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 .
Status of claims
Pending claims 1-7 and 9-14 have been examined on the merits.
Objection to Claims, Allowable Subject Matter
Claim 4-5 and 7 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.
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.
Claim 1-2 and 9-14 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.
Claim 1 and 2 recite a compound of chemical formula I, wherein the claim broadly defines R1 as encompassing numerous structurally diverse substituents including but not limited to H; C1-C6 alkyl; C2-C6 alkenyl; C2-C6 alkynyl; C3-C8 cycloalkyl; C3-C6cycloalkenyl; C1-C6 alkoxy; heterocycloalkyl or heterocycloalkenyl, aryl, CN; benzodioxolyl, halogen, with multiple optional substituents with Ra, Rb. However, the disclosed compounds are primarily directed toward a narrow species of substituted aryl and heteroaryl groups, such as indole, thiophene, furan, benzofuran, benzodioxol, pyridine and pyridazine derivatives bearing selected substituents. The specification does not provide representative species comprising the full scope of the claimed R1 genus. Similarly, although R2 is broadly defined to encompass H; alkyl; cycloalkyl; aryl, heteroaryl, heterocycloalkyl, heterocycloalkenyl groups with multiple optional substituents (Rc and Rd), the disclosed compounds are predominantly limited to substituted cyclohexyl and piperidinyl derivatives bearing a relatively small number of recuring substituents, such as secondary amine, amine, hydroxyalkyl, alkoxyalkyl, haloalkyl, aziridine, dioxolane, and related groups. The specification, however, provides working examples which do not reasonably represent the extensive compounds combinations and permutations encompassed by the broad R1 and R2 definitions. Furthermore, the specification only provides working examples of R3 as methyl, and V as a single bond; but does not disclose either Rp or Rq as cycloalkyl or (C=O)-alkyl. Therefore, a person of ordinary skill in the art (POSITA) would infer that the specification does no adequately demonstrate possession of the full claimed genus encompassing the wide and diverse substituents options as claimed.
Claim 9-15 recite a method for preventing or treating. However, the specification (page 39) defines the term “treatment” as follows: “the term “treatment” may mean all the acts, by which a symptom of an individual likely to develop or suffering from a disease gets better or takes a favorable turn by administering a compound according to any one of above (1) to (5) ...” From this definition, the specification does not provide a definitive definition of the phrase “treatment.” Instead, the specification describes that treatment “may mean” symptom improvement, indicating that this is merely one possible meaning rather than the exclusive meaning of the claim language. Herein, the phrase “may mean” suggests that “treatment” could encompass additional therapeutic outcomes or meanings that are not identified or described in the specification. Therefore, the specification is ambiguous and leaves unresolved what other therapeutic outcomes, if any, are encompassed with the claimed “treatment.” For example, the specification fails to identify whether treatment includes prolonging survival, reducing mortality, preventing recurrence, or other clinically recognized therapeutic outcomes. Furthermore, the definition describes that treatment applies to an individual “likely to develop or suffering from a disease.” An individual “likely to develop” a disease describes a patient who has not yet developed the disease and therefore corresponds to prophylactic treatment, whereas an individual “suffering from” a disease corresponds to therapeutic treatment of an existing disease. Therefore, the specification clearly conflates prevention and treatment within the phrase “treatment.”.
