DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Application Status and Election
Applicant’s amendment filed December 15, 2025, amending claims 5, 25 and 30, canceling claims 14, 16 and 29, and adding new claims 31, 32 and 32 are acknowledged.
Note that there are two claims numbered “32”. Misnumbered claim 32 reciting “wherein the predictive biomarker is a (a) FLT ITD, (b) a mutation in NPM1 or DNMT3a, (c) a mutation in any of the following splicing genes SDSF2, ZRSR2 or SF3B1” is objected to and has been renumbered claim 33.
Claims 1-13, 22-28 and 30-33 are pending.
New claim 32 is directed to a non-elected species (see Non-final OA mailed 4/14/2025, page 2). As such claims 3-4, 7, 9-13, 24, 26-28 and 32 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to nonelected species, there being no allowable generic or linking claim.
Claims 1-2, 5-6, 8, 22-23, 25, 30, 31 and 33 are under examination.
The cancelation of claim 16 renders the §102 rejection over Tarighat reference moot. Any other rejection or objection not reiterated herein has been overcome by amendment. Applicant’s amendments and arguments have been thoroughly reviewed, but are not persuasive to place the claims in condition for allowance for the reasons that follow.
Claim Rejections - 35 USC § 112(b)
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.
Claim 33 is 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. This is a new rejection necessitated by amendment.
Claim 33 recites “The method of claim 1, wherein the predictive biomarker is a (a) FLT ITD, (b) a mutation in NPM1 or DNMT3a, (c) a mutation in any of the following splicing genes SDSF2, ZRSR2 or SF3B1”. There are no conjunctions between options (a), (b) or (c). As a result, it is not clear if all of options (a), (b) and (c) are required, a subset of (a), (b) and (c) are required, or only one of (a), (b) or (c) is required. Therefore, the set of predictive biomarkers required for patient identification and PRMT5 inhibitor administration is indefinite.
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.
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, 22-23, 25 and 33 are rejected under 35 U.S.C. 103 as being unpatentable over Knudsen (US 20090023149 A1, of record) in view of Tarighat (Somayeh Tarighat Dissertation: Novel epigenetic role and therapeutic targeting of protein arginine methyltransferase 5 (PRMT5) in acute myeloid leukemia, (2014), Ohio State University). This rejection also addresses the elected species of (A) AML, and (B) mutations in DNMT3A. This is maintained rejection and a new rejection for new claim 33 necessitated by amendment.
Regarding claims 1-2, Knudsen discloses a method of identifying a patient diagnosed with cancer for treatment [0004]: "The invention features methods, kits, and devices for determining the sensitivity or resistance of a patient, e.g., a cancer patient, to a treatment,"; ([0009]) comprising: a) obtaining a biological sample comprising cancer cells from a patient diagnosed with cancer ([0016]): "the nucleic acid molecules are characterized by their ability to specifically identify nucleic acid molecules complementary to the microRNAs in a sample collected from a cancer patient."; ([0056]): "Using a tumor sample or a blood sample (e.g., in case of leukemia or lymphoma) from a patient, expression of the biomarker in the cells of the patient in the presence of the treatment agent is determined"); b) measuring the gene expression level of a predictive biomarker of a cancer treatment responsiveness in the biological sample ([0006], [0009], [0017], [0056]); c) identifying a patient predicted to be responsive to said treatment ([0009]); and d) administering an effective amount of a cancer treatment to the patient if the predictive biomarker is present ([0021]: "the treatment is, e.g., administration of a compound ... to a patient."; [0037]: "administering to a patient (e.g., a human) or living organism or exposing to a cell or tumor a compound (e.g., a drug ... to treat or prevent cancer or the symptoms of cancer (e.g., cryotherapy and radiation therapy)"; para [0056]). Knudson also teaches that to determine biomarkers for predictive inhibitor responsiveness, cancer cells lines are treated with the drug and assayed for growth inhibition (FIG 1, [0039]).
Knudson does teach predictive biomarkers for responding to a PRMT5 inhibitor.
Tarighat teaches that mutations in DNMT3A are often found in acute myeloid leukemia (AML) (page 23). Tarighat teaches a “C12” compound is capable of killing OCI-AML3 cells (Figure 2.3). Tarighat teaches that C12 is a PRMT5 inhibitor (Figure 2.3, legend, page 46). Tarighat teaches that OCI-AML3 cells are a cancer AML cell line, comprising a mutation in DNMT3A (Figure 2.3 and legend).
Regarding claims 1-2, it would have been obvious to one of ordinary skill in the art to have detected a mutation in DNMT3A as taught in Tarighat as a biomarker for treatment response of PRMT5 inhibitor in Knudsen's method of identifying a patient diagnosed with cancer for a treatment in order to detect AML patient sensitivity to PRMT5 inhibitor treatment for treatment optimization. It would have amounted to measuring a known biomarker that would be predicted to respond to PRMT5 inhibition and applying that biomarker into a known diagnostic and treatment pipeline. Because Tarighat teaches a DNMT3A mutation cell line is sensitive to the C12 PRMT5 inhibitor, the skilled artisan would have predicted that an AML patient with the DNMT3A mutation would respond to a PRMT5 inhibitor, similar to the cell culture results. The skilled artisan would have been motivated to use a PRMT5 inhibitor to treat patients having a DNMT3A mutation because Tarighat teaches C12 is capable of killing tumor cells with the DNMT3A mutation and derived from patient with AML.
