordinary skill in the art to select the claimed invention. An express teaching may be based on a statement in the prior art reference such as an art recognized equivalence.
GNPTAB is listed among a genus of therapeutic peptides that are suitable for being encoding in the AAV vectors therein (paragraphs [0014], [0059]). Wright discloses the species therein are equivalents: at paragraph [0153] Wright states, “All of the features disclosed herein may be combined in any combination. Each feature disclosed in the specification may be replaced by an alternative feature serving a same, equivalent, or similar purpose. Thus, unless expressly stated otherwise, disclosed features ( e.g., a recombinant vector ( e.g., AAV) plasmid, vector genome, or recombinant virus particle ( e.g., AAV)) are an example of a genus of equivalent or similar features.” Thus, it would have been obvious to select AAV8 and GNPTAB from the teachings of Wright.
With regard to the claimed requirement wherein the vector encodes a sequence with at least 80% identity to SEQ ID NO:1, Wright discloses the AAV vectors can encode GNPTAB for treating lysosomal storage disease (paragraphs [0014], [0059]). It would have been obvious to combine the known cDNA sequence of GNPTAB that is known in the art, as provided by Genbank Accession No. NM_024312.
It would have been obvious to further combine the disclosures of Wright and Genbank Accession No. NM_024312 with Grey in order to successfully package a cDNA encoding GNPTAB in a single stranded AAV vector. Wright discloses 1) the therapeutic peptide encoded on the rAAV is can encode GNPTAB; 2) that the total length of insert nucleic acid in the rAAV, comprising the AAV ITRs, the stuffer/filler sequences, promoter/enhancer elements, the heterologous peptide and polyA sequence have a combined length of between about 4.0-5.0 kb; and 3) that AAV single strand vectors have packaging constraints, known for accepting inserts of DNA from about 4 kb to about 5.2 kb (paragraph [0095] of Wright). In addition, Genbank Accession No. NM_024312 discloses a nucleic acid encoding the mature GNPTAB peptide is a minimum of 3768 base pairs in length (3.7kb).
Thus, a skilled artisan, combining Wright with Genbank Accession No. NM_024312 would have been aware of the affect of encoding a cDNA of 3.7 kb in the packaging constrained AAV genome limited to 4.0-5.2 kb. A skilled artisan would have been motivated to combine the rAAV with packaging constraints having a total insert size of 4.0-5.2 kb, encoding a 3.7 kb GNPTAB transgene, rendered obvious by Wright and Genbank Accession No. NM_024312, further with Gray because Gray discloses smaller chimeric enhancer/promoters are commonly used in gene transfer vectors, can be used in vectors with packaging constraints in order to maximize the space for transgenes.
A skilled artisan would have had a reasonable expectation of success in practicing the claimed invention at the time of filing, as the packaging constraints of single strand AAV vectors, the cDNA encoding human GNPTAB of 3.7 kb was known, and use of smaller enhancer/promoters in viruses with packaging constraints were all known at the time of the invention.
With regard to claim 2, Genbank Accession No. NM_024312 discloses the mature peptide coding nucleotides from nucleotides 285-3068 encodes the alpha subunit, and nucleotides 3069-4052 therein encodes the beta subunit (3767 base pairs total). Thus, this claim is obvious for the same reasons as stated above for claim 1.
With regard to claim 4, Genbank Accession No. NM_024312 discloses human N-acetylglucosamine-1-phosphate transferase. Thus, this claim is obvious for the same reasons as stated above for claim 1.
With regard to claim 5, Genbank Accession No. NM_024312 discloses the mRNA sequence for human N-acetylglucosamine-1-phosphate transferase, wherein the mature peptide coding nucleotides are from nucleotides 285-4052 therein (3767 base pairs). Alignment of the translation of the peptide disclosed therein with instant SEQ ID NO:1 shows 100% identity. Thus, this claim is obvious for the same reasons as stated above for claim 1.
With regard to claim 11, Wright discloses the viral genome comprises “stuffer/filler” sequences are intronic sequences (paragraph [0007], [0013], [0095]).
