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
Claims 4, 27, 28 and 29 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention and species, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on October 6, 2025.
Applicant’s election without traverse of Group I claims and SEQ ID NO: 2, 8 and 9 in the reply filed on October 6, 2025 is acknowledged.
Regarding Claims 8, 9, 13-16 and 26, examination is extended to all species claimed because a search for PIP4K2B and SEQ ID NO: 2, 8, and 9 did not reveal relevant prior art.
Claims 1-3 and 5-26 are under examination.
Claim Objections
Claims 12, 14, and 15 is objected to because of the following informalities:
Claims 12, 14 and 15 recite a “the binding entity”. Claim 11 recites “a binding moiety”, and Claim 13 recites “the binding moiety”. The claims do not use consistent claim terminology. To overcome this rejection, applicant may amend Claims 12, 14, and 15 to “the binding moiety”.
Appropriate correction is required.
Claim Rejections - 35 USC § 112(b)
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.
Claim 9 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.
Claim 9 recites the limitation "the peptide" in line 1. There is insufficient antecedent basis for this limitation in the claim. Claim 1 recites a method compromising degrading, modifying, or inhibiting one or more PIP4K isoforms, which may involve multiple peptides. Claim 8 recites the method of Claim 1 compromising administering phosphatidylinositol-5-phosphate 4-kinase compromising a mutation, but Claim 8 does not exclude additional peptides. Neither Claim 1 or Claim 8 recite the limitation “peptide”. The instant specification recites the use of additional peptides such as E3 ubiquitin ligases (p. 21, lines 25-27). Therefore, it is unclear which peptide is being referenced in Claim 9.
Claim Rejections - 35 USC § 112(a)
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 1-7, 10-13, 17-19 and 22 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 claims 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.
MPEP 2163.II.3.ii recites “The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice …, reduction to drawings …, or by disclosure of relevant, identifying characteristics, i.e., structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the inventor was in possession of the claimed genus … Satisfactory disclosure of a "representative number" depends on whether one of skill in the art would recognize that the inventor was in possession of the necessary common attributes or features possessed by the members of the genus in view of the species disclosed.”
Regarding Claim 1, the instant specification does not provide a representative number of species such that one skilled in the art would recognize the inventor had possession of the genus of methods comprising of degrading, modifying, or inhibiting PIP4K2B.
Claim Analysis
Claim 1 recites a method comprising degrading, modifying, or inhibiting one or more PIP4K isoforms in a mammalian subject, and therefore includes all methods of degrading, modifying or inhibiting a PIP4K isoform. Applicant has elected PIP4K2B for examination. Modification comprises protein modifications such as post-translational modifications. Inhibition comprises methods that influence upstream or downstream processes that inhibit expression.
Guidance Provided by the Specification
Applicant provides the structure and key residues of PIP42KB on pages 11-15 of the instant specification.
The instant specification teaches methods for degradation of PIP42KB on pages 21- 33. The methods described are general methods in which one skilled in the art would need to try multiple methods or screening assays with E3 ubiquitin ligases or antibodies to target PIP4K2B for degradation. Regarding E3 ubiquitin ligases, multiple examples with chemical structures of ligases are provided. Regarding antibodies, generic properties and structures of antibodies as well as methods to uncover antibodies are provided. The instant specification are no specific chemical structures provided.
The specification teaches methods for modification of PIP4K2B on pages 37-40. The methods described are the “use of microinjection, viral delivery, recombinase technologies, homologous recombination, TALENS, CRISPR, and/or ZFN” (p. 37). The methods described include references for the use of these methods, feature of vectors, and which amino acid substitutions are appropriate. The specification teaches the PIP4K N-terminal motif SEQ ID NO: 5 “can be deleted or degraded to generate a useful PIP4K polypeptide” (p. 9, lines 24-2). The specification teaches mutations in SEQ ID NO: 93 to SEQ ID NO: 95 in PIP4K2C to inhibit PIP4K interactions (p. 72, lines 21-30). The instant specification provides a reduction to practice of CRIPSR modification in Example 2, p.66-68.
