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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on March 2nd, 2026 has been entered.
All previous objections and rejections not reiterated herein were overcome by claim amendments and arguments, filed February 9th, 2026, have been fully considered and found persuasive. As such all objections and rejections not reiterated herein have been withdrawn.
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claim 14 is rejected under 35 U.S.C. 101 because the claimed invention is directed to an abstract idea without significantly more. The claim recites a method for the screening of active agents against psoriasis comprising the identification of a test compound's activity of an EZH2 inhibitor, wherein the EZH2 inhibitor is selected from the group consisting of: EPZ-6438 (tazemetostat), CPI-169, EPZ005687, EI1, GSK126, UNC1999, CPI-1205, EPZ011989, EBI-2511, PF-06726304, GSK503, and GSK343. This judicial exception is not integrated into a practical application because the only step of the claim is an identification step, which is an abstract idea, more specifically, a mental processes, wherein after well-understood, routine, and conventional data gathering activity there is an evaluation of the collected data. Thus the identification step is a mental processes step that can be performed by a human, to diagnosis or interpret the results. The claim does not include additional elements that are sufficient to amount to significantly more than the judicial exception because the only step in the method as claimed by claim 14 is the judicial exception, of a mental processes step.
Claim Rejections - 35 USC § 102
Response to Arguments
Applicant's claim amendments and arguments filed February 9th, 2026, with respect to the 35 U.S.C. 102(a)(1) rejection of instant claims 1 – 9, and 11 – 15 have been fully considered and have been found persuasive. The 35 U.S.C. 102(a)(1) rejection of instant claims 1 – 9, and 11 – 15 has been withdrawn.
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.
Claims 1 – 2, 5 – 6, 8, 11, and 14 are rejected under 35 U.S.C. 103 as being unpatentable over International Publication Number WO 2013/039988 A1 to Burgess et.al. (herein after Burgess’988; cited in the Office Action dated April 7th, 2025) in view of Liu et. al. ((2011), Comparison of gene expression profiles reveals aberrant expression of FOXO1, Aurora A/B and EZH2 in lesional psoriatic skins, Mol Bio Rep., 38, 4219 – 4224; cited in the Office Action dated April 7th, 2025) and Bradley et. al. ((2014), EZH2 Inhibitor Efficacy in Non-Hodgkin’s Lymphoma Does Not Require Suppression of H3K27 Monomethylation, Cell Press Chemistry & Biology, 1463 – 1475; cited in the Office Action dated November 3rd, 2025).
Regarding claims 1 – 2, 5 – 6, 8, 11, and 14, Burgess’988 teach that the disclosure relates to substituted azaindoles which inhibit EZH2 (page 1 line 4). Specifically, Burgess’988 teach substituted azaindoles of formula (I) (page 3 lines 1 – 2) that are useful for the treatment of disorders mediated by inhibiting EZH2 (page 5 lines 23 – 25). More specifically, Burgess’988 teach disorders mediated by inhibiting EZH2 includes psoriasis (claims 1) (page 22 line 22). Additionally, Burgess’988 teach that the compounds of the disclosure can be combined with or co-administered with other therapeutic agents (page 22 lines 25 – 26).
Moreover, Burgess’988 teach that pharmaceutical compositions comprising the EZH2 inhibitors of the disclosure may be adapted for administration by any appropriate route which includes topically by buccal, sublingual or transdermal (claims 1 and 2) (page 33 lines 19 – 24). Furthermore, Burgess’988 teach that that such compositions may be prepared by any method known in the art of pharmacy (claim 11), for example by bringing into association a compound of formula (I) with the carrier(s) or excipient(s) (claim 8) (page 33 lines 22 – 24). Additionally, Burgess’988 teach that the pharmtuically compositions comprising the EZH2 inhibitor can be adapted for vaginal administration as a cream, gel, or paste (page 35 lines 7 – 8 ). Now while Burgess’988 teach the formulation of creams, gels, and pastes for vaginal administration; given that Burgess’988 does teach that that such compositions may be prepared by any method known in the art of pharmacy and the relatively high skill of one of ordinary skill in the pharmaceutical arts it would have been obvious to such artisan to formulate a topical cream, gel or, paste to be applied directly to the skin (claim 8) using the appropriate topical carrier or excipient (claim 11).