Regarding claims 5-6, the teachings of Knudson and Tarighat are recited above as for claims 1-2. The obviousness of using the biomarker identification pipeline outlined in Knudson for the predictiveness and subsequent administration of Tarighat’s C12 PRMT5 inhibitor to AML patients having a DNMT3A mutation is recited above as for claims 1-2.
Regarding claim 8, Tarighat teaches the DNMT3A mutation in the OCI-AML3 cells lines is R288C.
Regarding claims 22-23, the teachings of Knudson and Tarighat are recited above as for claims 1-2. The obviousness of using the biomarker identification pipeline outlined in Knudson for the predictiveness and subsequent administration of Tarighat’s C12 PRMT5 inhibitor to AML patients having a DNMT3A mutation is recited above as for claims 1-2.
Regarding claim 25, Tarighat teaches the DNMT3A mutation in the OCI-AML3 cells lines is R288C.
Regarding new claim 33, the claim is indefinite for the reasons explained above in paragraph 10. For the purpose of compact prosecution, claim 33 is interpreted as requiring only one of options (a), (b) or (c). The teachings of Knudsen and Tarighat are recited above as for claims 1-2. The obviousness of having detected a mutation in DNMT3A as taught in Tarighat as a biomarker for treatment response of PRMT5 inhibitor in Knudsen's method of identifying a patient diagnosed with cancer for treatment optimization is recited above as for claims 1 and 2.
Claim 30 is rejected under 35 U.S.C. 103 as being unpatentable over Knudsen (US 20090023149 A1, of record) and Tarighat (Somayeh Tarighat Dissertation: Novel epigenetic role and therapeutic targeting of protein arginine methyltransferase 5 (PRMT5) in acute myeloid leukemia, (2014), Ohio State University) as applied to claims 1-2, 5-6, 8, 22-23, 25 and 33 above, and further in view of Bergman (US 20170298075 A1, published October 19, 2017). This is a maintained rejection.
The teachings of Knudsen and Tarighat are recited above and applied as for claims 1-2, 5-6, 8, 22-23, 25 and 33. Tarighat also teaches that general down regulation of PRMT5 reduces the growth of several AML cell lines (FIG 2.1.I).
Knudsen and Tarighat do not teach any of the PRMT5 inhibitors recited in claim 30.
Bergman teaches that PRMT5 is a pro-survival factor, which regulates cell proliferation ([0021]). Bergman teaches that PRMT5 is linked to human cancer ([0022]) and is a known target for the identification of novel cancer therapeutics ([0026]). Bergman teaches the synthesis of N-(2-Hydroxy-3-(1,2,3,4-tetrahydroisoquinolin-3-yl)propyl)-4-(morpholine-4-carbonyl)benzamide, herein referred to as Compound 1 (Example 1, [0699]-[0702]). Bergman teaches Compound 1 inhibits PRMT5 in vivo ([0870]). Bergman teaches the PRMT5 inhibitors of the invention can be used to treat cancer ([0054], [0152]), including AML ([0153]).
It would have been obvious to one skilled in the art before the effective filing dates of the claimed invention to have substituted the C12 PRMT5 inhibitor of Tarighat with Bergman’s compound 1 in the method of treating an individual having AML with a DNMT3A mutation rendered obvious above. It would have amounted to the simple substitution of one known PRMT5 inhibitor with another known PRMT5 inhibitor by known means to yield predicable results. The skilled artisan would have predicted that Compound 1 could be used to treat an AML-DNMT3A mutation patient because 1) Tarighat teaches that other means to inhibit PRMT5 are useful for killing AML tumor cells, and 2) Bergman teaches the PRMT5 inhibitors of the invention can be used to treat AML. Because the prior art recognizes the equivalence of C12 and Bergman’s compound 1 for the purpose of inhibiting PRMT5 in vivo, an express suggestion to substitute one equivalent component or process for another is not necessary to render such substitution obvious. MPEP 2144.06.II.
Claim 30 is rejected under 35 U.S.C. 103 as being unpatentable over Knudsen (US 20090023149 A1, of record) and Tarighat (Somayeh Tarighat Dissertation: Novel epigenetic role and therapeutic targeting of protein arginine methyltransferase 5 (PRMT5) in acute myeloid leukemia, (2014), Ohio State University) as applied to claims 1-2, 5-6, 8, 22-23, 25 and 33 above, and further in view of Machacek (US 20220363707 A1, priority to at least August 5, 2019). This rejection also addresses the elected species of (C) (2R,3R,3aS,6S,6aR)-6-((2-amino-3-bromoquinolin-7-yl)methyl)-2-(4-methyl-7H-pyrrolo[2,3-d]pyrimidin-7-yl)hexahydro-2H-cyclopenta[b]furan-3,3a-diol.
