Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Election/Restrictions
Applicant’s election without traverse of Group I claims 1-12 in the reply filed on 05/15/2026 is acknowledged.
Claims 13-35 withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected inventions, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 05/15/2026.
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.
Claims 1-12 are rejected under 35 U.S.C. 103 as being unpatentable over Fedoriw, US20190365710; Eram, ACS Chem Biol. 2016 March 18; 11(3): 772–781; Bromley WO2019243567 hereinafter, "CRTL"); Luo, MedComm (2020). 2025 Nov 16;6(12):e70482; Li Tngting, Oncotarget, Vol. 7, No. 15 20236-20248; Rhodes US20120245235; Choucair, Oncogene (2019) 38:4015–4027; Chang US20080274908; Fujita (2014). PLoS ONE 9(7): e103084.
Fedoriw teaches a method of treating cancer in a subject having elevated gene activity [0027] fig 10; [0129], said method comprising administering a therapeutically effective amount of a type I PRMT inhibitor to said subject (Abstract, methods of treating cancer in a subject in need thereof, e.g., in a human in need thereof, comprising determining the level of 5-Methylthioadenosine phosphorylase (MTAP) polynucleotide or polypeptide or the presence or absence of a mutation in MTAP in a sample from the human and administering to the human an effective amount of a Type I protein arginine methyltransferase (Type I PRMT) inhibitor); a method of treating cancer in a subject, said method comprising administering a therapeutically effective amount of a type I PRMT inhibitor to said subject (Abstract, methods of treating cancer
in a subject in need thereof, e.g., in a human in need thereof, comprising determining the level of 5-Methylthioadenosine phosphorylase (MTAP) polynucleotide or polypeptide or the presence or absence of a mutation in MTAP in a sample from the human and administering to the human an effective amount of a Type I protein arginine methyltransferase (Type I PRMT) inhibitor); a method of treating cancer in a subject, said method comprising administering a therapeutically effective amount of a type I PRMT inhibitor and a STAT1 activating compound to said subject (Abstract, methods of treating cancer in a subject in need thereof, e.g., in a human in need thereof, comprising determining the level of 5-Methylthioadenosine phosphorylase (MTAP) polynucleotide or polypeptide or the presence or absence of a mutation in MTAP in a sample from the human and administering to the human an effective amount of a Type I protein arginine methyltransferase (Type I PRMT) inhibitor; Paras. [0154], [0208], further active ingredient or ingredients for use in combination or co-administered with the present methods or combinations, including erlotinib which is a STAT1 activating compound); a method of treating cancer in a subject in need thereof, said method comprising: (i) detecting an elevated gene activity in a subject; and (ii) administering a therapeutically effective amount of a type I PRMT inhibitor to said subject (Abstract, methods of treating cancer in a subject in need thereof, e.g., in a human in need thereof, comprising determining the level of 5-Methylthioadenosine phosphorylase (MTAP) polynucleotide or polypeptide or the presence or absence of a mutation in MTAP in a sample from the human and administering to the human an effective amount of a Type I protein arginine methyltransferase (Type I PRMT) inhibitor if the level of the MTAP polynucleotide or polypeptide is decreased relative to a reference or if a mutation in MTAP polynucleotide or polypeptide is present, thereby treating the cancer in the human); a method of treating cancer in a subject in need thereof, said method comprising: (i) detecting an elevated gene activity in a subject; and (ii) administering a therapeutically effective amount of an anti-cancer agent to said subject, wherein said subject has been previously treated with a STAT1 activating compound (Abstract, methods of treating cancer in a subject in need thereof, e.g., in a human in need thereof, comprising determining the level of 5-Methylthioadenosine phosphorylase (MTAP) polynucleotide or polypeptide or the presence or absence of a mutation in MTAP in a sample from the human and administering to the human an effective amount of a Type I protein arginine methyltransferase (Type I PRMT) inhibitor if the level of the MTAP polynucleotide