Furthermore, Burgess’988 teach an assay protocol for evaluating the disclosed compounds ability to inhibit the methyltransferase activity of EZH2 (claim 14) within the PRC2 complex (page 215 lines 13 – 21). While the assay taught by Burgess’988 focused on the screening of the disclosed compounds in methods of treating cancer, as mentioned above, the prior art of Burgess’988 specifically taught an embodiment for the use of the compounds of the disclosure in treating psoriasis through the inhibition of EZH2. Thus it would have been obvious that the assay taught by Burgess’988 can be used to screen compounds that are useful against psoriasis since both disease share a common mechanistic pathway that involves the inhibition of EZH2 activity.
While Burgess’988 taught the use of EZH2 inhibitors for psoriasis the prior art reference failed to exemplify the topical use of the disclosed EZH2 inhibitor to treat psoriasis (claim 1). In addition, Burgess’988 fails to teach a method wherein theEZH2 inhibitor is CPI-169 (claims 1 and 5) or a method wherein the EZH2 inhibitor is administered with an additional agent active against psoriasis-associated symptoms (claim 6).
Nevertheless, Liu et. al. teach the identification of de-regulated expression of FOXO1, AURKA/B and EZH2 in lesional psoriatic skins (page 4219 column 2 paragraph 2). Furthermore, Liu et. al. teach that the expression of FOXO1, AURKA/B and EZH2 in lesional psoriatic skins were reversed upon Etanercept treatments (page 4219 column 2 paragraph 2). Additionally, Liu et. al. teach that aberrant expression of FOXO1, AURKA/B and EZH2 may contribute to the progress of psoriasis (page 4420 column 1 paragraph 1). Furthermore, Liu et. al. teach that it would be worthwhile to test whether the EZH2 inhibitor (DZNep) can enhance the therapeutic effects of Etanercept (claim 6) in psoriasis management (page 4223 column 1 paragraph 2). Thus Liu et. al. suggest a reasonable expectation of success for the inhibition of EZH2 in combination with etanercept for the treatment of psoriasis.
While Liu et. al. fails to teach the EHZ2 inhibitor as recited in newly amended claim 1, Liu et. al. does teach the administration of an EZH2 inhibitor, specifically, EZH2 (DZNep).
Nevertheless, Bradley et. al. teach that CPI-169 (claims 1 and 5) was identified as a more potent EZH2 inhibitor with improved microsomal stability (page 1468 column 2 paragraph 3). Furthermore Bradly et. al. teach that that CPI-169 significantly increased EZH2 thermal stability and–compared to CPI-360–maintained stabilization for a longer time period after compound removal (page 1468 column 2 paragraph 3).
Therefore, since the prior art of both Burgess’988, Liu et. al. taught that EZH2 inhibitors were possible treatment strategies for treating psoriasis and since the prior art of Bradley et. al. taught that CPI-169 was a more potent EZH2 inhibitor it would have been obvious to one of ordinary skill in the art to substitute either the substituted azaindoles of Burgess’988 or EZH2 (DZNep) of Liu et. al. with the more potent EZH2 inhibitor CPI-169.
Therefore, it would have been obvious before the effective filing date of the instant application to modify the invention of Burgess’988 to treat psoriasis using EZH2 inhibitor topically applied in view of Liu et.al. and Bradley et. al. specifically to use CPI-169 as a substitute for DZNep with Etanercept as the additionally agent active against psoriasis-associated symptoms. One would have been motivated to use CPI-169 instead of DZNEP as an EZH2 inhibitor because the prior art of Lui et. al. and Bradley et. al. teach both DZNEP and CPI-169 as inhibitors of EZH2. One of ordinary skill in the art would have had a reasonable expectation of success since aberrant expression of EZH2 may contribute to the progress of psoriasis.
