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 election without traverse of group I, as well as the species reducing the level of Aurora kinase, PROTAC, adult onset PKO or ADPKD, and PKD1 in the reply filed on 6/3/25 is acknowledged.
Claims 4, 6, 13, 15, 18, 31, 33, 36, and 40 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim.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 6/3/25.
Drawings
The drawings filed on 4/26/22 and 12/11/25 are objected to because they are not fully legible. The figures are very fuzzy and the text cannot be clearly ascertained.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1, 2, 10, 19, 22, 24, 34, 35, 38, and 44-48 are rejected 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. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
The claims are directed to a method of minimizing or delaying renal cystogenesis via administering any PROTAC that reduces the level of Aurora kinase A. However, the specification does not adequately describe the structure required for the PROTAC to achieve the recited function. The minimal species of the specification that are specific to Aurora kinase A are not representative of the entire claimed genus.
Claim 10 recites that the PROTAC reduces the level of Aurora kinase A protein, but the specification does not adequately describe the structure required for this function.
It is noted that the PROTAC is not required to have any specific structural relationship to any specific Aurora kinase A sequence, but can act on any possible target that has a secondary effect of reducing the level of Aurora kinase A in the subject, which is a genus of agents that have not been adequately described in the specification.
The specification discloses: In certain embodiments, the compound for reducing levels of Aurora kinase is a PROTAC. A PROTAC is a chimeric construct which is useful for facilitating intracellular degradation of a target protein. To facilitate a protein for degradation by the proteasome (e.g. Degradation of Aurora kinase), the PROTAC is comprised of a first moiety that binds to an E3 ubiquitin ligase and a second moiety that binds to Aurora kinase. These moieties are typically connected with a linker. The PROTAC brings the E3 ubiquitin ligase in proximity with the protein so that it is ubiquitinated and marked for degradation. The moiety of a PROTAC for binding to Aurora kinase can be any peptide, small molecule or antibody that binds to Aurora kinase (page 28).
The specification does not adequately describe the structure required for the PROTAC to reduce the level of Aurora kinase A. The specification does not adequately describe the structure required for the first moiety that binds to an E3 ubiquitin ligase and the second moiety that binds to Aurora kinase. The specification discloses that the moiety of a PROTAC for binding to Aurora kinase can be any peptide, small molecule or antibody that binds to Aurora kinase. Without further description of the structure required for the function, one would not be able to readily recognize which peptides, small molecules, or antibodies, for example, bind to Aurora kinase A.
The MPEP states that for a generic claim, the genus can be adequately described if the disclosure presents a sufficient number of representative species that encompass the genus. See MPEP § 2163. If the genus has a substantial variance, the disclosure must describe a sufficient variety of species to reflect the variation within that genus. See MPEP § 2163. Although the MPEP does not define what constitute a sufficient number of representative species, the courts have indicated what do not constitute a representative number of species to adequately describe a broad genus. In Gostelli, the courts determined that the disclosure of two chemical compounds within a subgenus did not describe that subgenus. In re Gostelli, 872, F.2d at 1012, 10 USPQ2d at 1618. Additionally, in Carnegie Mellon University v. Hoffman-La Roche Inc., Nos. 07-1266, -1267 (Fed. Cir. Sept. 8, 2008), the Federal Circuit affirmed that a claim to a genus described in functional terms was not supported by the specification’s disclosure of species that were not representative of the entire genus. Furthermore, for a broad generic claim, the specification must provide adequate written description to identify the genus of the claim. In Regents of the University of California v. Eli Lilly & Co. the court stated:
"A written description of an invention involving a chemical genus, like a description of a chemical species, 'requires a precise definition, such as by structure, formula, [or] chemical name,' of the claimed subject matter sufficient to distinguish it from other materials." Fiers, 984 F.2d at 1171, 25 USPQ2d 1601; In re Smythe, 480 F.2d 1376, 1383, 178 USPQ 279, 284985 (CCPA 1973) ("In other cases, particularly but not necessarily, chemical cases, where there is unpredictability in performance of certain species or subcombinations other than those specifically enumerated, one skilled in the art may be found not to have been placed in possession of a genus ...") Regents of the University of California v. Eli Lilly & Co., 43 USPQ2d 1398.
