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 .
Claims Status
Claims 12-15 and 19-20 are amended.
Claims 17, 23-24, 35-40, and 43 are withdrawn.
Claims 1-16,18-22,25-29, and 41-42 are under examination.
Withdrawn Objections
The objection raised against claim 28 is withdrawn in light of claim amendment. Applicant has amended claim 28 to correct for the typographical error by inserting the missing space between “to” and “claim”.
Withdrawn Rejections
Claims rejection-35 USC § 112
The rejection of claims 12-15, and 19-20 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112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement is withdrawn in light of claims amendment. Applicant has amended claims 12-15, and 19-20 by deleting the term “ a fragment or derivative thereof”. Accordingly, the rejection is withdrawn.
Allowable Subject Matter
Sequence search did not find any prior art with 100% identity to the claimed SEQ ID NO: 27. Therefore, claim 18 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.
Maintained Rejections
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.
Claims 1-16,19-22, 25-29,and 41-42 are rejected under 35 U.S.C. 103 as being unpatentable over Picconi et al (Methods & Clinical Development , 2014), in view of Groendahl et al (US 2019/0255193 A1), Lachman et al ( CA 2755473 A1), and Lisowski et al ( WO 2013/029030 A1).
Regarding claims 1-6,12-16, 19-20, Groendahl et al disclose an adeno-associated viral (AAV) vector comprising a nucleotide sequence encoding Complement Factor I (CFI), an inhibitor of the complement system, or a fragment thereof, for use in the treatment or prevention of age-related macular degeneration (AMO), wherein the vectors enable delivery of CFI to the eye. ([0001]). Groendahl et al also teach that the nucleotide sequence encoding CFI or the fragment thereof can be operably linked to a chicken beta-actin (CBA) promoter, a CAG promoter, or CMV promoter. ([0027-0028]).
It is noted that Groendahl et al do not teach an AAV viral vector comprising a nucleotide sequence encoding an inhibitor of the complement that is operably linked to a podocyte-specific promoter or a viral vector that is capable of specifically transducing podocyte.
Picconi et al teach the utilization of AAV 2/9 vector containing the minimal NPHS1 promoter, which is a podocyte-specific promoter, to drive kidney-specific expression of enhanced green fluorescence protein (eGFP).( See abstract). Picconi et al disclose that tail vein injection of the rAAV serotype 2/9 piggybacked with a minimal NPHS1 promoter driving the expression eGFP gene into pregnant mice results in kidney-specific glomerular expression of the eGFP in both pups and dams that was stable up to 12 weeks post injection. (See Figs.5- 6). It should be noted that the glomerulus contains podocytes, thereby the rAAV 2/9 vector reads on a viral vector that is capable of transducing podocytes. Picconi et al demonstrate that considerable expression of eGFP was detected in the kidneys of the dams treated with a vector containing the NPHS1 promoter, while minimal off-target expression was detected in other tissues. (See Figs.7-8). To summarize, Picconi et al teach that pseudotyped rAAV 2/9 vector can produce sustained fetal kidney expression of the GFP gene following maternal tail vein injection of pregnant mice, and that by adding a podocyte-specific promoter (NPHS1 promoter), expression can be restricted to the kidneys, specifically the glomerulus. Furthermore, Picconi et al suggest employing an AAV 2/9 vector containing a podocyte-specific promoter in gene therapy for the treatment or amelioration of genetic defects associated with kidneys. (See 1st column page 6).
Lachman et al teach a therapeutic use of recombinant or plasma-derived CFI, an inhibitor of the complement system, for the prevention, treatment, or amelioration of kidney diseases associated with complement overactivation, such as atypical haemolytic uraemic syndrome (aHUS), and membranoproliferative glomerulonephritis Type 2 (MPGN2), ( Pages 3-4th paragraph, page 5- 5th paragraph, page 6-4th paragraph).
