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 .
Amendments
This action is in response to papers filed 01/07/2026 in which claim 2 was amended, and no claims were cancelled or added. All of the amendments have been thoroughly reviewed and entered.
Applicant has amended claim 2 to overcome the 112(a) rejections; the 112(a) written description rejection is withdrawn but the enablement rejection of claims 2-3 and 29-34 is maintained.
Applicant argues, the amendment and declaration have overcome the 112(a) written description rejection and enablement rejection of claims 2-3 and 29-34, and the specification is enabling for the method as claimed.
Applicant’s arguments are not persuasive. The declaration and specification are not commensurate with the scope of the claims, let alone enabling. Arguments are further addressed at the end of each section presented below.
The nonstatutory double patenting rejection over US Application 17968984, now US Patent 12,565,648 is withdrawn because the patented claims recite miRNA agents that do not inhibit ZNF274. The nonstatutory double patenting rejection over Application 18/047831 is maintained.
Arguments applicable to rejections to amended claims are addressed below. Arguments that are no longer relevant are not addressed.
Objections and Rejections not reiterated here are withdrawn.
Election/Restrictions
Applicant's election without traverse of:
Species: transcription factors was previously withdrawn. Therefore all species of transcription factors recited in claim 2 are now being examined;
Applicant's election without traverse of:
Subspecies I: multiple sclerosis as recited in claim 4; and
Subspecies II: an agent that comprises one or more nucleic acid molecules that comprise a first nucleic acid sequence encoding a Cas protein and a second nucleic acid sequence encoding a guide RNA, as recited in claim 28;
in the reply filed 7/03/2024 was previously acknowledged and stands as these species now are amended into claim 2. All other species recited in claim 2; i.e., agent (i-ii) and all glial-cell related disorders (i-iii), are being treated as unelected species.
Claims 5-7, 21-27, and 33 withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim stands. Election was made without traverse in the reply filed on 7/03/2024.
With the cancellation of claims 4-5, 7, 21-22, and 28 in the response dated 05/16/2025, the withdrawal of cancelled claims is now moot.
Claims 6, 23-27, and 33 remain 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.
Accordingly, claims 2-3, 29-32, and 34-35 are under examination.
Maintained 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.
Enablement Rejection
Claims 2-3, 29-32, and 34-35 remain rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
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 as the specification does not provide enablement for a method of treating a human subject having a glial cell-related disorder said method comprising administering, to the subject, an effective amount of an agent that suppresses one or more transcription factors selected from the group consisting of (i) zinc finger protein 274 (ZNF274),(ii) Myc-associated factor X (MAX), and (iii) zinc finger protein Aiolos (JKZF3), wherein the glial cell-related disorder is: MS (elected species), and wherein the glial cell-related disorder is myelin deficiency.
i.e., the method of remyelinating cells or increasing the number of myelinating cells or effectuating any kind of change that can reasonably be considered an improvement in myelination for the treatment of multiple sclerosis in vivo by administering, to the human subject, an effective amount of an agent that suppresses one or more transcription factors selected from the group consisting of (i) zinc finger protein 274 (ZNF274), (ii) Myc-associated factor X (MAX), and (iii) zinc finger protein Aiolos (IKZF3), as required by the claims, is not enabled.
As stated in MPEP §2164.01(a), “there are many factors to consider when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any experimentation is ‘undue’.” These factors include, but are not limited to:
1. The breadth of the claims;
2. The nature of the invention;
3. The state of the prior art;
4. The level of skill in the art;
5. The level of predictability in the art;
6. The amount of direction provided by the inventor;
7. The presence or absence of working examples;
8. The quantity of experimentation necessarily needed to make or use the invention based on the disclosure.
See In re Wands USPQ 2d 1400 (CAFC 1988).
The Breadth of the Claims and The Nature of the Invention
Claims 2-3, 29-32, and 34-35 are directed to a method of treating a subject having a glial cell-related disorder wherein the disorder is a glial-cell related disorder (elected: multiple sclerosis) by administering to the subject an agent, wherein the agent is selected from the group consisting of (i) zinc finger protein 274 (ZNF274), (ii) Myc-associated factor X (MAX), and (iii) zinc finger protein Aiolos (IKZF3), wherein said administering suppresses one or more transcription factors selected from the group consisting of (i) zinc finger protein 274 (ZNF274), (ii) Myc-associated factor X (MAX), and (iii) zinc finger protein Aiolos (IKZF3) (claim 2).
