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 .
Application Status
The Amendments and Remarks filed 17 July 2026 are acknowledged and have been entered. Claims 19, 22, 27 and 30 have been amended. Claims 1-18, 20-25, 26, 28-29, 33-36, and 38-39 have been cancelled. Claims 19, 27, 30-32 and 37 are pending and being examined on the merits.
Any objection or rejection not reiterated herein has been overcome by applicant’s claim amendments.
Priority
This application is a 371 PCT of CN2021/098217 filed 06/04/2021. Acknowledgment is made of applicant's claim for foreign priority based on an application filed in China on 09/29/2020. Receipt is acknowledged of certified copies of papers and English translation required by 37 CFR 1.55.
Claim Objections
Claim 37 is objected to because of the following informalities:
Claim 37 recites: “the senescence of animal cell”. Claim 30 previously recites “the senescence of the animal cell.” The intended meaning of claim 37 appears reasonably ascertainable, and therefore a separate §112(b) rejection is not considered necessary. However, for grammatical clarity and consistency with claim 30, it would be remedial to amend the phrase to, for example: “the senescence of the animal cell is the senescence of…”or otherwise amend the claim to clearly express Applicant's intended limitation.
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 31 and 32 are 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 31 recites: “wherein the animal is a mammal.” However, claim 31 depends from claim 30, and claim 30 recites administration of a substance “on an animal cell, a tissue, an organ or an individual.” Claim 30 does not introduce or recite “an animal” as a claim element. Accordingly, there is insufficient antecedent basis for “the animal” in claim 31. Moreover, because claim 30 separately recites an animal cell, tissue, organ, and individual, it is unclear whether “the animal” of claim 31 is intended to limit the organism from which the animal cell is derived, the organism associated with the tissue or organ, the recited individual, or some other unrecited animal. Therefore, the scope of claim 31 is not reasonably certain.
Claim 32 recites: “wherein the mammal is a human or a mouse.” Claim 32 depends directly from claim 30. Claim 30 does not recite or otherwise introduce “a mammal.” Accordingly, there is insufficient antecedent basis for “the mammal”, and it is unclear which element of claim 30 is intended to be limited to a human or mouse. It is noted that merely changing the dependency of claim 32 to claim 31 would not completely resolve the issue because claim 31 itself presently lacks antecedent basis for “the animal.”
Claims 19, 27, 30-32 and 37 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 enabling particular embodiments involving inhibition of KAT7 for delaying or reducing cellular senescence in particular cell types and aged mice, does not reasonably provide enablement for treating and/or preventing senescence across every animal call, tissue, organ, and individual as broadly claimed. 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 use the invention commensurate in scope with these claims.
Nature of invention:
Claim 19 is directed to a method of preparing “a product for treating and/or preventing senescence,” comprising “formulating the substance into a pharmaceutically acceptable product for treating and/or preventing the senescence.” Independent claim 27 is drawn to a product “for treating and/or preventing senescence.” Claim 30 is drawn to a method for: delaying and/or treating and/or preventing senescence of an animal cell, a tissue, an organ or an individual, by administering a substance that reduces KAT7 content or activity, inhibits KAT7 gene expression, or knocks out KAT7 genes, wherein the substance is either the recited CRISPR/Cas9 system or WM-3835.
Breadth of claim
The claim therefore encompasses numerous cell types, tissues, organs, organisms, physiological states, causes of senescence, and mechanisms by which senescence may arise.