or polypeptide is decreased relative to a reference or if a mutation in MTAP polynucleotide or polypeptide is present, thereby treating the cancer in the human; Paras. [0154], (0208], further active ingredient or ingredients for use in combination or co-administered with the present methods or combinations, including erlotinib which is a STAT1 activating compound); a method of treating cancer in a subject in need thereof, said method comprising: (i) detecting a gene activity in a subject; and (ii) administering a therapeutically effective amount of a STAT1 activating compound to said subject (Abstract, methods of treating cancer in a subject in need thereof, e.g., in a human in need thereof, comprising determining the level of 5-Methylthioadenosine phosphorylase (MTAP) polynucleotide or polypeptide or the presence or absence of a mutation in MTAP in a sample from the human and administering to the human an effective amount of a Type I protein arginine methyltransferase (Type I PRMT) inhibitor if the level of the MTAP polynucleotide or polypeptide is decreased relative to a reference or if a mutation in MTAP polynucleotide or polypeptide is present, thereby treating the cancer in the human; Paras. [0154], [0208], further active ingredient or ingredients for use in combination or co-administered with the present methods or combinations, including erlotinib at [0208], [0214] which is a STAT1 activating compound. More on this later.
For the instantly recited PRMT1 inhibitor formula (II of claim 4 see Fedoriw page 15 column B [112].
The above noted erlotinib in Fedoriw reads on instant claim 3.
Eram teaches in Figure I, the instantly elected species PRMT1 inhibitor of formula II Eram teaches that protein arginine methyltransferases (PRMTs) play a crucial role in a variety of biological processes. Overexpression of PRMTs has been implicated in various human diseases including cancer.
CRTL discloses a method of treating cancer in a subject in need thereof (Abstract, present invention provides a method for predicting the treatment response to anti-cancer immunotherapy of a mammalian cancer patient, the method comprising: a) measuring the gene expression of ... STAT1; Pg. 12, Lns. 24-32, (also at claim 1 of CRTL) a method of treatment of cancer in a mammalian patient), said method comprising: (i) detecting an elevated STAT1 activity in a subject (Abstract, present invention provides a method for predicting the treatment response to anti-cancer immunotherapy of a mammalian cancer patient, the method comprising: a) measuring the gene expression of ... STAT1); and (ii) administering a therapeutically effective amount of an anti-cancer agent to said subject (Pg. 12, Lns. 24-32, a method of treatment of cancer in a mammalian patient, comprising ... administering immunotherapy (e.g. immune checkpoint blockage therapy) to the patient in need thereof).
According to Fujita, Isolation of specific genomic regions retaining molecular interactions is essential for comprehensive identification of molecules associated with the genomic regions. Recently, we developed the engineered DNA-binding molecule-mediated chromatin immunoprecipitation (enChIP) technology for purification of specific genomic regions. Here, we developed a retroviral expression system for enChIP using CRISPR. We showed that the target genomic locus can be purified with high efficiency by using this system. We also showed that contamination of potential off-target sites is negligible by using this system if the guide RNA (gRNA) for the target site has a sufficiently long unique sequence in its seed sequence. enChIP combined with stable isotope labeling using amino acids in cell culture (SILAC) analysis identified proteins whose association with the interferon (IFN) regulatory factor-1 (IRF-1) promoter region increases in response to IFNγ stimulation. The list of the associated proteins contained many novel proteins in the context of IFNγ-induced gene expression as well as proteins related to histone deacetylase complexes whose involvement has been suggested in IFNγ-mediated gene expression. Finally, we confirmed IFNγ-induced increased association of the identified proteins with the IRF-1 promoter by ChIP. Thus, our results showed that the retroviral enChIP system using CRISPR would be useful for biochemical analysis of genome functions including transcription and epigenetic regulation. See Abstract.