The claims are rejected under the written description requirement for failing to disclose adequate species to represent the claimed genus, the genus being PROTACs that reduce the expression of any Aurora kinase A sequence by mediating its degradation. The claims do not require any specific structural requirement between the PROTAC and the target sequence for the function.
The Guidelines for Examination of Patent Applications under the 35 USC § 112, first paragraph, “Written Description” Requirement”, published at Federal Register, Vol. 66, No. 4, pp. 1099-1111 outline the method of analysis of claims to determine whether adequate written description is present. The first step is to determine what the claim as a whole covers, i.e., discussion of the full scope of the claim. Second, the application should be fully reviewed to understand how applicant provides support for the claimed invention including each element and/or step, i.e., compare the scope of the claim with the scope of the description. Third, determine whether the applicant was in possession of the claimed invention as a whole at the time of filing.
Therefore, the scope of the claimed invention is broad and the skilled artisan would not be able to envisage the entire genus claimed of agents that inhibit the expression of any Aurora kinase such that the skilled artisan would recognize that the applicant was in possession of the claimed genus at the time of filing.
Response to Arguments
Applicant argues that the amended claims are limited to PROTACs that degrade AURKA, which are expressly taught in the specification (see, for instance, page 28; lines 12-25). The specification explains the PROTAC architecture (E3 ligase ligand + AURKA binder + linker) and the intended therapeutic context of PKD/renal cystogenesis (see, for instance, page 2, lines 9-18; page 21, lines 20-25; and page 27, line 25 to page 28, line 25).
However, the species of the specification are not representative of the entire claimed genus of any PROTAC that reduces the level of AURKA via mediating its degradation; and the specification does not adequately disclose the structure required for the function. As instantly drafted, the PROTAC of claim 1 can act upon a different target that has a secondary effect of reducing the level of AURKA via mediating its degradation, a genus of compounds that have not been adequately described in the specification. With respect to the PROTACs that are specific for AURKA directly, the specification discloses that the moiety of a PROTAC for binding to Aurora kinase can be any peptide, small molecule or antibody that binds to Aurora kinase. Without further description of the structure required for the function, one would not be able to readily recognize which peptides, small molecules, or antibodies, for example, bind to Aurora kinase A.
The specification discloses that to facilitate a protein for degradation by the proteasome (e.g. Degradation of Aurora kinase), the PROTAC is comprised of a first moiety that binds to an E3 ubiquitin ligase and a second moiety that binds to Aurora kinase. However, the structure required for each of the moieties to function as claimed has not been adequately described in the specification. The genus of PROTACs comprise an enormous genus of possible structures within them that have not been adequately described.
Applicant argues that representative AURKA-targeting PROTAC species JB170, JB300, SK3277, and Compound 1 are presented in the Declaration at paragraph 6. These compounds, individually and in various experiments, were shown to degrade AURKA and deliver efficacy (in vitro and/or in vivo). However, these species are not representative of the entire claimed genus.
With regards to the opinion declaration by Dr. Ian Smyth filed on 12/11/25, the declaration demonstrates that specific species of PROTACs reduced the level of AURKA by mediating its degradation; and that subcutaneous injection into mice reduced cyst formation in ADPKD mice.
This does not negate that the species are not representative of entire claimed genus.
Claims 1, 2, 10, 19, 22, 24, 34, 35, 38, and 44-48 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for a method of inhibiting Aurora kinase A with Alisertib (and the AURKA PROTACs of the specification), does not reasonably provide enablement for a method of minimizing or delaying any renal cystogenesis via any PROTAC that reduces the level of Aurora kinase at any amount. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention commensurate in scope with these claims.
Factors to be considered in a determination of lack of enablement include, but are not limited to:
(A) The breadth of the claims;
(B) The nature of the invention;
(C) The state of the prior art;
(D) The level of one of ordinary skill;
(E) The level of predictability in the art;
(F) The amount of direction provided by the inventor;
(G) The existence of working examples; and
(H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988)
The instant claims are directed to a method of minimizing or delaying any renal cystogenesis via broad systemic delivery of any PROTAC that reduces the level of Aurora kinase A by mediating its degradation at any amount.