Specification
At the paragraph bridging pages 1-2 of the specification the following is stated: Senescence in nature is a process of gradual decline in functions of various organ systems in a body, which will finally result in death of an individual. The degenerative changes in an organ function are driven by both genetic and environmental factors. With the senescence of a body, cells as the smallest functional units that make up the tissues and the organs also become senescent. Cell senescence refers to a changing process in which the cell proliferation and differentiation abilities and physiological functions gradually decline with the passage of time while cells executing life activities. The specification goes on to state, “Cell senescence as an inevitable process of life is affected by both genetic and environmental factors.” See page 2, 1st full paragraph, 1st sentence. All working examples are directed to delaying senescence in cells and mice. No working example demonstrates prevention of senescence in a cell, tissue or organism. The specification demonstrates KAT7 knockdown in human mesenchymal precursor cells and reports changes in senescence-associated markers, including SA-β-gal, p16, p21, and IL-6. The disclosure further demonstrates effects on replicative senescence in mesenchymal precursor cells. The specification also reports that KAT7 knockdown significantly delayed senescence in human primary hepatocytes. Example 6 evaluates WM-3835 in Werner syndrome human mesenchymal precursor cells and human primary hepatocytes and concludes that WM-3835 delayed senescence in those tested cellular systems. Accordingly, the specification is considered enabling for at least certain specifically disclosed cellular contexts involving mesenchymal precursor cells and hepatocytes.
State of the art
The state of the art demonstrates that cellular senescence is not a single uniform biological program. Hernandex (Hernandez-Segura et al. Trends in Cell Biology 28:436–453 (2018)) characterize the senescence phenotype as “highly variable and heterogeneous” and further explain that mechanisms behind common senescence characteristics are not widely conserved among all senescence programs [pg. 436, Highlights]. Hernandez-Segura further identifies numerous biologically distinct senescence programs, including replicative senescence, DNA-damage-induced senescence, oncogene-induced senescence, oxidative-stress-induced senescence, chemotherapy-induced senescence, mitochondrial-dysfunction-associated senescence, epigenetically induced senescence, and paracrine senescence. [pp. 437, Box 1]. Kirschner et al. similarly teach that cell type and the stimulus inducing senescence “can lead to variations in the phenotype of the senescence response.” Kirschner (Kirschner et al., Biochem. Soc. Trans. 48:765–773 (2020)) teaches that senescence phenotype varies with the affected cell type, physiological location, causal insult, and molecular pathways favored within the cells. [pg. 766; para 4].
Undue experimentation
In view of this recognized biological heterogeneity, the data showing that KAT7 inhibition delays senescence in certain mesenchymal precursor-cell and hepatocyte systems do not reasonably establish that KAT7 is a controlling or therapeutically useful pathway for every form of senescence encompassed by claim 30 in every animal cell, tissue, organ, or individual; nor does it show that KAT7 can prevent senescence.
To practice the full scope, one of ordinary skill would be required to determine, for numerous encompassed biological systems: whether KAT7 participates in the particular senescence pathway; whether inhibition of KAT7 delays, treats, or prevents that particular type of senescence; the effective extent and duration of KAT7 inhibition; appropriate dose and delivery conditions; whether inhibition of KAT7 produces the desired anti-senescence effect rather than apoptosis, differentiation, toxicity, or another cellular phenotype; and whether results obtained in the disclosed cell types can be extrapolated to the numerous undisclosed tissues and organs within the claim. Such experimentation would constitute more than routine optimization because the prior art expressly recognizes that senescence programs and their operative mechanisms vary according to cell type, stimulus, and physiological context.
Accordingly, considering the breadth of the claims, the limited number of representative biological systems demonstrated relative to that breadth, the recognized unpredictability of senescence biology, and the quantity of experimentation needed to determine whether KAT7 inhibition is effective throughout the full claimed genus, including preventing senescence, undue experimentation would be required.
Claims 31, 32, and 37 depend from claim 30 and do not overcome this deficiency. Although claim 37 narrows the animal-cell embodiment to mesenchymal precursor cells, mesenchymal stem cells, or hepatocytes, claim 37 remains dependent on the broader method of claim 30 and retains the broad delay/treatment/prevention language and alternative KAT7 inhibition modalities.
Claim Rejections - 35 USC § 102
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 27 is rejected under 35 U.S.C. 102(a)(1) as being anticipated by MacPherson (MacPherson et al. Nature 577:266–270 (2020), published online December 11, 2019).