Claims 11 and 14 recite wherein the hematologic malignancy is one or more types selected from lymphoma, non-Hodgkin lymphoma, diffuse large B-cell lymphoma, follicular lymphoma, leukemia, and multiple myeloma. The specification provides experimental support only using the Pfeiffer cell line (B lymphocyte) which is widely used as human B-lymphocyte model for diffuse large cell lymphoma (DLCL), which is a subtype of non-Hodgkin's lymphoma (NHL), as evidence by Pfeiffer (Pfeiffer, page 1). As such, the Pfeiffer cell line is representative only of that disease subtype and is not a representative experimental model for the broader genus of hematologic malignancy as claimed. The specification does not provide experimental evidence, representative disease models demonstrating that the claimed compounds are effective for treating broad genus of lymphoma, follicular lymphoma, leukemia, and multiple myeloma; nor does the specification describe that the Pfeiffer model is predictive of efficacy across these distinct malignancies. As evidence by Sharma (page 244), who demonstrates that treatment of cancer is inherently unpredictable, therapeutic response is influenced by both genomic heterogeneity between tumors and cellular heterogeneity within individual tumors. Sharma (page 244) also highlights that tumor subpopulations, including stem-cells, can exhibit distinct sensitivities to anticancer agents, causing treatment responses to vary even within the same cancer type. Therefore, efficacy demonstrated in a limited number of cancer cell models cannot reasonably be extrapolated to the full scope of the claimed cancers, as differences in tumor biology and cellular composition can substantially alter drug responses. Therefore, the specification’s failures to disclose proper model of treating broad genus of lymphoma, follicular lymphoma, leukemia, and multiple myeloma further supports the conclusion that the specification lacks adequate written description of the claimed subject matter. Pfeiffer (https://www.atcc.org/products/crl-2632” retrieved 07/30/2026), Sharma, S., Haber, D. & Settleman, J. Nat Rev Cancer 10, 241–253 (2010).
Enablement
Claims 9-14 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 enablement requirement. The claims contain 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 use the invention.
The specification does not reasonably provide enablement for treating a condition, disease, or disorder that is selected from cachexia; anorexia or anorexia nervosa; nausea; emesis; weight loss; failure to thrive; sarcopenia; muscle wasting; muscle weakness; frailty; osteoporosis; bone disorders; pain; neuropathic pain; anxiety; depression; hypertension; malnutrition; obesity; sexual dysfunction; and inflammatory disease.
The specification does not enable any person skilled in the art (POSITA) to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
The how to use requirement of the enablement statute, when applied to method claim, refers to operability and how to make the claimed method work "The factors to be considered (in making an enablement rejection) have been summarized as the quantity of experimentation necessary, the amount of direction or guidance presented, the presence or absence of working examples, the nature of the invention, the state of the prior art, the relative skill of those in that art, the predictability or unpredictability of the art and the breadth of the claims", In re Rainer, 146 USPQ 218 (1965); In re Colianni, 195 USPQ 150, Ex parte Formal, 230USPQ 546. The specification only demonstrates target inhibition and in vitro antiproliferative activity, while the claims require achieving therapeutic and prophylactic outcomes in living subjects without providing representative evidence or guidance that those outcomes can be achieved.
The instant claims encompass method for preventing or treating EZH1 or EZH2
activity-associated diseases, including lymphoma, non-Hodgkin lymphoma, diffuse large B-cell lymphoma, follicular lymphoma, leukemia, and multiple myeloma, as well as any other disease associated with EZH1 or EZH2 activity. Thus, the claims are not limited to a particular disease subtype, patient population, dosage regimen, route of administration, or therapeutic endpoint. Furthermore, the specification provides only biochemical EZH1/EZH2 inhibition assays and in vitro antiproliferative activity measured in cultured cells using CCK-8 assays. However, the specification does not demonstrate that administration of the claimed compounds prevents disease onset or treats established disease in any representative in vivo models; or even testing the compounds in an assay known to be correlated to clinical efficacy of such treatment. Consequently, practicing the full scope of the claimed methods would require undue experimentation. The specification fails to provide sufficient guidance or representative data to enable a POSITA to reasonably predict which claimed compounds would be effective for each of the large number and mechanistically distinct diseases recited in the instant claims without engaging in extensive trial-and-error experimentation.