With regard to claim 12, Wright does not disclose wherein the intron is an MVM intron. Gray discloses a prior art 800-bp mini-CMV/CBA promoter (CBA) comprises an SV40 intron (table 1), but that this promoter showed poor expression in motor neurons (Page 1146). Thus, Gray substitutes the SV40 intron with an intron from MVM to generate the 800-bp CBh promoter, and shows the new CBh promoter comprising the MVM intron has improved motor neuron expression compared to the prior art CBA 800-pb promoter (Table 1, page 1146, FIG 3). It would have been obvious to combine the disclosure of Wright with the disclosure of Gray to arrive at the claimed invention. A person of ordinary skill in the art would have had a reasonable expectation of success in substituting the SV40 intron of the CBA promoter with the MVM intron of the CBh promoter, as both are explicitly taught as being useful as intronic sequences in CMV/CBA promoters for driving expression of transgenes in AAV vectors. Therefore, these compositions are functional equivalents in the art, and substituting one for the other would have been obvious at the time of the invention. “When a patent ‘simply arranges old elements with each performing the same function it had been known to perform’ and yields no more than one would expect from such an arrangement, the combination is obvious.” See KSR International Co. v. Teleflex Inc., 82 USPQ2d 1385 (U.S. 2007) at 1395-1396, quoting Sakraida v. AG Pro, Inc., 425 U.S. 273 (1976) and In re Fout, 675 F.2d 297, 301 (CCPA 1982) (“Express suggestion to substitute one equivalent for another need not be present to render such substitution obvious”). A skilled artisan would have been motivated to use the MVM intron because Gray shows the MVM intron has improved expression in motor neurons compared to 800-bc CMV/CBA promoters comprising SV40 introns.
With regard to claim 13, Wright discloses the AAV vectors further comprise polyA sequences (paragraphs [0078], [0084], [0094]), including those from SV40 (paragraph [0084]).
With regard to claim 14, Wright does not disclose wherein the polyA sequence is a bovine growth hormone polyA sequence, as required by instant claim 14. However, Gray discloses the polyA sequence used within the 800-bp CBA and 800-bp CBh vectors cassettes utilize a BGH polyA signal (Table 1). A person of ordinary skill in the art would have had a reasonable expectation of success in substituting the BGH polyA sequences of Gray for the Sv40 polyA sequences of Wright, as both are explicitly taught as being useful as providing transcriptional termination sequences of transgenes in AAV vectors. Therefore, these compositions are functional equivalents in the art, and substituting one for the other would have been obvious at the time of the invention. “When a patent ‘simply arranges old elements with each performing the same function it had been known to perform’ and yields no more than one would expect from such an arrangement, the combination is obvious.” See KSR International Co. v. Teleflex Inc., 82 USPQ2d 1385 (U.S. 2007) at 1395-1396, quoting Sakraida v. AG Pro, Inc., 425 U.S. 273 (1976) and In re Fout, 675 F.2d 297, 301 (CCPA 1982) (“Express suggestion to substitute one equivalent for another need not be present to render such substitution obvious”).
With regard to claim 15, Wright discloses the AAV terminal repeat is an AAV1, AAV2, AAV3, AAV4, AAV5, AAV6, AAV7, AAV8, AAV9, AAV10, AAVrh10 serotype ITR (Paragraph [0026]).
With regard to claim 16, Wright discloses the rAAV vector comprises 2 AAV ITRs (paragraphs [0006], [0008]-[0011], Claim 2).
With regard to claim 30, Wright discloses the particles are formulated as pharmaceutical compositions (paragraphs [0020]-[0021], [0106]-[0107], [0137]-[0140], [0144], Claim 36).
With regard to claim 92, Wright discloses the vectors can be formulated as a kit (paragraph [0146]-[0147]).
With regard to new claim 126, Wright does not disclose wherein the promoter is a CMV/CBA promoter. However, Gray discloses a specific mini promoter, an 800-bp CMV enhancer/beta actin mini-promoter (CBA, comprising an SV40 intron), that can be used to increase the size of a transgene in viruses with packaging constraints (Abstract, pages 1143, 1147-1149, 1152). A person of ordinary skill in the art would have had a reasonable expectation of success in substituting the ubiquitous promoters of Wright for the CMV/CBA promoters of Gray, as both are explicitly taught as being useful for driving expression of transgenes in AAV vectors. Therefore, these compositions are functional equivalents in the art, and substituting one for the other would have been obvious at the time of the invention. “When a patent ‘simply arranges old elements with each performing the same function it had been known to perform’ and yields no more than one would expect from such an arrangement, the combination is obvious.” See KSR International Co. v. Teleflex Inc., 82 USPQ2d 1385 (U.S. 2007) at 1395-1396, quoting Sakraida v. AG Pro, Inc., 425 U.S. 273 (1976) and In re Fout, 675 F.2d 297, 301 (CCPA 1982) (“Express suggestion to substitute one equivalent for another need not be present to render such substitution obvious”). In addition, a skilled artisan would have been motivated to use the CBA promoter of Gray in the AAV vector encoding human GNPTAB of Wright for the same reasons as stated above for claim 1.