Claim 27 recites a product selected from a product for treating and/or preventing senescence and a product for inhibiting CCl4-induced hepatic fibrosis, wherein the active ingredient is either the specifically defined CRISPR/Cas9 system or WM-3835. Because these species are recited alternatively, disclosure of the WM-3835 species meets the active-ingredient limitation of the claim.
MacPherson identifies HBO1 as “also known as KAT7 or MYST2.” [Abstract]. MacPherson expressly teaches generation of WM-3835 and states that WM-3835 has increased potency against HBO1 [pg. 270, col. 1, para 2-3; Fig. 4a–c and accompanying text]. MacPherson further teaches that “WM-3835 is a cell-permeable small molecule” and that treatment with WM-3835 rapidly reduces H3K14 acetylation. [p. 270, col. 1, para 3]. MacPherson's Extended Data further reports an HBO1/KAT7 biochemical IC50 of about 0.030 µM for WM-3835, confirming that WM-3835 is an active inhibitor of HBO1/KAT7. [p. 270, col. 1, para 2; Extended Data Fig. 8a]. MacPherson additionally discloses an in-vivo-administered WM-3835 product. Specifically, BALB/c female mice were orally dosed with WM-3835 at 100 mg/kg twice daily, with WM-3835 formulated in 20% PEG400/10% Solutol [p. 270, col. 1, para 3; Extended Data Fig. 10c]. Thus, MacPherson discloses a product containing the expressly claimed active ingredient WM-3835.
The limitations that the product is “for treating and/or preventing senescence” or “for inhibiting carbon tetrachloride (CCl4)-induced hepatic fibrosis” express intended uses of the otherwise structurally recited WM-3835-containing product and do not impart a structural distinction over MacPherson's WM-3835 product. Accordingly, MacPherson anticipates claim 27.
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 19 is rejected under 35 U.S.C. 103 as being unpatentable over MacPherson (MacPherson et al. Nature 577:266–270 (2020), published online December 11, 2019).
Claim 19 recites a method of preparing a product comprising: providing a substance selected from the specifically defined KAT7-targeting CRISPR/Cas9 system or WM-3835; and formulating the substance into a pharmaceutically acceptable product.
MacPherson teaches HBO1, i.e., KAT7/MYST2, as a therapeutic target and expressly generates WM-3835 as an inhibitor thereof [pg. 266 Abstract; pg. 270, col. 1, para 2-3]. MacPherson expressly states that WM-3835 reduces HBO1-dependent H3K14 acetylation and that its cellular efficacy is primarily mediated through HBO1 inhibition. [p. 270, col. 1, para 2-3; Fig. 4d–f]. Thus, MacPherson teaches the claimed step of providing WM-3835. As to formulation, MacPherson teaches oral administration of WM-3835 to BALB/c female mice and expressly states that the compound was “formulated in 20% PEG400/10% solutol or vehicle.” [Extended Data Fig. 10c; pg. 270, col. 1, para 3]. MacPherson therefore expressly teaches formulating WM-3835 into a composition suitable for in-vivo administration. Although MacPherson does not employ the precise phrase “pharmaceutically acceptable product,” it would have been obvious to one of ordinary skill to formulate the expressly disclosed bioactive WM-3835 compound with pharmaceutically acceptable formulation components for administration, particularly because MacPherson itself prepares such a formulation and administers it orally to mice. The recitation that the resulting product is for treating/preventing senescence or inhibiting CCl4-induced hepatic fibrosis does not require a different manufacturing manipulation from providing WM-3835 and formulating the compound into a pharmaceutically acceptable product.
Claims 19, 27 and 30-32 are rejected under 35 U.S.C. 103 as being unpatentable over MacPherson (MacPherson et al. Nature 577:266–270 (2020), published online December 11, 2019) in view of Yu (Yu et al. Int. J. Biol. Sci. 2020, Vol. 16) and Sabatino (Sabatino et al. Front. Cell Dev. Biol. 7:297 (2019)).
