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 .
Election/Restrictions
Applicant’s election without traverse of Group 1, claims 1-2, 4, 9-11, 14, 19, 21, 23-24, 34-35, 38, and 40-43, in the reply filed on 06 March 2026 is acknowledged.
Claims 16 and 20 withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 06 March 2026.
Claim Status
Claims 3, 5-8, 12-13, 15, 17-18, 22, 25-33, 36-37, 39, 44-56 were previously canceled, claims 16 and 20 have been withdrawn as being drawn to a nonelected invention, and claims 1-2, 4, 9-11, 14, 19, 21, 23-24, 34-35, 38, and 40-43 have been considered on their merits.
Information Disclosure Statement
The listing of references in the specification is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered.
Claim Interpretation
Claim 1, 2, and 4 utilize the phrase “an AAV serotype that efficiently crosses the blood brain barrier” is understood to mean the AAV serotype is capable of crossing the blood brain barrier. The instant specification at paragraph [0143] states, “the control that serves as a reference to determine whether an AAV virion can ‘efficiently cross blood brain barrier’, is AAV virions that lack ability to cross blood brain barrier.”
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 24, 35, and 40-43 is 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 the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Regarding claim 24, the amino acid modifications to SEQ ID NO: 2 or 3 recite mutations at R726H and N736P, as an example. SEQ ID NO: 2 is only 535 amino acids long and SEQ ID NO: 3 is only 534 amino acids long, therefore, cannot possess mutations at positions 726 or 736.
Additionally, the mutations recited are relative terms which renders the claim indefinite. The amino acid positions of the mutations are not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention. The mutations appear to be relative to the positions relating to either SEQ ID NO: 2 or SEQ ID NO: 5, yet the sequences do not possess these mutations.
Regarding claim 35, directed to a mutated VP3 capsid protein, wherein the mutated VP3 comprises a mutation at an amino acid sequence corresponding to an amino acid selected from the group consisting of N263, G264, T265, S266T, G268, T270, T274, and E533, wherein all the amino acid positions correspond to a native VP1 sequence numbering of AAVrh10 or AAVrh74. The instant specification discloses the native sequence for AAVrh74 and table 1, which refers to See SEQ ID NO: 6 in US20150159173. The amino acids of the capsid sequence of AAVrh74 do not correspond to the amino acids required by the claim. Therefore, the amino acid positions of the mutations are not clearly defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention.
Regarding claims 40 and 41, directed to a mutated VP3 which comprises a mutation at an amino acid corresponding to an amino acid selected from the group consisting of R726 and N736, wherein the amino acid positions correspond to a native VP1 sequence numbering of AAVrh74. The instant specification discloses the native sequence for AAVrh74 and table 1, which refers to See SEQ ID NO: 6 in US20150159173. The amino acids of the capsid sequence of AAVrh74 do not correspond to the amino acids required by the claim. Therefore, the amino acid positions of the mutations are not clearly defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention.
Claim 42 is included in the rejection because it depends from claim 41 and does not remedy the issue.
Regarding claim 43, directed to wherein the AAV VP1 or VP2 viral structural protein is any AAV serotype selected from Table 1, which is not found in the claims. Where possible, claims are to be complete in themselves. Incorporation by reference to a specific figure or table "is permitted only in exceptional circumstances where there is no practical way to define the invention in words and where it is more concise to incorporate by reference than duplicating a drawing or table into the claim. Incorporation by reference is a necessity doctrine, not for applicant’s convenience." Ex parte Fressola, 27 USPQ2d 1608, 1609 (Bd. Pat. App. & Inter. 1993). See MPEP § 2173.05(s). It is suggested to amend the claims to include the data from Table 1 into the claims.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1-2, 4, 9-11, and 14 are rejected under 35 U.S.C. 102(a)(1)/(a)(2) as being anticipated by Li et al. (WO 2019/216932, published 14 November 2019, IDS ref.) as evidenced by Hacker et al. (Cancers 2020, 12, 1889, published 14 July 2020) and Pietersz et al. (Gene Therapy (2021) 28:435-446, published online 15 August 2020).