Claims 3 – 4, 9, and 12 – 13 are rejected under 35 U.S.C. 103 as being unpatentable over International Publication Number WO 2013/039988 A1 to Burgess et.al. (herein after Burgess’988; cited in the office action dated April 7th, 2025), Liu et. al. ((2011), Comparison of gene expression profiles reveals aberrant expression of FOXO1, Aurora A/B and EZH2 in lesional psoriatic skins, Mol Bio Rep., 38, 4219 – 4224; cited in the office action dated April 7th, 2025), and Bradley et. al. ((2014), EZH2 Inhibitor Efficacy in Non-Hodgkin’s Lymphoma Does Not Require Suppression of H3K27 Monomethylation, Cell Press Chemistry & Biology, 1463 – 1475; cited in the Office Action dated November 3rd, 2025) as they applied to claims 1 – 2, 5 – 6, 8, 11, and 14, in view of Gisondi et.al. ((2017), Treatment Approaches to Moderate to Severe Psoriasis, Int. J. Mol. Sci., 18, 1 – 8; cited in the office action dated April 7th, 2025) and Colombo et.al. ((2012), Calcipotriol and betamethasone dipropionate in the treatment of mild-to-moderate psoriasis: a cost effectiveness analysis of the ointment versus gel formulation, ClinicoEconomics and Outcomes Research, 4, 261 – 268; cited in the office action dated April 7th, 2025).
The teaching of Burgess’988, Liu et. al., and Bradley et. al. as they relate to claims 1, 8, and 11, from which claims 3 – 4, 9, and 12 – 13 depend, are given previously in this office action and are fully incorporated here.
However, Burgess’988, Liu et. al., and Bradley et. al. are silent about a method or pharmaceutical composition comprising an EZH2 inhibitor wherein the skin-permeable formulation (claim 3, 9, and 12) is selected from the group consisting of: creme, gel, lotion (claims 4, and 13).
Nevertheless, Gisondi et. al. teach that there are many factors influencing psoriasis severity which include the extent of the disease, the location of lesions, the degree of inflammation, the responsiveness to treatment, and the impact on quality of life (page 1 paragraph 1). Furthermore, Gisondi et. al. teach that treatments of pessaries can be classified as topical, systemic, or phototherapeutic (page 2 paragraph 2). Additionally, Gisondi et. al. teach that topical therapy alone is indicated in mild psoriasis (page 2 paragraph 2) and Gisondi et. al. teach that for patients with moderate to severe psoriasis topical therapy could be indicated in association with systemic treatments (page 2 paragraph 2 and page 3 paragraph 1).
However, Gisondi et. al. is silent about a method or pharmaceutical composition wherein the skin-permeable formulation is selected from the group consisting of: creme, gel, lotion (claims 3 – 4, 9, and 12 – 13).
Nevertheless, Colombo et.al. teach that topical therapy has an important role in the treatment of psoriasis (page 262 column 1 paragraph 3). Colombo et. al. teach a pharmacoeconomic simulation aimed at assessing the costs of two topical formulations gel and ointment showing different levels of adherence with treatment of mild-to-moderate psoriasis, applying it to the Italian population, and correlating costs with varying degrees of disease severity (page 262 column 1 paragraph 3 and column 2 paragraph 1). More specifically, Colombo et. al. teach the use of two formulations of calcipotriol and betamethasone dipropionate, that is, Dovobet® gel and ointment, in the treatment of mild-to-moderate psoriasis (page 262 column 2 paragraph 2).
Furthermore, Colombo et. al. teach that the use of Dovobet gel reduces the number of patients potentially needing treatment with more costly therapies by 5%, in spite of an increase in resource consumption for topical therapies (page 264 column 2 paragraph 1). Moreover, Colombo et. al. teach that the Dovobet gel strategy showed better overall adherence and, at the proposed selling price (€33.17), appears to be a more favorable choice than the ointment formulation from the clinical and economic points of view for the treatment of mild-to-moderate psoriasis (page 264 column 2 paragraph 3). While Dovobet is not an EZH2 inhibitor; Colombo et. al. suggest that the gel formulation as being a favorable choice over an ointment based formulation.
Therefore it would have been obvious before the effective filing date of the instant application to modify the method Burgess’988, Liu et. al., and Bradley et. al. to treat psoriasis using a topical application of an EZH2 inhibitor in view of Gisondi et. al. and Colombo et. al., that is in a gel skin-permeable formulation. One of ordinary skill in the art would have been motivated to make this modification for better compliance by the patient to the prescribed treatment regimen. One of ordinary skill in the would have a reasonable expectation of success because the gel formulation, for a conventional psoriasis therapy, showed better overall adherence and cost point for the patients.