MacPherson teaches HBO1, i.e., KAT7/MYST2, as a therapeutic target and expressly generates WM-3835 as an inhibitor thereof [pg. 266 Abstract; pg. 270, col. 1, para 2-3]. MacPherson further teaches that “WM-3835 is a cell-permeable small molecule”, that treatment with WM-3835 rapidly reduces H3K14 acetylation, and phenocopies genetic depletion of HBO1, thereby demonstrating that WM-3835 possesses biological activity through inhibition of HBO1/KAT7. [p. 270, col. 1, para 3; Fig. 4d-i]. MacPherson teaches oral administration of WM-3835 to BALB/c female mice and expressly states that the compound was “formulated in 20% PEG400/10% solutol or vehicle.” [Extended Data Fig. 10c; pg. 270, col. 1, para 3]. Thus, MacPherson teaches a product comprising the expressly claimed active ingredient, WM-3835, teaches that WM-3835 inhibits or reduces KAT7/HBO1, and teaches providing the expressly claimed WM-3835 species and formulating WM-3835 into an in-vivo-administrable pharmaceutical composition.
MacPherson does not expressly teach that the WM-3835-containing product is useful for treating and/or preventing senescence. MacPherson does not teach administering WM-3835 for delaying, treating, or preventing senescence.
Yu teaches that KLF6 and KAT7 are both upregulated under the studied disease conditions and further teaches that KAT7 binds relevant promoter regions in a KLF6-dependent manner [Abstract]. Yu teaches that “KLF6 was acetylated by KAT7 at lysine residue 100.” [Abstract]. Yu concludes that KAT7-mediated KLF6 acetylation increases KLF6 transcriptional activity [pg. 2354, col. 1]. Yu's in-vivo experiments further establish that KAT7 knockdown reduces KLF6 acetylation: In Thy-1 nephritis model rats pretreated with LV-shKAT7, Yu reports that KAT7 knockdown inhibited KLF6 acetylation and also reduced downstream inflammatory mediators and extracellular-matrix accumulation [pg. 2349, col. 2, para 3-4 – pg. 2350, col. 1, para 1; Fig. 7A–E]. Thus, Yu teaches that KAT7 is an upstream positive regulator of KLF6 activity and that reducing/inhibiting KAT7 reduces KLF6 acetylation/activity.
Sabatino reports that KLF6 silencing bypasses both oxidative and oncogene-induced senescence [Abstract]. Sabatino also reports that KLF6 expression itself was capable of triggering cellular senescence in normal and tumor cells [Abstract]. Sabatino further teaches that KLF6 upregulates the cyclin-dependent kinase inhibitor p21WAF1/Cip1 [pg. 1, Introduction]. Sabatino's experimental results establish that KLF6 silencing interfered with oxidative- and oncogene-induced senescence in NIH3T3 fibroblasts and that KLF6 expression induced senescence in normal and tumor contexts. [p. 2; col. 1 of introduction].
Regarding claim 19, it would have been obvious to one of ordinary skill before the filing date of the claimed invention, seeking to prepare a pharmaceutically acceptable product capable of delaying, treating, or preventing cellular senescence, to formulate the known KAT7 inhibitor WM-3835 taught by MacPherson for that purpose in view of the KAT7/KLF6 relationship taught by Yu and the KLF6/senescence relationship taught by Sabatino. MacPherson expressly demonstrates both a biologically active KAT7 inhibitor and formulation of that inhibitor into a composition suitable for administration. Yu teaches that inhibition of KAT7 decreases KLF6 acetylation/activity. Sabatino teaches that reduction of KLF6 activity interferes with the establishment of cellular senescence. Therefore, a skilled artisan would have reason to prepare and formulate WM-3835 as a pharmaceutical product for inhibiting or delaying senescence because a skilled artisan would have understood that WM-3835 could act upstream of the KLF6-dependent senescence pathway. One of ordinary skill would have a reasonable expectation of success would have existed because: MacPherson established that WM-3835 effectively inhibits KAT7/HBO1 activity; Yu experimentally established that reducing KAT7 reduces KLF6 acetylation; and Sabatino experimentally established that reducing KLF6 permits cells to bypass senescence. Accordingly, preparing and formulating WM-3835 into a pharmaceutically acceptable product for use in treating or preventing senescence would have represented a predictable application of a known KAT7 inhibitor to a known KAT7-regulated senescence pathway.