b) The direction concerning treating these diseases found in the specification merely states Applicants' intention to do so. However, the specification provides little guidance demonstrating that administration of the representative compounds produces the claimed therapeutic or prophylactic outcomes. For example, the specification provides only biochemical EZH1/EZH2 inhibition assays and in vitro antiproliferative activity measured in cultured cells using CCK-8 assays. The specification does not demonstrate that inhibition of EZH1 or EZH2, or reduce proliferation of isolated cells translates into prevention of disease prognosis or treatment of the established disease in a subject in need thereof. The specification does not provide representative in vivo therapy data demonstrating tumor regression, reduced leukemic burden, prolonged survival, delayed disease progression, or other clinically relevant measured of treatment following administration of the claimed compounds. The claimed invention resides in the unpredictable field of oncology therapeutics, where successful treatment depends upon substantially more than biochemical EZH1/EZH2 inhibition assays and in vitro antiproliferative activity. As evidenced by Biointron (page 2-3) which discloses that efficacy observed in vitro does not guarantee efficacy or safety in vivo; therefore, this means that the specification only establishes compound activity rather than therapeutic treatment. Biointron (page 3-4) further added that while in vitro results are valuable, they do not always translate directly to in vivo outcomes. Therefore in vitro inhibition alone does not reasonably establish that the claimed therapeutic method can be practiced without undue experimentation. This directly undermines reliance solely upon in vitro data. In this light, a POSITA would reasonably conclude that specification demonstrates only laboratory activity, not therapeutic effectiveness. (See (https://www.biointron.com/blog/in-vivo-vs-in-vitro-understanding-the-differences.html; retrieved 07/21/2026; “Biointron”)).
c) There is no working example of treatment of any rejected disease in humans or non-human animals.
d) The nature of the invention is clinical treatment or prevention of EZH1 or EZH2 activity
associated diseases, which involves physiological activity.
e) The pharmaceutical and oncology arts are highly unpredictable with respect to
therapeutic efficacy. Although inhibition of EZH1 or EZH2 may demonstrate target engagement, enzyme inhibition or reduced proliferation in cultured cells does not reliably predict prevention or treatment of disease in vivo. This unpredictability is illustrated by the development of clinically advanced EZH2 inhibitors. For example, GSK126, a selective EZH2 inhibitor developed by GlaxoSmithKline, demonstrated potent biochemical and cellular activity but exhibited only modest antitumor efficacy due pharmacokinetic limitations, and its clinical development was terminated (see Bhat, page 5-10). Likewise, Swanton (page 1595) emphasizes that therapeutic responses depend on complex interactions involving the tumor microenvironment, immune system, metabolism, and host physiology that cannot be replicated in isolated cell culture systems. Therefore, a POSITA would not reasonably predict that the disclosed in vitro EZH1/EZH2 inhibition and antiproliferative assays alone establish that the representative compounds, much less the full scope of the claimed compounds, are effective for preventing or treating the claimed EZH1 or EZH2-associated diseases without undue experimentation. (See Swanton, Charles, et al. “Embracing Cancer Complexity: Hallmarks of Systemic Disease.” Cell, vol. 187, no. 7, Mar. 2024, pp. 1589–616; Bhat KP, Ümit Kaniskan H, Jin J, Gozani O. Epigenetics and beyond: targeting writers of protein lysine methylation to treat disease. Nat. Rev. Drug Discov. 2021 Apr; 20(4):265-286).
f) The artisan using Applicant's invention would be a physician with a MD degree and
several years of experience.
g) It is well established that "the scope of enablement varies inversely with the degree of
unpredictability of the factors involved", and physiological activity is generally considered to be an unpredictable factor. See In re Fisher, 427 F.2d 833,839, 166 USPQ 18, 24 (CCPA 1970). Consistent with this principle, numerous EZH2 compounds, as an example, demonstrating promising preclinical activity have failed to consistently translate into clinical efficacy, illustrating the unpredictability of developing therapeutically effective against EZH1/EZH2-associated disease. As evidence Bhat (page 5-10) the EZH2 inhibitor GSK126 exhibited potent enzymatic inhibition and promising preclinical activity in lymphoma cell lines and animal models, yet its clinical development was ultimately discontinued because it failed to demonstrate sufficient clinical benefit and was associated with pharmacokinetic limitations and dose-limiting toxicity. These findings demonstrate that successful target inhibition and encouraging preclinical data do not reliably predict therapeutic efficacy in patients. (see Bhat KP, Ümit Kaniskan H, Jin J, Gozani O. Epigenetics and beyond: targeting writers of protein lysine methylation to treat disease. Nat. Rev. Drug Discov. 2021 Apr; 20(4):265-286).)