The specification states many diseases fall under the umbrella of glial cell-related disorders and myelin deficiency. Elected limitation is multiple sclerosis which is focused on here. The treatment end goals are broad and encompass:
[0066]: (1) preventing, delaying, or reducing the incidence and/or likelihood of the appearance of at least one clinical or sub-clinical symptom of the myelin deficiency developing in a subject that may be afflicted with or predisposed to the myelin deficiency, but does not yet experience or display clinical or subclinical symptoms of the myelin deficiency; or (2) inhibiting the myelin deficiency, i.e., arresting, reducing or delaying the development of the myelin deficiency or a relapse thereof or at least one clinical or sub-clinical symptom thereof; or (3) relieving the myelin deficiency, i.e., causing regression of the myelin deficiency or at least one of its clinical or sub-clinical symptoms. The benefit to a subject to be treated is either statistically significant or at least perceptible to the patient or to the physician.
as shown above from the applicants’ specification. Thus, it is unduly broad.
The State of the Prior Art
The state of the prior art with regard to treating a subject having a glial cell-related disorder or myelin deficiency or multiple sclerosis by administering to the subject an agent that suppresses one or more transcription factors from the list recited in the claims is limited.
Tiane et al., teach epigenomic and transcriptomic profiles of oligodendrocytes (OL) and oligodendrocyte precursor cells (OPC) during oligodendrocyte differentiation/maturation and renewal (Tiane et al., From OPC to Oligodendrocyte: An Epigenetic Journey. Cells. 2019 Oct 11;8(10):1236; IDS). They read that OPC differentiation is highly dependent on epigenetic regulation, which can be easily influenced by external stimuli from the surrounding microenvironment, such as sustained inflammation and inhibitory factors of the extracellular matrix. See Figure 1 for an overview of the transcriptional and epigenetic regulation of OPC proliferation and OL during development.
Hubler (Hubler et al. Nature. 2018 Aug; 560(7718): 372–376) notes the accumulation of 8,9-unsaturated sterols drives oligodendrocyte formation and remyelination. Further, sterols, regulated by small molecules, function as modulators of transcription factor function. Thus, the presence of small molecules, intentionally introduced or not, will affect myelination status.
Fernandez English abstract (Fernández et al. Medicine - Programa de Formación MédicaContinuada Acreditado Volume 11, Issue 77, April 2015 , Pages 4601-4609, English Abstract only), discloses how myelination is a treatment of CNS demyelination diseases such as multiple sclerosis.
Therefore, one of skill in the art would expect evidence of a myelination marker when considering a treatment for MS.
The level of ordinary skill in the art
An ordinary artisan in the area of drug development would have experience in screening chemical compounds for particular activities. Screening of new drug candidates, while complex, is routine in the art. The process of finding new drugs that have in vitro activity against a particular biological target, (i.e., receptor, enzyme, etc.) is well known. Additionally, while high throughput screening assays can often be employed, developing a therapeutic method, as claimed, is generally not well-known or routine, given the complexity of certain biological systems such as the brain.
Determining how a particular chemical will impact the CNS, where glial-cells reside, is not routine. There is no chemical targeting system at this time that can directly stimulate or block only a highly specific cluster of glial cells while avoiding effects on adjacent neurons where the same signal may have a different and unwanted effect. Further, the functioning of many neuronal systems and the pathology of many neurologic diseases involve complex systems involving a complex interaction between neurons and supporting glial cells (Kurosinski P, Götz J. Arch Neurol. 2002; 59(10):1524–1528).
Thus, the level of ordinary skill in the art of treating glial-cell related diseases is high, as an ordinary artisan in this art needs specialized knowledge of the complex nature of the CNS.
The Level of Predictability in the Art
Regarding claims 2-3, 29-32, and 34-35, the instant claimed invention is highly unpredictable. If one skilled in the art cannot readily anticipate the effect of a change within the subject matter to which that claimed invention pertains (i.e., suppress transcription factors in order to effectuate myelination changes), then there is a lack of predictability in the art. Moreover, it is noted that the pharmaceutical art is unpredictable, requiring each embodiment to be individually assessed for physiological activity. The court has indicated that the more unpredictable an area is, the more specific enablement is necessary in order to satisfy the statute. (See In re Fisher, 427 F.2d 833, 166 USPQ 18 (CCPA 1970)). This is because the claimed invention is not enabled based on the in vitro working examples.