Regarding claim 27, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention, seeking a product capable of inhibiting or delaying cellular senescence, to employ the WM-3835-containing product taught by MacPherson in view of the mechanistic teachings of Yu and Sabatino. MacPherson provided a known pharmacological inhibitor of KAT7/HBO1. Yu taught that KAT7 positively regulates KLF6 by acetylation and that reducing KAT7 reduces KLF6 acetylation. Sabatino independently established that KLF6 functions as a positive regulator of cellular senescence, because KLF6 silencing permits cells to bypass senescence whereas increased KLF6 expression promotes senescence. Thus the art collectively taught the following pathway: KAT7 activity → KLF6 acetylation/activity → cellular senescence; and MacPherson provided a known small-molecule inhibitor capable of acting at the upstream KAT7 step. One of ordinary skill therefore would have had reason to use WM-3835 as the active ingredient of a product intended to inhibit, delay, treat, or prevent cellular senescence, with a reasonable expectation that pharmacological inhibition of KAT7 would reduce KLF6 activation and thereby interfere with a KLF6-dependent senescence program.
Regarding claim 30, it would have been obvious to one of ordinary skill before the effective filing date of the claimed invention, seeking to inhibit or delay cellular senescence to use the known KAT7 inhibitor WM-3835 taught by MacPherson in view of the mechanistic teachings of Yu and Sabatino. MacPherson provided a known pharmacological tool for inhibiting KAT7/HBO1. Yu taught that KAT7 positively regulates KLF6 through KAT7-mediated KLF6 acetylation and that reduction of KAT7 decreases KLF6 acetylation. Sabatino independently taught that KLF6 is functionally involved in establishment of cellular senescence, because KLF6 silencing permits cells to bypass senescence whereas increased KLF6 expression promotes cellular senescence. The combined teachings therefore provided the following known relationship: KAT7 activity → KLF6 acetylation/activity → cellular senescence; and MacPherson supplied a known compound, WM-3835, for inhibiting the first component of that pathway. Accordingly, one of ordinary skill would have had reason to administer WM-3835 to cells susceptible to senescence in order to reduce KAT7-mediated KLF6 activation and thereby inhibit or delay a KLF6-dependent senescence program. One of ordinary skill would have reasonable expectation of success because Yu experimentally demonstrated that reducing KAT7 diminishes KLF6 acetylation, while Sabatino experimentally demonstrated that reduction of KLF6 permits cells to bypass senescence. Thus, applying the known KAT7 inhibitor of MacPherson to reduce the upstream KAT7 activity would have represented the predictable use of a known inhibitor to interfere with a known KAT7/KLF6/senescence signaling relationship.
Applicant's claim encompasses either the specifically recited CRISPR system or WM-3835. Therefore, it is unnecessary to establish that the prior art teaches the exact SEQ ID NOs. 1–4 because the WM-3835 species is sufficient to render the scope of claim 30 obvious.
Regarding claims 31 and 32, Sabatino expressly performs its senescence experiments using murine NIH3T3 fibroblasts, thereby teaching a mammalian cellular system. [Sabatino, p. 2, Materials and Methods]. MacPherson likewise uses both mouse and human experimental systems and administers WM-3835 to BALB/c mice. Accordingly, performing the obvious method in a mammalian system would have been obvious.