Claim 7 is rejected under 35 U.S.C. 103 as being unpatentable over International Publication Number WO 2013/039988 A1 to Burgess et.al. (herein after Burgess’988; cited in the office action dated April 7th, 2025), Liu et. al. ((2011), Comparison of gene expression profiles reveals aberrant expression of FOXO1, Aurora A/B and EZH2 in lesional psoriatic skins, Mol Bio Rep., 38, 4219 – 4224, cited in the office action dated April 7th, 2025), and Bradley et. al. ((2014), EZH2 Inhibitor Efficacy in Non-Hodgkin’s Lymphoma Does Not Require Suppression of H3K27 Monomethylation, Cell Press Chemistry & Biology, 1463 – 1475; cited in the Office Action dated November 3rd, 2025) as they applied to claims 1 – 2, 5 – 6, 8, 11, and 14, in view of Sun et. al. ((March 19, 2019), Berberine downregulates CDC6 and inhibits proliferation via targeting JAK-STAT3 signaling in keratinocytes, Cell Death and Disease, 10, 1 – 16; cited in the office action dated April 7th, 2025).
The teachings of Burgess’988, Liu et. al., and Bradley et. al. as they relate to claims 1, and 6, from which claim 7 depend, are given previously in this office action and are fully incorporated here.
However, Burgess’988, Liu et. al., Bradley et. al. are silent about whether the additional agent is an CDK4/6 inhibitor (claim 7).
Nevertheless, Sun et. al. teach although the molecular mechanisms involved in the pathogenesis of psoriasis are complex, growing evidence suggests that the activator of transcriptions 1 and 3 (STAT1 and STAT3), and nuclear factor-κB (NF-κB) is pivotal in the transcriptome network involved in the mechanism of psoriasis (page 2 column 1 paragraph 2). Furthermore, Sun et. al. teach that in particular, expression of constitutively active STAT3 (STAT3C) in keratinocytes leads to the spontaneous development of psoriasis in transgenic mice (page 2 column 1 paragraph 2). Moreover, Sun et. al. teach that CDK4/Cyclin D kinase was reported to be important in CDC6 transcription (page 4 column 2 paragraph 4). Thus, Sun et. al. suggest the targeting of CDK4 has a pathway for modulating CDC6 activity. Additionally, Sun et. al. teach that CDC6, induced by STAT3 activation in keratinocytes, is upregulated in psoriatic epidermal skin and contributes to proliferation of keratinocytes (page 2 column 1 paragraph 5). Moreover, Sun et. al. teach that Berberine (BBR), a plant alkaloid, inhibits CDK4/6-RB-CDC6 signaling, leading to cell cycle arrest and apoptosis in keratinocytes (page 2 column 2 paragraph 1). Furthermore, Sun et. al. teach that palbociclib significantly reduced both protein and mRNA levels of CDC6 in HaCaT cells (page 6 column 1 paragraph 1 and page 7 Figure 2h, i).
Therefore, it would have been obvious before the effective filing date of the instant application to modify the method of Burgess’988, Liu et. al., and Bradley et. al. to treat psoriasis using an EZH2 inhibitor in view of Sun et. al. that is to include a CDK4/6 inhibitor. One of ordinary skill in the art would have been motivated to make this modification because CDK4/6 is important in CDC6 transcription and thus STAT3 activation. One of ordinary skill in the art would have a reasonable expectation for success because Palbociclib, a CDK4/6 inhibitor, significantly reduced both protein and mRNA levels of CDC6 in HaCaT cells.
Claim 15 is rejected under 35 U.S.C. 103 as being unpatentable over Arifuzzaman et. al. ((2017), Selective inhibition of EZH2 by a small molecule inhibitor regulates microglial gene expression essential for inflammation, Biochemical Pharmacology, 137, 61 – 80; cited in the office action dated April 7th, 2025) and Bradley et. al. ((2014), EZH2 Inhibitor Efficacy in Non-Hodgkin’s Lymphoma Does Not Require Suppression of H3K27 Monomethylation, Cell Press Chemistry & Biology, 1463 – 1475).