In the instant case, the specification does not demonstrate:
For an agent that is specifically directed to any one of the transcription factors, when administered either in vitro or in vivo:
what would be the effective dose to achieve such treatment in vivo.
what evidence of remyelination, either in vitro or in vivo, is seen.
In addition, the expression of transcription factors at different time points in the adult glial progenitor cells is highly unpredictable.
The specification appears to rely on data from prior art and their biomarker study to predict that treatment will be achieved. For example, Example 7 in the specification shows adult miRNA signaling may repress the proliferative progenitor state and augur senescence.
Example 8 discloses prediction of upstream regulation of differentially expressed miRNAs in fetal and adult GPCs by querying the TransmiR transcription factor miRNA regulation database. Example 8, [0251] states “Through integration of transcriptional and miRNA profiling, pathway enrichment analyses, and target predictions, we propose a model of human GPC aging whereby fetal hGPCs maintain progenitor gene expression, activated proliferative programs, and prevent senescence, while repressing oligodendrocytic and senescent gene programs both transcriptionally, and post-transcriptionally via microRNA”. However, such an assumption cannot be made since the specification fails to demonstrate any data or evidence that administering any agent capable of suppressing transcription factors in vitro will also do so in vivo to levels sufficient to effectuate treatment.
Example 9 [0254] discusses re-initiation of mitotic expansion of glial progenitor cells, but is in the context of BCL11A transduction activated glial progenitor cells to re-initiate mitotic expansion and migratory colonization in host brains, and mentions myelinating oligodendrocytes. However, the BCL11A transcription factor does not relate to the transcription factors in the instant claims, which pertain to zinc finger protein 274, (IKZF3), MAX, and zinc finger protein Aiolos (IKZF3).
Given that the method requires administering to a subject an agent that suppresses one or more transcription factors without any specific reaction conditions that may impact the agent or compensatory increase in other transcription factors, it would be unpredictable that treatment would be achieved. Without experimentation demonstrating the efficacy of suppression of one or more transcription factors, the level of unpredictability remains high. The state of the art requires vast amounts of data, including analysis of the mechanisms of conditions associated with achieving treatment end-points, producing animal models based on the mechanisms of the agents administered and TFs suppressed, in vitro and in vivo experiments, and phase 0, I, II, III, and IV clinical trials.
Therefore, it is unpredictable that the claimed method would achieve its end-goal in vivo.
The Amount of Direction Provided by the Inventor and
The Presence or Absence of Working Examples
The specification does not enable any person skilled in the art to which it pertains to make and/or use the invention commensurate in scope with the claims.
The specification does not provide a working example of the claimed method. Other than contemplating the claimed methods, providing in vitro working examples or citing prior art involving miRNA and transcription factors, there is a lack of adequate guidance from the specification or prior art with regard to how to treat by suppressing one or more transcription factors from the list recited.
In addition, the specification does not provide enablement for delivering an agent to a subject to observe the desired biological activity as there is no working example showing that an agent was administered in vitro or in vivo to any subject (human, mouse, worms…). There are no working examples showing myelin changes in vitro or in vivo or what the results of the suppression of TFs were on in a subject having a myelin deficiency, by administering the agents.
The specification states [paragraphs 0051 and 0052] that, “A transcription factor can have a positive effect on gene transcription and, thus, may be referred to as a "transcription activator," "activator" or a "transcriptional activation factor." An exemplary activator (or transcriptional activation factor) is signal transducer and activator of transcription 3 (STAT3). As illustrated in Figure 4F of the present disclosure, in the context of adult glial progenitor cells, STAT3 is predicted to activate a set of senescence- associated genes (e.g., BIN1, DMTF1, CD47, CTNNA1, RUNX2, RUNX1, MAP3K7, and OGT), glial cell-associated genes (e.g., PLP1, CNP, PMP22, SEMA4D, CLDN11, GPR37, MYRF, MAG, BCAS1, ST18, ERBB4, CERS2, LPAR1, and GJB1), and downstream transcription factors (e.g., MAX, E2F6, and IKZF3)”, and “A transcription factor can also negatively affect gene expression and, thus, may be referred to as "transcription repressor," "repressor" or a "transcription repression factor." Exemplary repressors (or transcription repression factors) involved in glial progenitor cells senescence include, without limitation, ZNF274, MAX, E2F6, and IKZF3. As illustrated in Figure 4G of the present disclosure, in the context of adult glial progenitor cells, ZNF274, MAX, E2F6, and IKZF3 are predicted to repress sets of proliferation-associated gene targets (e.g., YAP1, LMNB1, PATZ1, TEAD1, FN1, TP53, CDK1, CCND2, CDKN2D, CENPH, MKI67, CDK4, CENPF, CDK5, CDKN3, and CHEK1), glial cell- associated genes (e.g., CHRDL1,ST8SIA1, PTPRZ CA10, PDGFRA, BCAN, NXPH1, CSPG4, and, PCDH15), and downstream transcription factors (e.g., BLC11A, EZH2, HDAC2, NF1B, MYC, HMGA2, and TEAD). However, predicting that these transcription factors have these effects in adult glial progenitor cells does not provide enablement that administering an agent to a subject in vivo that will suppress these will have the claimed effect.