The specification teaches methods for inhibition of PIP4K2B on pages 33-36. The methods described are the use of inhibitory nucleic acids, siRNA, or antisense oligonucleotides. The methods describe key characteristics including complimentary sequences, hairpins, and length of the nucleic acid. The instant specification provides a reduction to practice of inhibitory nucleic acids in Example 2, p.66-68, using shRNA.
Guidance Provided by the Art
The following art is cited below: Troup, R., et. al., Exploration of Targeted Anti-tumor Therapy, Vol. 1, p 273-312, October 30, 2020.
Regarding degradation, Troup teaches that targeted degradation of proteins by E3 ubiquitin ligases have a high degree of unpredictability: ‘Beyond structural biology, devising bioactive PROTACs is often complicated by issues surrounding their pharmacokinetic properties, notably cell permeability, metabolic stability, and solubility. As a result, the cell activity of a PROTAC is difficult to predict” (p. 301). No prior art guidance was found for degradation by E3 ubiquitin ligases targeting PIP4K isoforms.
Conclusion
Claim 1 recites a method comprising degrading, modifying, or inhibiting one or more PIP4K isoforms in a mammalian subject not limited to any particular method. Regarding degradation, the specification teaches methods to E3 ubiquitin ligases and antibodies without a reduction to practice such that one skilled in the art would recognize the inventor had possession of the invention. Regarding modification, the instant specification provides guidance on genetic modifications, but no guidance on modifications such as post-translational modifications. Regarding inhibition, the specification teaches inhibitory nucleic acids, but inhibition may include chemical inhibitors or inhibitors that act on processes upstream or downstream of expression of PIP4K2B. Troup teaches that there remains a high amount of unpredictability in the art for E3 ubiquitin ligases. Therefore, one skilled in the art would not conclude the inventor had possession of the claimed invention as a representative number of methods have not been described in the instant specification, and Claim 1 is rejected under 35 USC 112(a) for written description.
Dependent Claims
Claims 2-7, 10-13, 17-19, and 22 are also rejected under 35 USC 112(a) because they fail to limit the scope of Claim 1 to overcome the written description rejection.
Regarding Claims 2-4, and 7, the dependent claims do not limit the scope of degrading, modifying, or inhibiting one or more PIP4K isoforms and therefore fail to limit the scope of Claim 1 to overcome the rejection.
Regarding Claims 5, 6, and 10, the specification teaches mutations in SEQ ID NO: 93 to SEQ ID NO: 95 in PIP4K2C to inhibit PIP4K interactions with PIP5K1A while maintaining PIP4K activity (p. 72, lines 21-30). Claims 5, 6 and 10, however, still encompass methods of degradation and other forms of inhibition including chemical inhibitors, and therefore fail to limit the scope of Claim 1 to overcome the rejection.
Regarding Claims 11 and 12, while the claims limit the method to administering a binding moiety, the specification does not provide support for degradation or modifications such protein post-translational modifications as described for Claim 1.
Regarding Claim 13, the specification provides a general method for degradation through E3 ubiquitin ligases, but as described above for Claim 1, the specification does not provide specific guidance and does the art teaches that there remains a high amount of unpredictability.
Regarding Claims 17-19 and 22, the specification recites the use of antibodies and small molecule inhibitors, but the specification does provide for specific antibodies or molecular inhibitors.
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.
Claims 1, 2, 5, 6, 17 and 18 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Lamia, K. et. al., Molecular and Cellular Biology, Vol. 24, No. 11, p. 5080-5087, published June 2004.
Regarding Claim 1, Lamia teaches a method of comprising of degrading or inhibiting PIP4K2B, described as PI5P4Kβ in Lamia, in a mammalian subject to generate a subject with a population of modified mammalian cells: “To assess the physiological importance of PI5P4Kβ, we generated mice lacking this protein” (p. 5080, col. 2). Therefore, Claim 1 is anticipated by Lamia.