Regarding claims 1 and 4, Li teaches a polyploid adeno-associated virus (AAV) capsid, wherein the capsid comprises capsid protein VP1, wherein said capsid protein VP1 is from one or more than one first AAV serotype, wherein said capsid protein VP2 is from one or more than one first AAV serotype and capsid protein VP3, wherein said capsid protein VP3 is from one or more than one second AAV serotype and wherein at least one of said first AAV serotype is different from at least one of said second AAV serotype and is different from at least one of said third AAV serotype, in any combination (Abstract). Li teaches generating rAAV with mixed or mosaic capsid shells has been to add AAV helper plasmids encoding the capsid proteins (VP1, VP2, and VP3) from a mixture of AAV serotypes (para. [0011]). Li teaches the capsids can be from any of the AAV serotypes, including the 12 serotypes of AAV isolated for gene therapy, other species, mutant serotypes, shuffled serotypes of such genes, or any other AAV serotype desired (para. [0012]). Li teaches a polyploid virus AAV2/8/9 was made from capsids of three serotypes, AAV2, AAV8, and AAV9 (para. [0020]). AAV9 is well known in the art to cross the blood-brain barrier as evidenced by Hacker. Hacker teaches for CNS-directed gene therapy, AAV9 possess the ability to cross the blood-brain-barrier (BBB) when applied intravenously and AAVrh10 is considered as an alternative to AAV9 (p. 4, section 2.3.2). Li teaches a haploid vector construct wherein VP2/VP3 are from serotype 9 (claim 4) and VP1 is from serotype 5 (Fig. 13 and 14). Li teaches enhanced AAV transduction from haploid AAV vectors by assembly of AAV virions with VP1/VP2 from one AAV vector and VP3 from an alternative one by application of rational polyploid methodology (Example 2, para. [00480]). Therefore, since the polyploid capsid of Li utilized the AAV9 VP3 protein and AAV9 is known in the art to efficiently cross the BBB, the capsid of Li reads on a population of rational polyploid AAV virions capable of crossing the BBB comprising at least one AAV VP1 or VP2 and VP3 structural proteins, wherein the VP1 or VP2 are from a different serotype than that of the VP3 viral structural protein which is capable of crossing the BBB.
Regarding the limitations directed to the capabilities of the AAV virions crossing the BBB in the last paragraph of the claim, these limitations read as intended results of a composition claim. Where the claimed and prior art products are identical or substantially identical in structure or composition, or are produced by identical or substantially identical processes, a prima facie case of either anticipation or obviousness has been established. In re Best, 562 F.2d 1252, 1255, 195 USPQ 430, 433 (CCPA 1977). MPEP 2112.01(I).
Regarding claim 2, Li teaches after systemic injection of 2x1010 vg of AAV vectors into mice, it was found that haploid AAV vectors composed of VP1/VP2 from serotypes 7, 8, 9, and rh10 and VP3 from AAV2 or AAV3 display a 2- to 7-fold increase in transduction across multiple tissue types, including liver, heart, and brain, when compared to AAV2-only and AAV3-only capsids (non-rational polyploid AAV particle) (para. [00495]). Li discloses their teachings provide insight into current AAV production strategies that can increase transduction across multiple tissue types (para. [00495]). The systemic injection and transduction in the brain read as the population of rational polyploid AAV virions crossed the blood-brain-barrier relative to non-rational polyploid AAV particle. The remaining limitation of the claim are presented in the alternative, therefore, are not required by the claim.
Regarding claim 9, the limitations directed to the CNS biodistribution of the AAV virion population are regarded as an intended result of a composition claim, as such, if the reference teaches the structure of the composition as claimed then it would necessarily possess the same functionality. Thus, since Li teaches the population of rational polyploid AAV virions of claim 1, the teachings of Li read on the limitations of claim 9.