Taken together, employing an AAV vector encoding for an inhibitor of the complement system, such as CFI, under the control of a podocyte-specific promoter, is a product of combining prior art elements according to known methods to yield predictable results. Groendahl et al disclose an AAV vector comprising a nucleotide sequence encoding an inhibitor of the complement system (i.e. CFI), but fail to suggest using a podocyte-specific promoter or an AAV vector with a tropism to podocyte. Picconi et al strongly suggest utilizing a vector with kidney tropism such as an AAv 2/9 vector with a podocyte-specific promoter, in gene therapy to repair or ameliorate genetic defects associated with kidneys. The teachings of Lachman et al provide motivation for ordinary skill in the art to use an inhibitor of the complement system, such as CFI, to treat kidney diseases associated with the overactivation of complement system. Thus, one would have been motivated to utilize the pseudotyped rAAV 2/9 vector comprising a nucleotide sequence encoding the inhibitor of the complement system that is operably linked to a podocyte-specific promoter, to restrict its expression to the kidneys, specifically the podocytes and to treat kidney’s diseases associated with complement overactivation. One would be motivated to employ the recombinant vector of Picconi to specifically deliver the CFI to podocytes rather than using the recombinant or plasma-derived CFI, as taught by Lachman et al, which would have the disadvantage of delivering this protein ubiquitously (body and brain). A person of ordinary skill in the art who had reviewed Groendahl et al could have come across Picconi and Lachmann and immediately noticed the strong possibility of modifying the vector of Groendahl to comprise an rAAV 2/9 containing a podocyte-specific promoter to express CFI in podocytes. One would have been motivated to make this modification to specifically and efficiently deliver CFI transgene into the podocytes sparing other tissues.
Regarding claims 21-22, and 42, Groendahl et al teach an AAV vector comprising inhibitor of the complement sequence consisting of a polypeptide SEQ ID NO:1 that is identical to SEQ ID NO:11.
Regarding claims 7-11,and 41, following the discussion in claim 1 above, Groendahl et al in view of Picconi et al and Lachman render obvious claim 1. However, none of the cited prior art teach an AAV vector comprising LK03 capsid proteins with an amino acid sequence of SEQ ID NO: 2.
Lisowski et al disclose recombinant adeno-associated viral (AAV) comprising LK03 capsid, which consists of amino acid with SEQ ID NN:31 that is 100% identical to SEQ ID NO:2 of the instant claim. [00140]. Lisowski et al disclose that an rAAV vector comprising the LK03 capsid can be used to facilitate the expression of gene of interest in a variety of cells in a mammal, with an increased tropism to kidney cells. (See [0015], [0048], and [00199]). For example, Lisowski et al also demonstrate that an AAV comprising LK03 capsid has a high tropism to kidney cells such FRhk-4 and Hek 293 cells. ( See Figs.34,45-46)
Therefore, claims 7-11 and 41 are also a product of combining prior art elements according to known methods to yield predictable results, the predictable results being the generation of a recombinant viral construct AAV vector comprising LK03 capsid protein with amino acid sequence of SEQ ID NO: 31. Given that Lisowski et al demonstrate that an AAV vector comprising LK03 capsid has high tropism to Kidney, it would have been prima facie obvious to modify the vector of Groendahl et al to comprise an LK03 capsid proteins in order to target the AAV to Kidney. One would have been motivated to make this modification because Lisowski et al demonstrate that an AAV vector comprising LK03 capsid with SEQ ID NO:31 has a high tropism to Kidney. A person of ordinary skill in the art would have a reasonable expectation of success, when building an expression vector, that taking the LK03 capsid comprising SEQ ID 31, as described by Lisowski et al, and incorporating it in the vector encoding an inhibitor of the complement system, that the vector of claim 1 would be successfully synthesized.
Regarding claims 25-26, following the discussion above, the combined teachings of Groendahl et al , Picconi, and Lachman render obvious claim 1. Groendahl et al also disclose an AAV vector that includes a woodchuck hepatitis post transcriptional regulatory element (WPRE) that is operably linked to the nucleotide sequence encoding CFI, as well as a bovine growth hormone poly-A signal that is also operably linked to the nucleotide sequence encoding CFI. ([0242-0245]).
Regarding claim 27, following the discussion in claim 1 above, none of the cited prior art teach nucleotide sequence encoding an inhibitor of the complement system that is operably linked to a Kozak sequence.