Regarding Claim 2, Lamia teaches a method for PIP4K2B. Therefore, Claim 2 is anticipated by Lamia.
Regarding Claim 5, Lamia teaches a method where PIP4K2B expression is completely inhibited and therefore PIP4K2B is inhibited from interacting with endogenous PIP4K isoforms or PIP5K in a mammalian subject. Therefore, Claim 5 is anticipated by Lamia.
Regarding Claim 6, Lamia teaches a method where PIP42KB expression is completely inhibited and therefore has reduced scaffolding or interaction of one or more isoforms with at least one other PIP4K or PIP5K. Therefore, Claim 6 is anticipated by Lamia.
Regarding Claim 17, Lamia teaches a method of modifying PIP4K2B gene sequences. Therefore, Claim 17 is anticipated by Lamia.
Regarding Claim 18, Lamia teaches a method of inhibiting expression of PIP4K2B. Therefore, Claim 18 is anticipated by Lamia.
Claims 1, 2, 5-7, and 17-21 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Bultsma, Y. et. al., Biochemical Journal, Vol. 430, No. 2, p. 223-235, published August 13, 2010.
Regarding Claim 1, Bultsma teaches a method of inhibiting PIP4K2B, described as PIP4Kβ in Bultsma, in a population of mammalian cells to generate a population of modified mammalian cells using siRNA in HEK-293 cells: “PIP4Kβ (PIP4K2B siGENOME siRNA…) were transfected into HEK-293 cells” (p. 224, col. 2; p. 231 Figure 5D). Therefore, Claim 1 is anticipated by Bultsma.
Regarding Claim 2, Bultsma teaches a method for PIP4K2B. Therefore, Claim 2 is anticipated by Bultsma.
Regarding Claim 5, Bultsma teaches a method of inhibiting PIP4K2B expression, and therefore PIP4K2B is inhibited from interacting with endogenous PIP4K isoforms or PIP5K in a mammalian subject. Therefore, Claim 5 is anticipated by Bultsma.
Regarding Claim 6, Bultsma teaches a method of inhibiting PIP42KB expression and therefore has reduced scaffolding or interaction of one or more isoforms with at least one other PIP4K or PIP5K. Therefore, Claim 6 is anticipated by Bultsma.
Regarding Claim 7, Bultsma teaches a method of inhibiting PIP4K2B expression in human cells, but Bultsma does not teach the inhibition modulates PIP5K or PI3K activity. However, Wang (Wang, D. et. al., Cell Reports, Vol. 27, No. 7, p. 1991-2001, published May 14, 2019) teaches that PIP4K2B inhibits PIP5K in human cells: “PIP5K1A activity is inhibited in vitro by addition of 2- to 10-fold molar excess of PIP4K2A, PIP4K2B, or PIP4K2C” (p. 1996, Figure 3, B-D). MPEP 2112.I-II states, “"[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. IRECO Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. … There is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference.” Therefore, the method of Bultsma, which inhibits PIP4K2B, inherently possesses the ability to modulate PIP5K activity, and Claim 7 is anticipated by Bultsma.
Regarding Claim 17, Bultsma teaches a method comprising of administering an inhibitor of PIP4K2B. Therefore, Claim 17 is anticipated by Bultsma.
Regarding Claim 18, Bultsma teaches a method of inhibiting expression of PIP4K2B. Therefore, Claim 18 is anticipated by Bultsma.
Regarding Claims 19 and 20, Bultsma teaches a method of inhibiting expression of PIP4K2B using siRNA, a nucleic acid inhibitor. Therefore, Claims 19 and 20 are anticipated by Bultsma.
Regarding Claim 21, Bultsma teaches a siRNA targeting PIP4K2B with 100% identity to SEQ ID NO: 9 (p. 224, col. 1); an alignment is below. Therefore, Claim 21 is anticipated by Bultsma.