The specification discloses that co-deletion of Aurka in mice resulted in rescue of Inpp5eΔ/Δ-dependent cystogenesis (page 61).
The specification discloses Alisertib, a specific Aurka kinase inhibitor, potentiated cystogenesis in mouse models of ADPKD mediated by loss of Pkd1 (page 63).
These results are not commensurate in scope with a method of minimizing or delaying any renal cystogenesis via broad systemic delivery of any PROTAC that reduces the level of any Aurora kinase A at any amount. The specification is specific to delivery of Aurora kinase A specific PROTACs and ADPKD. The claims are not limited to delivery of any specific PROTAC or the treatment of ADPKD.
Zou et al. (Cell Biochem Funct. 2019;37:21–30) teach that although it is very promising to use PROTAC for drug development, it remains of many concerns about the clinical application. These concerns include the off‐target, cellular permeability, stability, and large molecular weight. Another problem is the difficulty of synthesis of the hybrid molecule, including optimizing the linker length and composition (page 27).
As outlined above, it is well known that there is a high level of unpredictability in the art for therapeutic in vivo applications. The scope of the claims in view of the specification as filed together do not reconcile the unpredictability in the art to enable one of skill in the art to make and/or use the claimed invention, namely a broad method of minimizing or delaying renal cystogenesis via delivery of any PROTAC that reduces any level of AURKA encompassing in vivo effects.
MPEP 2164.01
Any analysis of whether a particular claim is supported by the disclosure in an application requires a determination of whether that disclosure, when filed, contained sufficient information regarding the subject matter of the claims as to enable one skilled in the pertinent art to make and use the claimed invention.
Also, MPEP 2164.01(a)
A conclusion of lack of enablement means that, based on the evidence regarding each of
the above factors, the specification, at the time the application was filed, would not have taught one skilled in the art how to make and/or use the full scope of the claimed
invention without undue experimentation. In re Wright, 999 F.2d 1557,1562, 27
USPQ2d 1510, 1513 (Fed. Cir. 1993).
Given the teachings of the specification as discussed above, one skilled in the art could not predict a priori whether introduction of any agent within the instantly recited genus in vivo by the broadly disclosed methodologies of the instantly claimed invention, would result in successful minimizing or delaying any renal cystogenesis. To practice the claimed invention, one of skill in the art would have to de novo determine; the stability of the molecule in vivo, delivery of the molecule to the whole organism, specificity to the target tissue in vivo, dosage and toxicity in vivo, and entry of the molecule into the cell in vivo and the effective action therein. Without further guidance, one of skill in the art would have to practice a substantial amount of trial and error experimentation, an amount considered undue and not routine, to practice the instantly claimed invention.
A conclusion of lack of enablement means that, based on the evidence regarding each of the above factors, the specification, at the time the application was filed, would not have taught one skilled in the art how to make and/or use the full scope of the claimed invention without undue experimentation (see MPEP 2164.01(a)).
Response to Arguments
Applicant argues that the claims are now limited to PROTACs that target and degrade AURKA for the treatment of renal cystogenesis. This is a well-defined genus, and the specification provides detailed guidance on the design and function of such PROTACs (see, for instance, page 28; lines 12-25).
Contrary to applicant’s arguments, this is not a well defined genus. The claims are directed to delivery of an undefined genus of PROTACs that have the function of reducing the level of AURKA by mediating its degradation. The species of the specification are not representative of the entire claimed genus and do not demonstrate that any PROTAC specific for any target that has an effect of reducing the level of AURKA by any amount by mediating its degradation would result in the predictable minimization or delay of renal cystogenesis.
Applicant argues that while Zou discusses general challenges in the field of PROTAC development, Zou does not teach that PROTACs targeting AURKA are inoperable, nor does Zou suggest that these challenges cannot be overcome for specific targets. In fact, the Declaration demonstrates that multiple, AURKA-targeting PROTACs (JB170, JB300, SK3277, and Compound 1) can degrade AURKA and deliver efficacy in both in vitro and in vivo models of renal cystogenesis. Declaration, 6-8, FIGS. Xa-Xe. These results directly address the concerns raised by the Examiner in referencing Zou regarding permeability, stability, and functional efficacy, as the compounds were shown to be active in relevant biological systems, including animal models. Declaration, 110.