Claim(s) 122-125 remain rejected under 35 U.S.C. 103 as being unpatentable over WO2014/144486 to Wright, of record, further in view of Genbank Accession No. NM_024312, earliest priority 1993; 8 pages, of record, and Gray et al. Optimizing Promoters for Recombinant Adeno-associated Virus-Mediated Gene Expression in the Peripheral and Central Nervous System Using Self-Complementary Vectors. Human Gene Therapy, 2011. 22:1143-1153, of record, cited on Applicant’s IDS dated 12/07/2018, as evidenced by Niwa et al. Efficient Selection for High-Expression Transfectants with a Novel Eukaryotic Vector. Gene, 1991. 108:193-200, of record.
With regard to claim 122, Wright discloses recombinant adeno-associated viral particles comprising vectors encoding heterologous peptides for therapeutic use, wherein the viral genome comprises “stuffer/filler” sequences in order to improve packaging (Abstract; paragraphs [0034]-[0042], [0058], FIG 1). Wright discloses the heterologous peptides are flanked by, and operably linked one or more AAV inverted terminal repeats and a promoter/enhancer element, including ubiquitous enhancers from CMA or ubiquitous promoters such as chicken beta-actin (paragraphs [0018], [0040], [0084]-[0092], [0104]). Wright teaches the heterologous peptides are operably linked to polyA sequences, including those from SV40 (paragraph [0084]). Wright discloses the AAV vector typically accept inserts of DNA having a defined size range from about 4 kb to about 5.2 kb (paragraph [0095]). Wright discloses the AAV vectors are single stranded (paragraph [0042]).
Wright discloses the heterologous peptides encoded on the vector include N-acetylglucosamine-1-phosphate transferase for treating lysosomal storage disease (paragraphs [0014], [0059]).
Wright discloses the rAAV vectors encoding N-acetylglucosamine-1-phosphate transferase (GNPTAB) are packaged into AAV particles, including AAV8 (paragraphs [0004]-[0005], [0014], [0021], [0026], [0038]-[0039], [0045]-[0049]).
However, with regard to claim 122, Wright does not disclose wherein the promoter is a CAG promoter that has been shortened by deleting or substituting one or more nucleotides in its enhancer, promoter, intron or exon regions, nor that the N-acetylglucosamine-1-phosphate transferase protein is comprises an amino acid sequence that is at least about 80% identical to instant SEQ ID:1.
Gray discloses chimeric hybrid CMV enhancer/beta actin promoters are commonly used in gene transfer vectors, operably linked to both therapeutic and reporter genes (page 1144, Table 1), including the 1.6 kb CAGGS promoter (page 1144). Gray discloses an 800-bp CMV enhancer/beta actin mini-promoter (CBA, comprising an SV40 intron) or an 800-bp CMV enhancer/beta actin mini-promoter (CBh, comprising an MVM intron) function in scAAV vectors (Table 1; FIGs 1, 2, 3, 4). Gray teaches the smaller promoters can be used on vectors with packaging constraints (Abstract, pages 1143, 1147-1149, 1152).
Gray discloses the 800-bp CBA promoter is derived from the 1.6 kb CAGGGS promoter, wherein the CBA intron was replaced with a smaller SV40 intron (page 1144). Niwa (cited in Gray) is cited solely to show the CMV enhancer/Chicken beta-actin hybrid promoter of the prior art (referenced as CAGGGS promoter within Gray) is: 1) also called a CAG promoter; and 2) comprises a CMV enhancer operably linked to the promoter and first exon and intron of chicken beta-actin gene, and a splice acceptor of the rabbit beta-globin gene (See Abstract, FIG 1 of Niwa). Thus, the 800-bp CBA promoter comprising the SV40 intron in Gray is a CAG promoter that has been shortened by deleting or substituting one or more nucleotides in its enhancer, promoter intron or exon regions, as required by instant claim 122.
The cassettes of Gray show the ubiquitous, truncated CMV/CBA promoters are 800 base pairs long (Abstract, Table 1). The polyA sequences of Gray are derived from SV40 (226 bp) and BGH (207 bp) see Table 1). Thus, Gray establishes an expression cassette comprising the 800-bp (CBA or CBh) promoter and an approximate 200 bp polyA tail:
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Greyscale
Gray also acknowledges single-stranded AAV vectors have packaging restraints, stating, “AAV has a single-stranded 4.7-kb genome, and after removal of 4.4kb of the viral genome recombinant vectors can be packaged with a similar-sized foreign piece of DNA” (page 1143).
Genbank Accession No. NM_024312 discloses the mRNA sequence for human N-acetylglucosamine-1-phosphate transferase, wherein the mature peptide coding nucleotides are from nucleotides 285-4052 therein (3768 base pairs). Alignment of the translation of the peptide disclosed therein with instant SEQ ID NO:1 shows 100% identity.