Bultsma 1 AGATCAAGGTGGACAATCA 19
|||||||||||||||||||
SEQ ID NO: 9 708 AGATCAAGGTGGACAATCA 726
Claims 1 and 23 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Choi, S. et. al., Nature Cell Biology, Vol. 21, p. 462-475, published March 18, 2019.
Regarding Claim 1, Choi teaches a method comprising inhibiting PIP4K2B, described as PIPKII- β in Choi, in a population of mammalian cells to generate a population of modified mammalian cells: “each of the nuclear-localized PIP kinases was deleted by the clustered regularly interspaced short palindromic repeats (CRISPR)–CRISPR-associated protein 9 (Cas9) system in MDA-MB-231 breast carcinoma cells … deletion of PIPKII-α, PIPKII-β” (p. 426, col. 1; p. 463, Fig. 1a). Therefore, Claim 1 is anticipated by Choi.
Regarding Claim 23, Choi teaches a method which comprises CRISPR-mediated knockout of PIP4K2B. Therefore, Claim 23 is anticipated by Choi.
Claims 1, 11 and 12 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Gray, N. and Zhang, T., WO 2016/210291 A1, published December 29, 2016.
Regarding Claim 1, Gray teaches a method of inhibiting PIP4K2B in a population of mammalian cells to generate a population of modified mammalian cells through administering PIP4K2B inhibitors: “The compounds of Formula (I), and pharmaceutically acceptable salts, solvates, hydrates, polymorphs, cocrystals, tautomers, stereoisomers, isotopically labeled derivatives, prodrugs, and compositions thereof, may inhibit the activity of a kinase… In certain embodiments, the kinase is … PIP4K2B protein.” (p. 3, [0008]); “A "subject" to which administration is contemplated refers to a human” (p. 32, [0077]). Therefore, Claim 1 is anticipated by Gray.
Regarding Claim 11, Gray teaches a method of inhibiting PIP4K2B compromising of administering a binding moiety: “The compounds of the present invention may bear multiple binding motifs for binding to a kinase … In certain embodiments, the PIP4K2 is PIP4K2B protein” (p. 111, [00213]). Therefore, Claim 11 is anticipated by Gray.
Regarding Claim 12, Gray teaches a method wherein the binding entity binds with specificity to PIP4K2B: “For example, Ring A may form a hydrogen bond with a Cys residue of PIP4K (e.g. … Cys318 of PIP4K2B enzyme)” (p. 111, [00213) Therefore, Claim 12 is anticipated by Gray.
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.
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 3 is rejected under 35 U.S.C. 103 as being unpatentable over Lamia, K. et. al., Molecular and Cellular Biology, Vol. 24, No. 11, p. 5080-5087, published June 2004 and Bultsma, Y. et. al., Biochemical Journal, Vol. 430, No. 2, p. 223-235, published August 13, 2010 and as applied to Claim 1 above, and further in view of Lamia, K. et. al., Molecular and Cellular Biology, Vol. 24, No. 11, p. 5080-5087, published June 2004.
Regarding Claim 3, Lamia and Bultsma teach Claim 1.
Lamia and Bultsma do not teach a subject has or is suspected of having diabetes, metabolic syndrome, insulin resistance, obesity or a combination thereof.
Lamia recites a suggestion to use their method for a subjecting having obesity or diabetes: “The insulin hypersensitivity, reduced adiposity, and lack of major anatomical or physiological defects observed thus far in adult PI5P4Kβ -/- mice make PI5P4Kβ an attractive target for the development of inhibitors that may be useful in the treatment of obesity and type 2 diabetes.” Lamia also teaches mutations in the tubby gene in mice leads to obesity and diabetes (p. 5080).