Regarding claim 15, Arifuzzaman et. al. teach EZH2, the catalytic subunit of the Polycomb repressive complex 2 (PRC2), is a histone methyltransferase (HMT) that mediates transcriptional silencing through histone H3 at lysine 27 (H3K27) to generate trimethylated H3K27 (H3K27me3) (page 61 column 1 paragraph 1). Furthermore, Arifuzzaman et. al. teach that EZH2 is critically associated with the regulation of inflammation and autoimmune diseases (page 61 column 2 paragraph 1). Arifuzzaman et. al. teach the selective small molecule inhibitor of EZH2, EPZ-6438, is emerging as a promising therapeutic agent for the treatment of non-Hodgkin Lymphoma (NHL) because it has superior potency and drug-like properties as well as oral bioavailability (page 62 column 1 paragraph 2). Furthermore, Arifuzzaman et. al. teach a comparative gene expression analysis of primary microglial cells upon stimulation with LPS, EPZ-6438, and LPS + EPZ-6438 using massively parallel cDNA sequencing (RNA-seq), which paved the way for unbiased and efficient assays of the transcriptome of any mammalian cell (page 62 column 1 paragraph 3). Additionally, Arifuzzaman et. al. teach a comprehensive analysis of the selective small molecule inhibitors of EZH2 and EPZ-6438-mediated gene expression profiles and networks in LPS-stimulated microglial cells using a transcriptome RNA-seq assay and bioinformatics analyses (page 62 column 1 paragraph 4).
In the study, Arifuzzaman et. al. teach that the cells were maintained in a humidified incubator with 95% air and a 5% CO2 atmosphere at 37 oC and the cells were treated with 10 µM EPZ-6438, 1 µM R848 (Resiquimod) and LPS (10 ng/ml) for the specified times under normal culture conditions (page 62 column 2 paragraph 1). Arifuzzaman et. al. teach that in BV-2 cells treated with EPZ-6438 showed lower expression for NFKB1/2, that is IκBζ, then the BV-2 cells not treated with EPZ-6438 (page 65 Figure 3 A and 3H). While the culture conditions taught by Arifuzzaman et. al. focused on the comparative gene expression of primary microglial cells upon stimulation with LPS, as mentioned above, the prior art of Arifuzzaman et. al. specifically taught an EZH2 inhibitor cultured with cells. Additionally, the prior art of Arifuzzaman et. al. taught the outcome which was the suppression of the expression for NFKB1/2, that is IκBζ. Thus it would have been prima facie obvious that the culture conditions taught by Arifuzzaman et. al. can be used to culture cells with suppressed cellular NF-kappa-B inhibitor zeta (IκBζ) expression.
Additionally, while Arifuzzaman et. al. fail to teach a method wherein the EHZ2 inhibitor is one as recited in newly amended claim 15, Arifuzzaman et. al. does teach the administration of a EZH2 inhibitor, specifically, EZH2 EPZ-6438; thus, it would have been obvious to substitute the prior art taught EZH2 inhibitor of EPZ-6438 for any of the EZH2 inhibitors recited in claim 15.
Nevertheless, Bradley et. al. teach CPI-169 (claim 15) was identified as a more potent EZH2 inhibitor with improved microsomal stability (page 1468 column 2 paragraph 3). Furthermore Bradly et. al. teach that that CPI-169 significantly increased EZH2 thermal stability and–compared to CPI-360–maintained stabilization for a longer time period after compound removal (page 1468 column 2 paragraph 3). Thus it would have been obvious to substitute the prior art taught EZH2 inhibitor of EPZ-6438 for the EZH2 inhibitor CPI-169 as recited in claim 5 with the expectation that both EPZ-6438 and CPI-169 will behave similarly.