Xu et al teach that the utilization of an AAV vector for gene therapy can be optimized by including transcriptional and post-transcriptional elements such as a promoter, enhancer, intron, and a poly(A) sequence. According to Xu et al, including such elements would improve the expression efficiency of each viral particle, allowing for fewer viral particles to be injected. (See Introduction, 2nd column 1st paragraph page 266). For example, Xu et al teach that inserting the woodchuck hepatitis virus post-transcriptional regulatory element (WPRE), a powerful viral enhancer element, between the luciferase gene and the poly(A) in an AAV construct encoding for luciferase increased luciferase expression 2- to 7-fold in vitro and 2- to 50-fold more in vivo,. (See abstract and Material and Methods section 2.1. “ adenovirus vectors” page 267). The construct of Xu et al also included the insertion of Kozak consensus sequences around the start codon of the luciferase gene, and the poly A tail derived from the bovine growth hormone,. ( See Material and Methods section 2.1. “ adenovirus vectors” page 267). Xu et al suggest that “ Inclusion of the WPRE, combined with the optimization of transcriptional regulatory elements at the stage of Ad vector design, will substantially reduce the quantity of viral particles that must be injected in order to reach a therapeutic level of transgene expression”. ( see Discussion, 1st column-last paragraph, page 270). Therefore, it would have been prima facie obvious for one of ordinary skill in the art at the time the invention was filed to combine the teachings of Groendahl, Picconi, Lachman and Xu to utilize AAV serotype 2/9 vector containing a kidney-specific promoter and specific transcriptional regulatory elements that is operably linked to nucleotide sequence encoding an inhibitor of the complement sequence to increase the transduction efficiency, and, subsequently, the expression of viral particles into the podocytes. The combined teachings of Groendahl et al , Picconi, and Lachman et al render obvious utilizing rAAV 2/9 vector and podocyte-specific promoter to produce podocyte-specific CFI expression. Xu et al teach that the inclusion of the WPRE, along with other regulatory elements such as Kozak consensus sequence and the bGH poly A sequence, substantially reduces the number of viral particles that must be injected to achieve a therapeutic level of transgene expression. Thus one would have been motivated to combine the teachings of Groendahl, Picconi, Lachman and Xu to utilize the rAAV 2/9 vector containing the podocyte-specific promoter and specific regulatory elements to specifically deliver the therapeutic protein (i.e. CFI) to the injured podocytes rather than the whole body, because such vector would allow for the specific and efficient delivery of CFI transgene into the kidney while sparing other tissues. Combining prior art elements according to known methods to yield predictable results. See MPEP 2143 (I)(A).
Regarding claims 28-29, Groendahl et al also teach an isolated cells comprising an AAV vector encoding for an inhibitor of the complement system, also disclosed a pharmaceutical composition comprising AAV vector encoding for an inhibitor of the complement system, or the isolated cell comprising AAV vector encoding for an inhibitor of the complement system in combination with a pharmaceutically acceptable carrier, diluent or excipient.( [0019-0020]).
Response to Arguments
Applicant's arguments filed 05/26/2026 have been fully considered but they are not persuasive.
Response to Applicant’s remarks regarding claim 18
Applicant notes that the office action indicates under the “ Allowable Subject Matter”
that SEQ ID NO: 27 is free of the art, and since claim 18 specifies the inclusion of SEQ ID NO: 27, the claim is believed to be allowable. This argument is not persuasive as it is not consistent with what was noted in the office action. The statement under the “ Allowable Subject Matter” section merely reflects that the sequence search did not find any prior art disclosing SEQ ID NO:27. Such statement was not intended as a determination that claim 18, as presently claimed, is in condition for allowance. It should be noted that claim 18 depends from claim 3, which depends from claim 1, and therefore incorporates all of the limitations of those claims. Claims 1 and 3 remain rejected under 25 U.S.C 103 for the reasons discussed above. Accordingly, claim 18 is objected to because it includes all the limitation of the rejected base claim.
Nature of the invention
Applicant argues that claim 1 is directed to a viral vector configured for podocyte-associated use and that the applied references do not disclose or suggest such a configuration. This argument is not found persuasive because the rejection does not rely upon a single reference to disclose every limitation of the claim. Rather, the rejection is based upon the combined teachings of Groendahl, Picconi, and Lachmann. As set forth above in the rejection, Groendahl et al teach an AAV vector encoding complement factor I (CFI), an inhibitor of the complement system. Picconi et al teach use of a podocyte-specific promoter (NPHS1) to restrict transgene expression to podocytes and further teach kidney-directed AAV delivery. Lachmann, on the other hand, teach the therapeutic desirability of complement inhibition in complement-mediated renal diseases. The combination of these teachings would have suggested a viral vector encoding a complement inhibitor under the control of a podocyte-specific promoter for treatment of complement-mediated kidney disease. Accordingly, Applicant has not shown an error in the rejection.