It would be obvious to one skilled in the art before the effective filing date to use the teachings of Lamia or Bultsma and suggestion of Lamia to use their method to generate a population of modified mammalian cells which have or is suspected of having diabetes or obesity, including mice with mutations in the tubby gene. One skilled in the art would have reasonable expectation of success because Lamia reports no decreased survival in adult PI5P4Kβ -/- mice (p. 5086, col. 2) and Bultsma’s method created viable human cells. Therefore, Claim 3 is obvious over Lamia and Bultsma in further view of Lamia.
Claims 24 and 25 are rejected under 35 U.S.C. 103 as being unpatentable over Choi, S. et. al., Nature Cell Biology, Vol. 21, p. 462-475, published March 18, 2019 as applied to Claims 1 and 23 above, and further in view of Cailleau, R. et. al., Journal of the National Cancer Institute, Vol. 53, No. 3, p. 661-674, published September 1, 1974.
Regarding Claim 24, Choi teaches Claim 23 including incubating the cells with CRISPR reagents to generate a modified population of cells.
Choi does not teach isolating a population of cells from the subject.
Cailleau teaches a method of isolating cells from a subject to generate the MDA-MB-231 cell line: “During 1973, 4 new epithelial tumor cell lines were isolated from pleural effusions from breast cancer patients. We describe 3 of these lines: … MDA-MB-231” (p. 661, Summary).
It would be obvious to one skilled in the art to combine the teachings of Choi and Cailleau to create the method of Claim 1 comprising isolating a population of cells from the subject as taught by Cailleau and incubating the cells with CRISPR to generate a modified population of cells with modified PIP4K2B as taught by Cailleau. The method would be predictable because Cailleau successful generated several cell lines, and Choi used the same cells, MDA-MB-231, to create a modified population of cells. Therefore, Claim 24 is obvious over Choi in further view of Cailleau.
Regarding Claim 25, Choi teaches guide RNAs that target to the PIP4K2B genomic site: “Guide RNA sequences … 5′-GACGCTGAGGATCGGCTCGC-3′ and 5′-CGATCCTCAGCGTCCTGATG-3′ for the gene encoding PIPKII-β” (p. 476, CRISPR-Cas9 cell line generation). Therefore, Claim 25 is obvious over Choi in further view of Cailleu.
Allowable Subject Matter
Claims 8, 14-16, and 26 are 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.
The following art is cited below: Bondeson, D. and Crews, C., Annual Review of Pharmacology and Toxicology, Vol. 57, p. 107-123, published online October 12, 2016 and Gray, N. and Zhang, T., WO 2016/210291 A1, published December 29, 2016.
Regarding Claims 8, 9, and 26, a prior art search failed to reveal prior art for a mutation in SEQ ID NO: 1-5 and 96 with respect to PIP4K isoforms or motivation for mutating the sequences for administration to a mammalian subject.
Regarding Claim 14, Gray teaches Claim 11, but does not teach the agents that bind to an epitope with 95% sequence identity to SEQ ID NO: 6, 8, or 10. A prior art search for SEQ ID NO: 6, 8, or 10 failed to reveal any relevant prior art.
Regarding Claim 15, Gray teaches Claim 11, but does not teach agents that bind to an epitope with 95% sequence identity to SEQ ID NO: 1-5, 93 or 96. A prior art search for the sequences failed to reveal any relevant prior art.
Regarding Claim 16, a prior art search did not reveal prior art for inhibiting structural interaction between PIP4K isoforms and endogenous cellular structures or proteins. Gray teaches inhibitors for PIP4K isoforms that inhibit Kinase activity (p. 153-154, [00324]), but Gray does not tech the inhibitors inhibit structural interaction between PIP4K isoforms and endogenous cellular structures or protein.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Krishna Nuggehalli Ravindra whose telephone number is (571)272-2758. The examiner can normally be reached M-Th, alternate F, 8a-5p est.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Neil Hammell can be reached at (571) 270-5919. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/K.N.R./Examiner, Art Unit 1636
/NEIL P HAMMELL/Supervisory Patent Examiner, Art Unit 1636