Claim 37 is rejected under 35 U.S.C. 103 as being unpatentable over MacPherson (MacPherson et al. Nature 577:266–270 (2020), published online December 11, 2019) in view of Yu (Yu et al. Int. J. Biol. Sci. 2020, Vol. 16) and Sabatino (Sabatino et al. Front. Cell Dev. Biol. 7:297 (2019)) as applied to claim 30 and further in view of Sydor (Sydor et al., Scientific Reports 7:8119 (2017)).
As explained above, MacPherson teaches WM-3835 inhibition of KAT7/HBO1; Yu teaches KAT7-mediated KLF6 activation; and Sabatino teaches KLF6 involvement in cellular senescence. The combination does not expressly identify hepatocytes as the target senescent cell.
Sydor supplies this cell-type-specific teaching. Sydor teaches that KLF6 is biologically active in hepatocytes and reports that KLF6 was induced in hepatocytes in acute liver injury and in CCl4-treated mice [Abstract]. Specifically, Sydor teaches that KLF6 was induced in hepatocytes in acute liver failure and in mice treated with acetaminophen or carbon tetrachloride [pg. 1]. Sydor further teaches that in mice having hepatocyte-specific KLF6 knockout, cell proliferation following partial hepatectomy was increased relative to controls [Abstract]. Sydor's teaches enhanced hepatocyte proliferation in the absence of KLF6 [pg. 2, Fig. 2B]. Sydor also teaches that KLF6 transactivates genes controlling proliferation, including p21. [pg. 2].
It would therefore have been obvious to one of ordinary skill before the effective filing date of the claimed invention, seeking to apply the KAT7/KLF6 anti-senescence strategy suggested by MacPherson, Yu, and Sabatino to a biologically appropriate cell type, to apply the method to hepatocytes because Sydor expressly establishes that KLF6 is an active growth-regulatory pathway in hepatocytes and that loss of KLF6 increases hepatocyte proliferation. Sydor's finding that KLF6 is induced in CCl4-treated liver further strengthens the reason to investigate the KAT7/KLF6 pathway in hepatocytes experiencing chemically induced liver injury [pg. 4]. Accordingly, one of ordinary skill would have had reason to inhibit the upstream KAT7/KLF6 signaling pathway in hepatocytes using the known KAT7 inhibitor WM-3835, with a reasonable expectation that reducing KAT7-mediated KLF6 activation would interfere with the KLF6-mediated growth-arrest/senescence pathway established by Sabatino.
Response to Arguments
Applicant's arguments filed 07/17/2026 have been fully considered
Applicant argued that the cited Wang reference fails to disclose the presently claimed specific sgRNA configuration. In view of the amendments and upon reconsideration, this argument is persuasive with respect to the prior Wang anticipation rejection. That rejection has therefore been withdrawn.
However, the amended claims expressly recite the specifically defined CRISPR system OR WM-3835. MacPherson independently discloses the expressly claimed WM-3835 species as a KAT7/HBO1 inhibitor before the effective filing date. Therefore, the absence of Applicant's particular sgRNA sequences from Wang does not overcome the present rejections.
To the extent Applicant relies upon the working examples as evidence of unexpected results, the Office acknowledges that the specification provides evidence that KAT7 inhibition delays senescence in particular cellular systems. However, Applicant has not established on this record that the observed results are unexpected relative to the closest prior art combination, which before the filing date taught the claimed WM-3835 inhibitor, the KAT7→KLF6 regulatory relationship, and the role of KLF6 in senescence. Moreover, any evidence of unexpected results must be commensurate in scope with the claims. Claim 30 remains broadly directed to animal cells, tissues, organs, and individuals and to delaying, treating, and/or preventing senescence.
Conclusion
No claims allowed.
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/TIFFANY NICOLE GROOMS/Examiner, Art Unit 1637
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