Shortcomings of the Groendahl reference
Applicant argues that Groendahl is directed to age-related macula
degeneration and therefore cannot serve as the primary reference. This is also not found persuasive because the rejection as currently stands does not rely upon Groendahl for the treatment indication of the age-related macular degeneration. Rather, Groendahl et al is relied upon for teaching an AAV vector encoding CFI. The therapeutic indication disclosed by Groendahl does not limit the applicability of its technical teachings where those teachings are relevant to the claimed subject matter.
As per the MEPEP (2141) “ a reference need not be from the same field of endeavor as the claimed invention in order to be analogous art. Bigio, 381 F.3d at 1325, 72 USPQ2d at 1212. This is consistent with the Supreme Court's instruction in KSR that "[w]hen a work is available in one field of endeavor, design incentives and other market forces can prompt variations of it, either in the same field or a different one." KSR, 550 U.S. at 417, 82 USPQ2d at 1396. The Federal Circuit reads KSR as "direct[ing] us to construe the scope of analogous art broadly" because "familiar items may have obvious uses beyond their primary purposes, and a person of ordinary skill often will be able to fit the teachings of multiple patents together like pieces of a puzzle." Wyers v. Master Lock Co., 616 F.3d 1231, 1238, 95 USPQ2d 1525, 1530 (Fed. Cir. 2010) (quoting KSR, 550 U.S. at 402, 127 S. Ct. at 1727).
Applicant further argues that Groendahl lacks a podocyte-specific promoter. While the office agrees, however, that feature is supplied by Picconi et al. Applicant is reminded that obviousness does not require that every limitation be disclosed by the primary reference. 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., 800F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
Shortcomings of the Picconi reference
Applicant argues that Picconi merely reports expression of GFP and therefore does not teach complement inhibition. This is also not found persuasive because Picconi et al is not relied upon for the therapeutic payload. Rather, Picconi et al is relied upon for teaching a gene-delivery platform capable of restricting expression to podocyte through the NPHS1 promoter. Therefore, one with ordinary skill in the art would have recognized that the identity of the transgene maybe varied while retaining the promoter’s specific function of restricting expression. Substitution of one known transgene for another represent no more than the predictable use of prior art elements according to their established function. In other words, Applicant has not provided persuasive evidence that replacing GFP with CFI would have produced unexpected results.
Furthermore, Applicant is reminded that 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).
Shortcomings of the Lachmann reference
Applicant argues that Lachmann et al concerns protein therapy rather than gene therapy. This is not found persuasive because Lachmann et al is cited solely for its teaching that complement inhibition through CFI is therapeutically useful for treating complement-mediated kidney disease. As set forth above, Lachmann et al is not relied upon to teach viral vectors, promoters, or gene delivery. References need not be combinable only where they employ identical therapeutic modalities. Lachmann et al is cited for recognizing the therapeutic utility of CFI in kidney diseases. This is supported by Lachmann et al statement that “Diseases such as aHUS and AMD might be tackled by targeted intervention in the C3b feedback and iC3b generation pathways”. (See section “ Therapeutic considerations” on page 18-19 in Lachmann disclosure ). This is not merely identifying disease biology. Rather, it is proposing a therapeutic intervention for aHUS, which is complement-mediated renal disease. Lachmann et al is also relied upon for its explicit teachings that increasing Factor I ( i.e. CFI ) is therapeutically beneficial for treating complement-mediated kidney diseases such as aHUS, and that raising the concentration of Factor I is the preferred therapeutic strategy ”. (See section “ Therapeutic considerations” on page 18-19 in Lachmann disclosure ). On the other hand, Groendahl et al is relied upon for teaching an AAV vector encoding CFI, Groendahl et al also show that CFI can be successfully expressed in vivo from a viral vector and that the expressed CFI was therapeutically active. ( See [0341] in Groendahl disclosure). Therefore, a person with ordinary skill in the art would have recognized the viral vector of Groendahl as an alternative delivery modality for achieving the therapeutic increase in Factor I advocated by Lachmann. Substituting a known delivery system for a known therapeutic protein to achieve the same biological effects represent predictable use of prior art elements according to their established function.
Applicant is reminded that 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).
No motivation to select the primary reference
Applicant argues that no person of ordinary skill in the art would have selected Groendahl.