Regarding claims 10 and 11, Li teaches a haploid vector construct wherein VP2/VP3 are from serotype 9 and VP1 is from serotype 5 (Fig. 13 and 14). Li does not teach the VP1 or VP2 is selected from AAV rhesus monkey serotype, therefore, reads as at least one of VP1 or VP2 is not selected from AAV rhesus monkey serotype (claim 10). The VP1 from serotype 5 reads as a AAV serotype that does not cross the blood brain barrier (claim 11) as evidenced by Pietersz, who discloses AAV9 and AAVrh10 are known to cross the blood-brain barrier after IV administration, while AAV5 does not (Pietersz, p. 444, 2nd column).
Regarding claim 14, Li teaches polyploid virus AAV2/8/9 made from capsids of three serotypes (AAV2, 8 and 9) demonstrated neutralizing antibody escapes ability was significantly improved against sera immunized with parental serotypes (para. [0020]).
Thus, the reference anticipates the subject matter of claims 1-2, 4, 9-11, and 14.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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.
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.
Claims 19 and 21 is rejected under 35 U.S.C. 103 as being unpatentable over Li et al. (WO 2019/216932, published 14 November 2019, IDS ref.) in view of Mietzsch et al. (Journal of Virology, Vol. 94, Issue 6, March 2020).
Regarding claims 19 and 21, Li teaches polyploid AAV vectors which are composed of capsids from two or more AAV serotypes may take advantages from individual serotypes for higher transduction but in certain embodiments eliminate the tropism from the parents (para. [0010]). Li teaches the polyploid viruses might have the ability to escape the neutralization by Nabs since the majority of Nab recognize conformational epitopes and polyploid virions can have changed its surface structure (para. [0010]). Li teaches diseases of the central nervous system can be treated using an AAV, wherein the AAV comprises a recipient AAV that can be any AAV serotype and a donor capsid that is selected from one or more of AAV1, AAV2, AAV3, AAV4, AAV5, AAV7, AAV8, AAV9 or AAV10 (para. [00433]). Li teaches a substantially homogeneous population of virions wherein only one of the three structural proteins is from a different serotype and wherein the one viral structural protein different from the other two viral structural proteins is VP3 (see Li claims 4 and 8). Li teaches the VP1 and/or VP2 can be AAV8 and the VP3 can be AAVrh10 (Table 1 and Li claims 16, 22, and 23).
While Li does not exemplify the virion comprising VP1 and VP2 from AAV8 and VP3 from AAVrh10, the teachings and claims of Li suggest this embodiment. The claims are directed to Table 1 which discloses AAVrh10 as an option for the second AAV serotype, which corresponds to the serotype for the VP3 protein, and the claims and table disclose AAV8 serotype as an option for the VP1 and VP2 proteins.
Additionally, Mietzsch teaches adeno-associated viruses (AAVs) from clade E, which includes rhesus isolate 10 (AAVrh.10) and AAV8, are often used as vectors in gene delivery applications, wherein, unlike representative AAV8, AAVrh.10 is capable of crossing the blood brain barrier (BBB), thereby enabling the delivery of therapeutic genes to the central nervous system (Abstract). Mietzsch teaches the capsid structures of AAV8 and AAVrh.10 are similar, with only minor differences observed in the previously described surface variable regions, suggesting that specific residues S269 and N472, absent in AAV8, may confer the ability to cross the BBB in AAVrh.10 (Abstract). Mietzsch teaches recombinant adeno-associated virus vectors (rAAVs), based on AAV8 and AAVrh.10, have been utilized in multiple clinical trials to treat different monogenetic diseases (Abstract). Mietzsch teaches the capsid structure information provides a platform for engineering to improve receptor retargeting or tissue specificity (Abstract). Mietzsch teaches AAV variants isolated from rhesus macaque tissues are being developed for a variety of gene delivery applications because of the lower percentage of preexisting neutralizing antibodies against their capsid in the human population and their higher transgene expression in a variety of tissues in comparison to other AAV serotypes (para. bridging pp. 2-3). Mietzsch teaches AAVrh.10 is reported to cross the BBB and efficiently transduce neuronal cells similar to AAV9, which belongs to clade F (p. 3). Mietzsch teaches the capsid surface information will aid future engineering at tempts to generate AAVrh.10 variants with the ability to (i) escape preexisting neutralizing antibodies based on information on known epitopes for other AAVs or (ii) target different cell types based on tissue tropism information (p. 12, Conclusions).