h) The breadth of the claims involves all of the thousands of compounds as well as the
numerous EZH1 or EZH2-associated diseases. However, and as mentioned above, the state of the art further demonstrates the unpredictability of EZH1 or EZH2-targeted therapies. As evidenced by Bhat (page 5-10), demonstrating EZH2 inhibitors have shown mixed clinical outcomes. For example, although the FDA has approved Tazemetostat for the treatment of epithelioid sarcoma and follicular lymphoma, however, other inhibitors, such as GSK126, for refractory non-Hodgkin lymphoma and multiple myeloma, fails to demonstrate a meaningful therapeutic effects or adequate clinical efficacy, leading to trial termination. These variables outcomes indicate that the therapeutic effects of EZH2 inhibition are not universally predictable across cancer types. Moreover, there is currently no FDA-approved therapy indicated for preventing EZH1 or EZH2-assocaited diseases, despite the specification defining “prevention” as inhibiting or delaying disease occurrence. The specification, however, provides only biochemical EZH1/EZH2 inhibition assays and in vitro antiproliferative data, without any representative prevention models or in vivo therapeutic efficacy studies. There is no reasonable basis to conclude that inhibition of EZH1 or EZH2 activity predict therapeutic efficacy for all EZH1 or EZH2-assocaite diseases. Consequently, a POSITA would be required to engage in undue experimentation to determine appropriate compounds, dosing regimens, treatment protocols, and therapeutic endpoints across the full scope of the claimed methods.
MPEP 2164.0l(a) states, "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)." That conclusion is clearly justified here and undue experimentation will be required to practice Applicants' invention.
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 1-3 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.
Claims 1-3 recite R1, at least one H of C1-C6 alkyl; C3-C8 cycloalkyl; heterocycloalkyl, heterocycloalkenyl, aryl, heteroaryl, CN, benzodioxolyl, and halogen, may be substituted or unsubstituted with Ra, which does not clearly identify the scope of the permitted substitution(s). It is ambiguous whether “at least one H” applies to at least one hydrogen on one selected group, on each listed group, or on multiple listed groups, including Ra. For example, several of the recited R1 possibilities, such as, halogen and cyano, are either incapable of further substitution or do not contain substitutable hydrogen atoms, yet the claim does not clearly distinguish these substituents from those intended to be optionally substituted. Thus, it is unclear which R1 embodiments are eligible for “at least one H.”
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 text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
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.
Claims 1-3, 6, and 9-11 are rejected under 35 U.S.C. 103 as being unpatentable over Kanno et al., US PG-PUB 2018/0282313 A1 (“Kanno”) in view of Stuckey et al. ( J. of Biol. Chem., vol. 296, Jan. 2021, p. 100349) (“Stuckey”).
Regarding claims 1-2, 6, and 9-11, Kanno (abstract) teaches 1,3-benzodioxole derivatives represented by the general formula (I) or a pharmacologically acceptable salt thereof. Kanno (abstract; page 2, [0041] and page 4) teaches compounds of formula I have anticancer effect on cancers dependent on EZH1 alone, cancers dependent on EZH2 alone, and cancers dependent on both EZH1 and EZH2, including but not limited to human diffuse large B-cell lymphoma which is a is a type of hematologic malignancy. Furthermore, Kanno (page 70, emphasis added to the R5) teaches compound 55: N-[(4,6-Dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-2- ethyl-7-[6-(4-ethylpiperazin-1-yl)-3-pyridyl]-4-methyl-2-(tetrahydropyran-4-yl)-1,3-benzodioxole-5-carboxamide, wherein R1 is pyridine substituted with N-ethylpiperazine; R3 is ethyl; V is bond;
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R2 is tetrahydropyran; R4 is methyl; R5 is a methyl; and R6 methyl.
Kanno, however, does not explicitly teach a sulfur linker to the R5 substituent to form a 4-thiomethyl containing compound.