This is not found persuasive because prima facie case of obviousness is not limited to selecting references from identical therapeutic fields. The proper inquiry is whether the art is analogous and reasonably pertinent to the particular problem with which the inventor was concerned, in order to be relied upon as a basis for rejection of the claimed invention. See In re Oetiker, 977 F.2d 1443, 24. In this case, Groendahl et al teach an AAV expression vector encoding the identical class of therapeutic molecule recited in the claims (i.e. CFI). Accordingly, Groendahl et al constitutes a relevant prior art despite its disclosure of ocular disease.
Applicant further argues that the office improperly stated “ that one could have come across” Groendahl. The office acknowledges applicant’s criticism of this phrasing. However, the rejection does not merely rely upon the possibility that one could have encountered Groenadahl. Rather, the rejection relies upon the explicit teachings of the cited references demonstrating.
Known AAV-mediated CFI delivery (Groendahl)
Known podocyte-specific promoter (Picconi), and
The recognized utility of CFI in renal diseases (Lachmann).
These teachings collectively provide sufficient reason to combine under KSR.
No motivation to combine
Applicant argues that a person of ordinary skill in the art interested in retinal disease would not have consulted Picconi or Lachmann. This is not found persuasive because the rejection is not built upon a retinal researcher seeking kidney therapy. Rather, the rejection is based upon what would have been obvious to a person with ordinary skill in the art seeking to employ CFI gene therapy in the treatment of complement-mediated renal disease. As previously stated, once such objective is recognized through Lachmann, Picconi provides an explicit teaching of podocyte-specific expression using the NPHSI promoter. The proposed modification merely substitutes a known-tissue specific promoter for the ubiquitous promoter taught by Groendahl to achieve its known function of restricting expression to podocytes.
The selected references do not suggest the claimed invention
Applicant further argues that the office improperly relies upon Applicant’s disclosure to identify the advantages of podocyte-specific expression and the use of gene therapy to treat complement-mediated renal disease. This is also not found persuasive because Picconi et al expressly teach restricting transgene expression to podocyte. Tissue-specific promoters are conventionally employed to reduce off-target expression. Accordingly, the motivation to substitute Picconi’s promoter into Groendahl’s construct arises directly from prior art itself and not from Applicant’s disclosure. Applicant has not identified any claim limitation that remains absent after consideration of the combined teachings.
No reasonable expectation of success
Applicant argues that the office relies upon boilerplate reasoning. This is also not found persuasive because each component of the proposed combination perform exactly the function for which it was previously known. As such, Groendahl successfully express CFI. Picconi et al successfully restrict expression to podocytes. Lachmann et al identifies complement inhibition as therapeutically useful in kidney disease. Applicants has not produced objective technical evidence demonstrating incompatibility between these teachings.
Lisowaski fails to cure the deficiencies of Groendahl, Picconi, and Lachmann
Applicant argues that Lisowski et al principally teach liver tropism. This is not found persuasive because the office relies upon Lisowski only for its disclosure that LK03 exhibits increased kidney tropism relative to conventional capsids. The cited portions demonstrate suitability of LK03 for kidney-directed gene delivery.
Argument against the restriction requirement
Applicant asserts that the office incorrectly characterized Applicant’s election a being made without traverse. This argument is not found persuasive because while Applicant submitted remarks in the election response, those remarks did not distinctly and specifically identify any error in the restriction requirement as required by 37 CFR 1.143. Instead, Applicant argued that the restriction requirement would become “improper or moot” if the claims were subsequently determined to be patentable over Colgan et al. Such argument does not explain why the restriction requirement, as made, was improper. Accordingly, Applicant’s election was properly treated as an election without a proper traverse, and no error is found in the office’s characterization.
As per Applicant’s request for a rejoinder, rejoinder is not appropriate at this time. Pursuant to MPEP § 821.04(a) withdrawn claims are eligible for rejoinder only when an allowable claim encompassing the elected invention is present. Since the elected claims remain rejected under 35 U.S.C 03, there presently no allowable claim that would support rejoinder.
Conclusion
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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to FATIMAH KHALAF MATALKAH whose telephone number is (703)756-5652. The examiner can normally be reached Monday-Friday,7:30 am-4:30 pm EST.
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/FATIMAH KHALAF MATALKAH/Examiner, Art Unit 1638
/Tracy Vivlemore/ Supervisory Primary Examiner, Art Unit 1638
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