Taken together, the active ingredient PRMT1 inhibitor and their inherent biochemical property underlying the claimed method of the base claims are known in the art. PRMT1 and STAT1 one are inexorably linked. For example, Luo is a Review article titled PRMT1 in Health and Disease: Emerging Perspectives From Molecular Mechanisms to Therapeutic Strategies, which teaches the limitations of the dependent claims. Applicant is encouraged to use word search technique to locate the relevant citations. For example, a search in Luo for multiple teachings can be found for the term ‘interferon’ which read on claim 7. Likewise, a search for CD4 reveals at page 20 of 31 column A, last paragraph that significant upregulation of PRMT1 in CD4+ T cells. These are examples of teachings relevant to the limitations of dependent claims within the purview of one of skill in the art. For example, it is common knowledge that resistance (see claim 2) occurs when pathogens or cancer cells mutate and no longer respond to medications designed to kill them. See in this regard,
Li Tingting, Protein arginine methyltransferase 1 may be involved in pregnane x receptor-activated overexpression of multidrug resistance gene during acquired multidrug resistant. PRMT1 may be an important co-activator of PXR in activating MDR1 gene during acquired resistance, and PRMT1 inhibitor combined with chemotherapy drugs may be a new strategy for overcoming tumor MDR. Claim 5 recites list of known cancers., see in this regard, Choucair, which teaches that the arginine methyltransferase PRMT1 regulates IGF-1 signaling in breast cancer. With regards to claim 6: see Chang for gene expression profiling methods for the diagnosis of melanoma and Rhodes for a system for classifying a patient's cancer as belonging to one or more Cancer Modules of 1 of 15 different cancer types is provided. The Cancer Modules are useful to identify patient populations and individual patients demonstrating specific prognosis, risk of metastasis and/or recurrence, response or lack of response to drugs, and the like. claim 6 recites gene signatures reflecting classic Interferon (IFN) response and immune activation. Interferon (IFN) response and immune activation; claim 7 elevated levels of interferons, These and limitations of claims 8, 9 mutations, and known characteristic of cancers (claims 10-11) such as heavily infiltrated tumor are also within the purview of one of skill in the art. For example Fujita teaches that IFNc-induced increased association of the identified proteins with the IRF-1 promoter by ChIP that would be useful for biochemical analysis of genome functions including transcription and epigenetic regulation.
As such the claims are drawn to combination of the inventions by the prior arts done in a manner obvious to one of ordinary skill in the art. Patent for the combination of known elements wherein their functions remain the same withdraws “what is already known into field of its monopoly and diminishes resources available to skilled men”. Sakraida v. Ag Pro, Inc.189 USPQ 449, 425 US 273, (1976).
Accordingly, the claims do not recite an unobvious distinction over the prior art. Further, a reference is relevant not only for what it expressly teaches, but also for what it would have conveyed to one of ordinary skill in the art. See In re Opprecht, 12 USPQ2d 1235, 1236 (Fed. Cir. 1989); In re Bode, 193 USPQ 12 (CCPA 1976). In light of the foregoing discussion, the Examiner finds that the claimed subject matter as a whole would have been obvious to one of ordinary skill in the art at the time the invention was made, in view of the cited references and the knowledge generally available in the art. Accordingly, the claims are rejected under 35 U.S.C. § 103.
The art made of record and not relied upon is considered pertinent to applicant's disclosure. Li, The Dual Role of STAT1 in Ovarian Cancer: Insight Into Molecular Mechanisms and Application Potentials, Frontiers in Cell and Developmental Biology, Volume 9, 2021, 1-13
Any inquiry concerning this communication or earlier communications from the examiner should be directed to NIZAL S CHANDRAKUMAR whose telephone number is (571)272-6202. The examiner can normally be reached M-F 8-5 EST.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Andrew Kosar can be reached at (571) 272-0913. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/NIZAL S CHANDRAKUMAR/ Primary Examiner, Art Unit 1625
Prosecution Insights