Nonetheless, Stuckey (page 1-2) discloses second-generation EZH2 inhibitors, comparable to Kanno’s teachings, with activities against non-Hodgkin’s lymphoma, a common type of hematologic malignancy. Thus, this indicates that the combined teachings of Kanno and Stuckey discloses EZH2 inhibitors are effective treatment option against hematologic malignancy such as, non-Hodgkin’s lymphoma and human diffuse large B- cell lymphoma, as an example. Furthermore, Stuckey (page 3, emphasis added to the R5) compares compounds (cmpd 1, cmpd 3, cmpd 13 and DS-3201b) that differ primarily in the presence or absence of the sulfur linker. Stuckey (page 3 and 6) demonstrates that cmpd 3 or cmpd 13, which contains the sulfur linker, exhibit longer target residence time than cmpd 1 or DS-3201b, which lacks the sulfur linker. In fact, Stuckey (page 3 and 6) demonstrates cmpd 13 has a significantly higher residence time, about 3 months, compared to DS-3201b, indicating the essential role of the 4-thiomethyl group in enhancing the compound’s inhibitory activity, and thereby promoting stronger engagement with target and potentially reducing off-target. Therefore, a POSITA would have recognized that incorporation of a sulfur linker is beneficial for structural modification
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improving inhibitor-target interactions. Furthermore, it would have been obvious with a reasonable expectation of success to a POSITA before the effective filing date of the claimed invention to modify compound 55 by incorporating the sulfur linker to attach to the R5 substituent to form a 4-thiomethyl, with a reasonable expectation of improving binding residence time and overall inhibitor performance as an effective treatment option against hematologic malignancy including non-Hodgkin’s lymphoma and human diffuse large B- cell lymphoma, as an example.
Regarding claim 3, and as applied to claims 1-2 above, Kanno discloses compound 55 comparable to the claimed compound, except that R2 substituent is tetrahydropyran rather than the claimed cyclohexyl or piperidine; and R3 substituent as ethyl and methyl. However, Kannon (page 2) teaches a general formula I and explicitly discloses that R2 may be selected from cycloalkyl or heterocycloalkyl groups containing either nitrogen, oxygen, and a sulfur atom. Thus, Kanno identifies oxygen- and nitrogen-containing heterocyclic rings, as well as cycloalkyl groups, as known alternative substituents for the same position. Additionally, Kannon (page 3) discloses R3 as a C1- C6 alkyl group. Kannon (page 31-52) also discloses numerous compounds bearing a methyl substituent at the R3, demonstrating that both methyl and ethyl are suitable alternatives for the same position. Therefore, a POSITA would have found it obvious to substitute the ethyl group of compounds 55 with the alternative methyl group, and to replace the tetrahydropyran with piperidine or cyclohexyl as a predictable alternative within the disclosed genus with expectation of retaining the desired EZH2 inhibitory activity, thereby arriving at the claimed invention.
Subject Matter Free of the Art of Record
The subject matter of claims 4-5 and 7 is free of the art of record. The closest prior art Kanno et al., US PG-PUB 2018/0282313 A1 in view of Stuckey et al. (J. of Biol. Chem., vol. 296, Jan. 2021, p. 100349). For example, Kanno describes a pharmaceutical composition exhibiting anticancer activity, mediated by EZH1 or EZH2 alone, or both EZH1 and EZH2, including applications to human diffuse large B-cell lymphoma. However, there is no motivation for a POSITA to modify the teaching of Kanno to arrive at the claimed invention. Since claims 12-14 are directly or indirectly dependent on claim 5, they are free of the art of record. It is important to note, even though these method claims may be free of the prior art, but they are not allowable due to 112(a) issues. Thus, these claims are not allowable until the 112(a) rejection is overcome.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to PIERRE PAUL ELENISTE whose telephone number is (571)270-0589. The examiner can normally be reached Monday - Friday 8:00 am - 5:00 pm (EST).
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, JAMES H ALSTRUM-ACEVEDO can be reached at (571) 272-5548. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/P.P.E./Examiner, Art Unit 1622
/JAMES H ALSTRUM-ACEVEDO/Supervisory Patent Examiner, Art Unit 1622
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