The specification in [0242] shows that forced, premature expression of the adult-enriched GPC repressors, E2F6, IKZF3, MAX, and ZNF274, are individually sufficient to induce multiple features of the aged GPC transcriptome in young, iPSC-derived GPCs MKI67 and CDK1, genes whose upregulation are associated with active cell division, were significantly repressed at two or more timepoints in each over-expression paradigm (Figure 5, Panel D). This was consistent with their diminished expression in adult GPCs (Figure 3, Panel F), and suggested their direct repression by E2F6, MAX, and ZNF274 (MKI67), or by all four (CDK1). CDKN1A/p21 was upregulated in response to each of the tested repressors at all time points, while CDKN2A/p16 was similarly upregulated in all timepoints in ZNF274- transduced hGPCs, as well as in the E2F6-over-expressing GPCs at day 7 (Figure 5, Panel D).
The specification in Examples 5 - 9 only express transcription factors (Example 5) and determine miRNA expression pattern (Example 6) in iPSC, and predict miRNA signature in adult glial progenitor cells (Example 7 and 8), and overexpress a transcription factor in the brain of a chimeric mouse model (Example 9). The scope of the claim does not encompass overexpressing an agent rather, suppressing it. As such, according to the specification, the act of overexpressing a transcription factor by an agent is unnecessary. Thus, the claims encompass a generic process without any indication what condition parameters are needed to achieve/assess a state wherein treatment is achieved.
In the absence of information other than correlation of transcription factors with phenotypic observations in vitro, but nothing with respect to treatment in the specification as well as the state of the art, a person of ordinary skill in the art would reasonably require an undue quantity of experimentation.
The as-filed specification has no working examples for either in vitro or in vivo administration of the agent that suppresses one or more transcription factors in a subject having a myelin deficiency. Therefore, the working examples fail to demonstrate any data or evidence that administering an agent that suppresses one or more transcription factors in a subject having a glial cell-related disorder or myelin deficiency in vivo will be an effective treatment for that disorder or deficiency.
In the absence of such information in the specification as well as the state of the art, a person of ordinary skill in the art would reasonably require an undue quantity of experimentation.
Conclusion of 35 U.S.C. 112(a) (Enablement) Analysis
MPEP §2164.01(a), 4th paragraph, provides that, “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 1157, 1562; 27 USPQ2d 1510, 1513 (Fed. Cir. 1993).
After applying several Wands factors and analysis to claims 2-4 and 28-32, in view of the applicant’s entire disclosure, it is concluded that the practice of the invention as claimed would not be enabled for a method of treating a subject by administering to the subject an agent that would suppress at least one transcription factor as recited in claim 2 and as discussed above.
Dependent claims are rejected for not rectifying the lack of enablement in the claims they depend from.
Therefore, claims 2-3, 29-32, and 34-35 are rejected under 35 U.S.C. §112(a) for failing to disclose sufficient information to enable a person of skill in the art to use the invention commensurate in scope with these claims.
Response to Applicant’s Remarks:
On Pg. 6-7 of the Remarks, Applicant states that:
Claim 2 has been amended to recite gRNA to ZNF274.
=> This is persuasive, as it pertains to the previous rejection for lack of enablement, but not the current one for the reasons enumerated above.
On Pg. 7 onwards, Applicant state:
The declaration and the specification (Fig. 1) discloses, " CRISPRi-mediated epigenetic knockdown of E2F6 and ZNF274, both alone and in combination, sharply suppressed genes associated with senescence, such as pl6/CDKN2A (Panel A), p21/CDKNJA (Panel B), and IL la (Panel C)”.