Therefore, it would have been obvious to one of ordinary skill in the art to arrive at the population of rational polyploid AAV virions comprising VP1 and VP2 from AAV8 and VP3 from AAVrh10 based on the teachings of Li and Mietzsch with a reasonable expectation of success because Li teaches the capsids can be from any of the AAV serotypes, including the 12 serotypes of AAV isolated for gene therapy, other species, mutant serotypes, shuffled serotypes of such genes, or any other AAV serotype desired (para. [0012]). One would be motivated to arrive at the population of rational polyploid AAV virions comprising VP1 and VP2 from AAV8 and VP3 from AAVrh10 based on the teachings of Li and Mietzsch because both AAV8 and AAVrh.10 have been utilized in multiple clinical trials to treat different monogenetic diseases and combining capsid serotypes are known to reduce humoral response relative to the humoral response elicited by the parental serotype which include AAV8 (claims 19 and 21) as disclosed by Li and Mietzsch.
Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill before the effective filing date of the claimed invention.
Claims 23-24, 34-35, and 40-43 are rejected under 35 U.S.C. 103 as being unpatentable Li et al. (WO 2019/216932, published 14 November 2019, IDS ref.) as evidenced by Hacker et al. (Cancers 2020, 12, 1889, published 14 July 2020) and Pietersz et al. (Gene Therapy (2021) 28:435-446, published online 15 August 2020) as applied to claims 1-2, 4, 9-11, and 14 above, and further in view of High et al. (US 2018/0187213 A1, published 05 July 2018, IDS ref.) as evidenced by Duan (Molecular Therapy, Vol. 26, No. 10, October 2018).
Li anticipates the subject matter of claims 1-2, 4, 9-11, and 14, and thus, also render them obvious.
Regarding claims 23-24 and 42-43, Li teaches polyploid AAV vectors which are composed of capsids from two or more AAV serotypes may take advantages from individual serotypes for higher transduction but in certain embodiments eliminate the tropism from the parents (para. [0010]). Li teaches a substantially homogeneous population of virions wherein only one of the three structural proteins is from a different serotype and wherein the one viral structural protein different from the other two viral structural proteins is VP3 (see Li claims 4 and 8). Li teaches the capsids can be from any of the AAV serotypes, including the 12 serotypes of AAV isolated for gene therapy, other species, mutant serotypes, shuffled serotypes of such genes, or any other AAV serotype desired (para. [0012]). An isolated AAV for gene therapy of Li would include AAVrh74, as this vector is known to be used for gene therapy, as evidenced by Duan. Duan teaches Duan teaches AAVrh74 has been used in clinical trials of systemic AAV gene therapy (p. 2340, 2nd column). Li teaches the VP1 and/or VP2 can be AAV8 (claim 43) (Table 1 and Li claims 16, 22, and 23). Li teaches examples of AAV capsid proteins that can be included in the capsid in combination with other capsid proteins include AAV8 and AAVrh (para. [00150]).
While Li does not exemplify the virion comprising VP3 from AAVrh74, the teachings and claims of Li suggest this embodiment.
Therefore, it would have been obvious to one of ordinary skill in the art to arrive at the population of rational polyploid AAV virions comprising VP3 from AAVrh74 based on the teachings of Li with a reasonable expectation of success because Li teaches the capsids can be from any of the AAV serotypes, including the 12 serotypes of AAV isolated for gene therapy, other species, mutant serotypes, shuffled serotypes of such genes, or any other AAV serotype desired (para. [0012]). One would be motivated to arrive at the population of rational polyploid AAV virions comprising VP3 from AAVrh74 based on the teachings of Li because Li teaches combining capsid serotypes are known to reduce humoral response relative to the humoral response elicited by the parental serotype.