The species of PROTACs of the declaration are not commensurate in scope with the instantly claimed genus of PROTACs that reduce the level of AURKA by any amount.
Applicant argues that representative AURKA-targeting PROTAC species JB170, JB300, SK3277, and Compound 1 are presented in the Declaration at paragraph 6. These compounds, individually and in various experiments, were shown to degrade AURKA and deliver efficacy (in vitro and/or in vivo). However, these species are not commensurate in scope with the entire claimed genus.
With regards to the opinion declaration by Dr. Ian Smyth filed on 12/11/25, the declaration demonstrates that specific species of PROTACs reduced the level of AURKA by mediating its degradation; and that subcutaneous injection into mice reduced cyst formation in ADPKD mice; which is not enabling for a method of minimizing or delaying renal cystogenesis via broad delivery via any means of any PROTAC that reduces the level of AURKA by any amount.
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.
Claim(s) 1, 2, 10, 19, 22, 24, 34, 35, 38, and 44-48 is/are rejected under 35 U.S.C. 103 as being unpatentable over Dere et al. (WO 2018/039581 A1), in view of Zou et al. (Cell Biochem Funct. 2019;37:21–30), and Lehmann et al. (J Am Soc Nephrol 26: 2778–2788, 2015).
Dere et al. teach methods of treating a renal condition in a subject associated with high AURKA-HDAC6 signaling, comprising administering a therapeutically effective amount of a combination of an HDAC6 inhibitor and an (Aurora Kinase A) AURKA inhibitor to the subject.
Dere et al. teach: In an embodiment of the methods provided herein, the renal disease is, or is associated with, ciliopathy, Von Hippel-Lindau (VHL) disease, renal cystogenesis, renal cell carcinoma, and Tuberous Sclerosis Complex (TSC), and the like.
Dere et al. teach that the cell can be a renal cell, such as a renal epithelial cell. The cell can be human (instant claims 44 and 45).
Dere et al. teach: The data establishing AURKA as a substrate of VHL presents new opportunities for intervention, not only in RCC, but also in other cancers such as colorectal carcinoma, where genomic data from patients reveals the existence of VHL mutations, elevated AURKA and ciliary defects. Importantly, the demonstration that primary cilia can be rescued with AURKA and HDAC6 inhibitors provides proof-of- concept that targeting the VHL-AURKA-HDAC6 axis may have therapeutic efficacy. Future studies using in vivo cancer models, as well as ciliopathy models such as polycystic kidney disease (PKD), in which AURKA signaling is dysregulated, now become candidates for therapeutic targeting of the VHL-AURKA-HDAC6 axis.
Therefore, Dere et al. teach a method of treating renal cystogenesis via delivery of an agent that inhibits Aurora Kinase A to a subject. Claims 10, 19, and 22 recite outcomes that necessarily would flow from the method steps rather than reciting additional method steps.
Dere et al. does not teach that the inhibitor is a PROTAC that reduces the level of AURKA by mediating its degradation. However, it would have been obvious for the inhibitor to be a PROTAC because Zou et al. tach that PROTAC, proteolysis targeting chimera, have been developed for inducing the protein degradation by a targeting molecule. This technology takes advantage of a moiety of targeted protein and a moiety of recognizing E3 ubiquitin ligase and produces a hybrid molecule to specifically knock down a targeted protein. Given the teachings of Zou et al., one would reasonably expect that a PROTAC would be a suitable inhibitor of Aurora Kinase (instant claim 1).
Dere et al. does not teach that the method comprises treating PKD, but does offer motivation for the method to treat PKD. Dere et al. teaches that polycystic kidney disease (PKD) is a condition in which AURKA signaling is dysregulated and that therefore AURKA inhibitors are candidates for therapeutic targeting of the VHL-AURKA-HDAC6 axis. Additionally, it would have been obvious to determine if the subject has renal cystogenesis, more specifically PKD before treating them because the goal is to treat an individual that does in fact have the condition (instant claims 2, 35, 38, and 46)..