The declaration further states: one of skill in the art would recognize that suppressing ZNF274, MAX, and/or IKZF3 could be used to treat a glial cell-related disorder. Applicants stress that contrary to Office’s insistence on disclosure of working examples, compliance with the enablement requirement does not depend upon whether an example is disclosed or not.
Applicants further state the issue of enablement should not be viewed in a vacuum, but in the context of the knowledge accumulated in the art and available to skilled artisans. See United States v. Telectronics, Inc., 857 F.2d 778, 785, 8 USPQ2d 1217, 1223 (Fed. Cir. 1988). The Examiner has to consider not only the instant disclosure, but also the knowledge accumulated in the art in the relevant area.
In view of the above, Applicants state that it would not require undue experimentation for one of skill in the art to practice the method of amended claim 2.
This is not found persuasive because:
The rejection is directed to the lack of enablement of a method of treating a human subject having a glial cell-related disorder, wherein the glial cell-related disorder is myelin deficiency, as recited; i.e., the inventive contribution is not described/enabled. The argument presented are not directed to this recitation. Therefore, an enablement rejection of Claims 2-3, 29-32, and 34-35 is maintained.
Regarding b. - d. above, Wands factors against the instant application are:
(A) The breadth of the claims – broader than what is disclosed;
(C) The state of the prior art – limited;
(D) The level of ordinary skill – invention is beyond the skill-level of the ordinary skilled artisan;
(E) The level of predictability in the art – unpredictable because of naturally occurring cross-talk between transcription factors;
(F) The amount of direction provided by the inventor – disclosure provided is not pertinent to invention. Disclosure is about overexpressing factors; recited claims are directed to suppressing factors; claims require treatment, specifically a benefit in terms of myelination, no myelination changes are shown or reliably predicted to occur;
(G) The existence of working examples – non-existent; and
(H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure – tremendous.
Thus, enablement requirement requires not one or any but a consideration of all the above Wands factors put together.
Regarding b-c. above, the declaration is persuasive in showing that direct repression of E2F6 and ZNF274 indeed results in CDKN1A/p21 upregulation at the time points tested; CDKN2A/p16 was similarly upregulated at the time points tested.
However, the declaration does not address how these results corelate to myelination. A mere statement that such a correlation exists is not deemed sufficient to overcome the scope of enablement rejection. Applicants have also not provided any art that shows that such a correlation exists.
Regarding d. above, as discussed for b-c above, Applicants must provide any knowledge in the art they see as persuasive.
Further, the rejection is also directed to: an effective amount of an agent that can suppress each of the transcription factors, as recited. The arguments are not directed to this recitation.
Therefore, the enablement rejection presented above is necessitated by amendment and directed to lack of enablement of the method of treating a human subject having a glial cell-related disorder, wherein the glial cell-related disorder is MS and myelin deficiency as claimed. Claims 2-3, 29-32, and 34-35 are rejected for not complying with the enablement requirement.
Double Patenting
Claims 2-3, 29-32, and 34-35 remain provisionally rejected on the grounds of nonstatutory double patenting as being unpatentable over claims 1-10 and 14-20 of copending Application No. 18/047,831 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the instant application is anticipated by the cited application in view of the suppressing agent claimed in the conflicting patent or application anticipates the claimed agent in the application being examined. Claims 11-13 are not included in the rejection because they are directed to different species of agents than instant.
Instant claim 1
18/047,831 claim 1
A method of …, said method comprising: administering, to the population of adult glial progenitor cells, an effective amount of an agent that suppresses one or more transcription factors selected from the group consisting of (i) zinc finger protein 274 (ZNF274), (ii) Myc-associated factor X (MAX), (iii) E2F transcription factor 6 (E2F6), (iv) zinc finger protein Aiolos (IKZF3), and (v) signal transducer and activator of transcription 3 (STAT3).
A method of rejuvenating, or enhancing the development potential of, a glial progenitor cell or a progeny thereof, said method comprising suppressing in the glial progenitor cell or the progeny a transcription repressor selected from the group consisting of E2F6, ZNF274, MAX, and IKZF3.
Any additional limitations of the reference claims are encompassed by the open claim language “comprises” found in the instant claims.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
No claim is allowed.
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.
Correspondence
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SHABANA MEYERING, Ph.D. whose telephone number is (703)756-4603. The examiner can normally be reached M - F: 9am to 5pm EST.
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/SHABANA S MEYERING/Examiner, Art Unit 1635
/SHABANA S MEYERING/ Examiner, Art Unit 1635
/CATHERINE KONOPKA/ Primary Examiner, Art Unit 1635