Li as evidenced by Duan are silent to the mutated sequence of AAVrh74.
However, High teaches SEQ ID NO: 2 which comprises, with 100% identity, instant SEQ ID NO: 2. High teaches AAVRh74 and AAVRh74 variants (reads as mutants) can be used to deliver polynucleotides, such as gene coding sequences, to express proteins that provide a desirable or therapeutic benefit, as well as for inhibitory nucleotides that reduce or inhibit expression of an undesirable or defective gene, thereby treating a variety of diseases (para. [0011]). Since the first two lines of claim 24 identifies the mutated AAVrh74 VP3 sequence having the amino acid sequence of instant SEQ ID NO: 2, it is understood that instant SEQ ID NO: 2 is a mutated sequence, therefore, the SEQ ID NO: 2 of High reads on the limitations of the claim. The other limitations of claim 24 are listed in the alternative, as such, not required by the claim. The instant specification indicates instant SEQ ID NO: 2 comprises the W581VV modification (Instant spec. para. [00246]), therefore, the sequence of High reads as a mutated AAVrh73 capsid sequence (claim 42).
Therefore, it would have been obvious to one of ordinary skill in the art to utilize the sequence of High in the population of virions of Li as evidenced by Duan with a reasonable expectation of success because High teaches AAVRh74 and AAVRh74 variants can be used to deliver polynucleotides, such as gene coding sequences, to express proteins that provide a desirable or therapeutic benefit, as well as for inhibitory nucleotides that reduce or inhibit expression of an undesirable or defective gene, thereby treating a variety of diseases. One would be motivated to utilize the sequence of High in the population of virions of Li as evidenced by Duan because High discloses a sequence comprising instant SEQ ID NO: 2 and Li teaches mutant serotypes can be utilized to make polyploid capsids and combining capsid serotypes are known to reduce humoral response relative to the humoral response elicited by the parental serotype.
Regarding claim 34, the limitation directed to the virions allowing repeat dosing, these limitations read as intended results of a composition claim. Where the claimed and prior art products are identical or substantially identical in structure or composition, or are produced by identical or substantially identical processes, a prima facie case of either anticipation or obviousness has been established. In re Best, 562 F.2d 1252, 1255, 195 USPQ 430, 433 (CCPA 1977). MPEP 2112.01(I).
Therefore, the claim is interpreted as requiring at least one AAV VP1 or VP2 viral structural proteins and a AAV VP3 viral structural protein; wherein the VP1 and VP2 viral structural proteins are each from any AAV viral serotype except for a Rhesus AAV serotype, and the VP3 viral structural protein is selected from a rhesus monkey AAV serotype; wherein the population of rational polyploid AAV virions evade neutralizing antibodies against a parental AAV rhesus monkey serotype of the VP3 viral structural protein, and wherein the VP3 structural protein of the rational polyploid virions is a AAV rhesus monkey mutated viral structural protein VP3. As such, the teachings of Li as evidenced by Duan in view of High read on the limitations of the claim, as set forth in the rejection of claims 23 and 24 above.
Regarding claims 35 and 40-41, the scope of the claims are unclear as discussed in the 112(b) rejection above. Therefore, the claim is interpreted as the population of rational polyploid AAV virions, wherein the AAV rhesus monkey mutated viral structural protein VP3 is from a mutated AAVrh74 VP3 viral structural protein. As such, since the references teach a mutated AAVrh74 VP3 protein, the teachings of Li as evidenced by Duan in view of High read on the limitations of the claims.
Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill before the effective filing date of the claimed invention.
Allowable Subject Matter
Claim 38 is free of the art and thus has allowable subject matter.
The following is a statement of reasons for the indication of allowable subject matter: The required amino acid mutations, R727H and N737P corresponding to a native VP1 sequence numbering of AAVrh10, of the viral structural protein VP3 was found to be free of the art.
Claim 38 is objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims.
Conclusion
No claims are allowed.
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/N.A.H./Examiner, Art Unit 1631
/LAURA SCHUBERG/Primary Examiner, Art Unit 1631
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