It would have been obvious to determine if the person has the condition before treating them, which is routine before treatment of a condition (instant claim 34). It would have been obvious to diagnose the PKD via screening for mutations in PKD1 or PKD2 or screening for mutations in the KIF3A gene because Lehmann et al. teach that deletion of KIF3A accelerates renal cyst formation. Lehmann et al. teach that Vhl/Kif3a double mutation also increased the frequency of cysts that displayed multilayered epithelial growth, which correlated with an increased frequency of misoriented cystic epithelial cell divisions (abstract). Therefore, it would have been obvious to screen for mutations in the KIF3A gene when identifying a subject having renal cystogenesis (instant claims 47 and 48).
It would have been obvious for the age to be at least one month, which is the requirement of instant claim 24, because the majority of the patients for PKD or renal cystogenesis would be over one month in age.
Response to Arguments
Applicant argues that Dere focuses on HDAC6 inhibitors, optionally in combination with AURKA inhibitors (e.g., alisertib). Dere proposes inhibiting kinase activity of AURKA-not degrading AURKA protein with PROTACs-and does not disclose PROTACs at all. Dere et al. is not relied upon for any teachings regarding PROTACs.
Applicant argues that Zou provides a generic review of PROTAC technology; Zou does not identify AURKA as a PKD target nor discuss renal disease; Zou highlights significant design uncertainties (off-target, permeability, linker optimization, molecular weight, synthesis challenges), undermining any reasonable expectation of success. Although there are challenges, Zou in fact offers motivation to utilize PROTACs by teaching the benefits of PROTACs and that they are promising for drug development.
Applicant argues that Lehmann addresses KIF3A deletion accelerating cyst formation and misoriented divisions (diagnostic relevance). While Lehmann may support diagnosis/stratification, Lehmann provides no suggestion to use AURKA-targeting PROTACs to treat cystogenesis. Lehmann is not relied upon for such.
Applicant argues that both Nikonova et al., PNAS 2014 (Nikonova 2014) and Nikonova et al., Frontiers in Oncology 2015 (Nikonova 2015) report that treatment with the AURKA kinase inhibitor alisertib exacerbates cystogenesis in ADPKD models. Nikonova 2014, p. 12862. In contrast, inhibition of EGFR kinase (which is also associated with ADPKD) using erlotinib had the opposite effect and restrained cystogenesis. Nikonova 2015, Abstract. This direct comparison demonstrates that not all pathogenic kinase inhibition is beneficial in PKD, and that AURKA inhibition in particular can be detrimental. Nikonova 2015, p. 9. Accordingly, a person skilled in the art would not be motivated by Nikonova 2014 and Nikonova 2015 to pursue AURKA inhibition for the treatment of PKD, let alone to develop a more complex modality such as a PROTAC targeting AURKA, without a specific rationale or evidence suggesting it would be effective.
One would have been motivated to inhibit AURKA to treat renal cystogenesis because Dere et al. teach a method of treating renal cystogenesis via delivery of an agent that inhibits Aurora Kinase A to a subject.
Applicant argues that the declaration demonstrates an unexpected efficacy of four different AURKA-targeting PROTACs. The four different PROTACs are JB170, JB300, SK3277, and Compound 1. Declaration, 16. All Aurora kinase (AURKA) targeting PROTACs significantly reduce the level of Aurora kinase A by mediating its degradation. Declaration, FIG. Xa. Compound 1 exposure did not alter cell count after 48 hrs in HK2 normal human proximal tubule cell lines, but dramatically reduced cell counts in the autosomal dominant polycystic kidney disease (adult onset PKD or ADPKD) cell line WT9-12. Declaration, 7, FIGS. Xb-Xc. Compound 1, 1 mg/kg IV injection into late-stage ADPKD mice, reduced kidney AURKA levels 48 hrs post-injection. Declaration, 8, FIG. Xd. Compound 1, chronic 1 mg/kg twice weekly SC injections, also reduced cyst formation in ADPKD mice. Declaration 8, FIG. Xe.
The claims are not limited to delivery of the PROTACs of the declaration or to a result commensurate in scope with the declaration.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). 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 Amy R Hudson whose telephone number is (571)272-0755. The examiner can normally be reached M-F 8:00am-6:00pm.
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/AMY ROSE HUDSON/Primary Examiner, Art Unit 1636