It would have been obvious to combine the disclosure of Wright, on single-stranded AAV vectors encoding therapeutic peptides, including N-acetylglucosamine-1-phosphate transferase, further with the disclosures of Gray and Genbank Accession No. NM_024312.
With regard to the claimed requirement wherein the capsid is an AAV8 vector and the transgene is GNPTAB, Wright particularly enumerates a specific list of transgenes and a specific list of AAV particles for delivering them.
If the claimed invention and the structurally similar prior art species share any useful property, that will generally be sufficient to motivate an artisan of ordinary skill to make the claimed species
See also
MPEP2144.08 II(A)(4)b (Consider the Express Teachings).
If the prior art reference expressly teaches a particular reason to select the claimed species or subgenus, Office personnel should point out the express disclosure and explain why it would have been obvious to one of ordinary skill in the art to select the claimed invention. An express teaching may be based on a statement in the prior art reference such as an art recognized equivalence.
GNPTAB is listed among a genus of therapeutic peptides that are suitable for being encoding in the AAV vectors therein (paragraphs [0014], [0059]). Wright discloses the species therein are equivalents: at paragraph [0153] Wright states, “All of the features disclosed herein may be combined in any combination. Each feature disclosed in the specification may be replaced by an alternative feature serving a same, equivalent, or similar purpose. Thus, unless expressly stated otherwise, disclosed features ( e.g., a recombinant vector ( e.g., AAV) plasmid, vector genome, or recombinant virus particle ( e.g., AAV)) are an example of a genus of equivalent or similar features.” Thus, it would have been obvious to select AAV8 and GNPTAB from the teachings of Wright.
With regard to the claimed requirement that the vector encode a CAG promoter that has been shortened, a person of ordinary skill in the art would have had a reasonable expectation of success in substituting the ubiquitous promoters of Wright for the CBA promoter (CAG promoter comprising the SV40 intron) of Gray, as both are explicitly taught as being useful for driving expression of transgenes in AAV vectors. Therefore, these compositions are functional equivalents in the art, and substituting one for the other would have been obvious at the time of the invention. “When a patent ‘simply arranges old elements with each performing the same function it had been known to perform’ and yields no more than one would expect from such an arrangement, the combination is obvious.” See KSR International Co. v. Teleflex Inc., 82 USPQ2d 1385 (U.S. 2007) at 1395-1396, quoting Sakraida v. AG Pro, Inc., 425 U.S. 273 (1976) and In re Fout, 675 F.2d 297, 301 (CCPA 1982) (“Express suggestion to substitute one equivalent for another need not be present to render such substitution obvious”). A skilled artisan would have been motivated to use the 800-bp chimeric CMV enhancer/beta actin promoter of Gray in the AAV vectors because 1), Wright discloses the vectors can encode ubiquitous promoters (paragraphs [0092]); 2) Wright and Gray disclose single stranded AAV vectors have size constraints (paragraph [0095] of Wright; page 1143 of Gray); and 3) Gray discloses its 800-bp CBA (CAG shortened promoter) can be used in vectors with size constraints and allows for more coding sequences in the vector has improved benefits (pages 1143, 1147-1149, 1152 of Gray).
With regard to the claimed requirement wherein the vector encode a sequence with at least 80% identity to SEQ ID NO:1, Wright discloses the AAV vectors can encode N-acetylglucosamine-1-phosphate transferase for treating lysosomal storage disease (paragraphs [0014], [0059]). It would have been obvious to combine the known cDNA sequence of N-acetylglucosamine-1-phosphate transferase that is known in the art, as provided by Genbank Accession No. NM_024312.
A skilled artisan would have had a reasonable expectation of success in practicing the claimed invention, as AAV single strand vectors were known for accepting inserts of DNA from about 4 kb to about 5.2 kb (paragraph [0095] of Wright, the CMV/CBA promoters and poly A segments sizes of Gray and the known cDNA coding human N-acetylglucosamine-1-phosphate transferase combine to fit within the 4-5.2 kb size constraints of AAV single strand AAV vectors.
With regard to claims 123-125, Genbank Accession No. NM_024312 discloses human N-acetylglucosamine-1-phosphate transferase, which has at least 95% identity to, or is identical to SEQ ID NO:1. Thus, this claim is obvious for the same reasons as stated above for claim 122.
Conclusion
No claims are allowed.
FINAL REJECTION
THIS ACTION IS MADE FINAL. 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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KAA
/CHRISTOPHER M BABIC/Supervisory Patent Examiner, Art Unit 1633
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