Therefore, it would have been obvious before the effective filing date of the instant application to modify the method of Arifuzzaman et. al. for a method for the suppression of the cellular IκBζ expression comprising the addition of to treat psoriasis using an EZH2 inhibitor in view of Bradley et. al. specifically to use CPI-169 as the EZH2 inhibitor. One would have been motivated to use CPI-169 instead of EPZ-6438 as an EZH2 inhibitor because the prior art of Arifuzzaman et. al. and Bradley et. al. teach both EPZ-6438 and CPI-169 as inhibitors of EZH2. One of ordinary skill in the art would have had a reasonable expectation of success because BV-2 cells treated with EPZ-6438 showed lower expression for NFKB1/2, that is IκBζ, then the BV-2 cells not treated with EPZ-6438. And thus there would have been a reasonable expectation that since the prior art taught both EPZ-6438 and CPI-169 as EZH2 inhibitors both EPZ-6438 and CPI-169 will behave similarly, that is lower expression for NFKB1/2, that is IκBζ.
Response to Arguments
Applicant's claim amendments and arguments filed February 9th, 2026, with respect to the 35 U.S.C. 103 rejection of claims 1 – 9, and 11 – 15 have been fully considered and but they are not persuasive.
Applicant argues that the combination of the cited prior art does not teach or suggest every element of the present claim 1 (see applicants remarks page 8 paragraphs 1 – 3).
In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
As stated in the above prior art rejection, both the prior art of Burgess’988 and Liu et. al. taught that EZH2 inhibitors were possible treatment strategies for treating psoriasis. Moreover, the prior art of Bradley et. al. taught that CPI-169 was a more potent EZH2 inhibitor. Thus all three prior art references teach three different compounds that are EZH2 inhibitors. Moreover, both the prior art references of Burgess’988 and Liu et. al. teach the use of EZH2 inhibitors in treating psoriasis with Liu et. al. specifically teaching that aberrant expression of FOXO1, AURKA/B and EZH2 may contribute to the progress of psoriasis (page 4420 column 1 paragraph 1) and that it would be worthwhile to test whether the EZH2 inhibitor (DZNep) can enhance the therapeutic effects of Etanercept (claim 6) in psoriasis management (page 4223 column 1 paragraph 2). Therefore, given the teaching as presented above it would have been obvious to one of ordinary skill in the art to substitute either the substituted azaindoles of Burgess’988 or EZH2 (DZNep) of Liu et. al. with the more potent EZH2 inhibitor CPI-169 in a method of treating psoriasis.
Applicant argues that there is no reason, suggestion or motivation to combine the cited prior art (see applicants remarks page 12 paragraphs 2 – 3).
In response to applicant’s argument that there is no teaching, suggestion, or motivation to combine the references, the examiner recognizes that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). In this case, of the prior art rejection as stated previously the prior art rejection it would have been obvious to one of ordinary skill in the art to substitute either the substituted azaindoles of Burgess’988 or EZH2 (DZNep) of Liu et. al. with the more potent EZH2 inhibitor CPI-169 in a method of treating psoriasis.
Applicant argues that there was superior and unexpected properties of the present claims (see applicants remarks page 14 paragraph 3, page 15 paragraphs 1 – 2, and page 16 paragraphs 1 – 2).
The examiner contends that for a showing of unexpected results there must be a comparison between the claimed subject matter with the closest prior art to be effective to rebut a prima facie case of obviousness. In re Burckel, 592 F.2d 1175, 201 USPQ 67 (CCPA 1979).(MPEP 716.02( e)). Moreover, The evidence relied upon should establish "that the differences in results are in fact unexpected and unobvious and of both statistical and practical significance." Ex parte Gelles, 22 USPQ2d 1318, 1319 (Bd. Pat. App. & Inter. 1992)(MPEP 716.02(b)).
Double Patenting
Response to Arguments
Applicant’s terminal disclaimer, filed February 9th, 2026, with respect to the provisionally nonstatutory double patenting (NSDP) rejection of the instant claims 1 – 9, and 11 – 15 over claims 1 – 11 of copending Application No. 17/707741 to Kramer et. al. (herein after Kramer’741) (reference application) have been fully considered and are persuasive. The provisional NSDP rejection of instant claims 1 – 9, and 11 – 15 has been withdrawn.
Conclusion
Claims 1 – 9, and 11 – 15 are rejected.
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/DAWANNA SHAR-DAY WHITE/Examiner, Art Unit 1627