The applied Machacek reference has a common assignee with the instant application. Based upon the earlier effectively filed date of the reference, it constitutes prior art under 35 U.S.C. 102(a)(2). The rejection under 35 U.S.C. 103 below might be overcome by: (1) a showing under 37 CFR 1.130(a) that the subject matter disclosed in the reference was obtained directly or indirectly from the inventor or a joint inventor of this application and is thus not prior art in accordance with 35 U.S.C.102(b)(2)(A); (2) a showing under 37 CFR 1.130(b) of a prior public disclosure under 35 U.S.C. 102(b)(2)(B); or (3) a statement pursuant to 35 U.S.C. 102(b)(2)(C) establishing that, not later than the effective filing date of the claimed invention, the subject matter disclosed and the claimed invention were either owned by the same person or subject to an obligation of assignment to the same person or subject to a joint research agreement. See generally MPEP § 717.02.
The teachings of Knudsen and Tarighat are recited above and applied as for claims 1-2, 5-6, 8, 22-23, 25 and 33. Tarighat also teaches that general down regulation of PRMT5 reduces the growth of several AML cell lines (FIG 2.1.I)
Knudsen and Tarighat do not teach any of the PRMT5 inhibitors recited in claim 30.
Machacek teaches that PRMT5 is a pro-survival factor, which regulates cell proliferation ([0021]). Machacek teaches that PRMT5 is linked to human cancer ([0005]) and is a known target for the identification of novel cancer therapeutics ([0008]). Machacek teaches the synthesis of (2R,3R,3aS,6S,6aR)-6-((2-amino-3-bromoquinolin-7-yl)methyl)-2-(4-methyl-7H-pyrrolo[2,3-d]pyrimidin-7-yl)hexahydro-2H-cyclopenta[b]furan-3,3a-diol, herein referred to as Compound 8 (Example 8, [0717]-[0725]). Machacek teaches Compound 8 inhibits PRMT5 in vivo ([1018], Table 26). Machacek teaches the PRMT5 inhibitors of the invention can be used to treat cancer including AML ([0279]).
It would have been obvious to one skilled in the art before the effective filing dates of the claimed invention to have substituted the C12 PRMT5 inhibitor of Tarighat with Machacek’s Compound 8 in the method of treating an individual having AML with a DNMT3A mutation rendered obvious above. It would have amounted to the simple substitution of one known PRMT5 inhibitor with another known PRMT5 inhibitor by known means to yield predicable results. The skilled artisan would have predicted that Compound 8 could be used to treat an AML-DNMT3A mutation patient because 1) Tarighat teaches that other means to inhibit PRMT5 are useful for killing AML tumor cells, and 2) Machacek teaches the PRMT5 inhibitors of the invention can be used to treat AML. Because the prior art recognizes the equivalence of C12 and Machacek’s compound 8 for the purpose of inhibiting PRMT5 in vivo, an express suggestion to substitute one equivalent component or process for another is not necessary to render such substitution obvious. MPEP 2144.06.II.
Claim 31 is rejected under 35 U.S.C. 103 as being unpatentable over Knudsen (US 20090023149 A1, of record) and Tarighat (Somayeh Tarighat Dissertation: Novel epigenetic role and therapeutic targeting of protein arginine methyltransferase 5 (PRMT5) in acute myeloid leukemia, (2014), Ohio State University) as applied to claims 1-2, 5-6, 8, 22-23, 25 and 33 above, and further in view of Baiocchi (US 20160046578 A1, published February 18, 2016). This is a new rejection of a new claim necessitated by amendment.
The teachings of Knudsen and Tarighat are recited above and applied as for claims 1-2, 5-6, 8, 22-23, 25 and 33. Tarighat also teaches that MV411 cells have an FLT3 internal tandem duplication (FLT3 ITD), which are killed by (i.e., respond to) the PRMT5 C12 inhibitor (Fig 2.3A). Tarighat teaches cells that have a wildtype FLT3 gene require a higher IC50 dose than the FLT3 ITD cell line (Fig 2.3A), indicating that the FLT3 ITD cells are responsive to the PRMT5 inhibitor.
Knudsen and Tarighat do not teach cells or patients comprising both an FLT3 ITD and a DNMT3a mutation.
Baiocchi teaches knocking down expression of PRMT5 (i.e., inhibiting PRMT5) reduces the proliferation capacity of the cells taken from a patient with an FLT3-ITD mutation more than of cells taken from an FLT-WT patient (i.e., the patient’s cells are predicted to respond to the PRMT5 inhibitor when having an FLT3-ITD mutation) (FIG. 29C-D).
It would have been obvious to one skilled in the art before the effective filing date of the claimed invention to have also detected the FLT3 gene status in the method rendered obvious above for claim 1. It would have amounted to measuring two known biomarkers in patients that would be predicted to respond to PRMT5 inhibition and applying that biomarker into a known diagnostic and treatment pipeline. Because both Tarighat and Baiocchi teaches that AML cells having an FLT3-ITD mutation are sensitive to PRMT5 inhibition, the skilled artisan would have predicted that an AML patient with both the DNMT3A and FLT3-ITD mutations would respond to a PRMT5 inhibitor, similar to the cell culture results. The skilled artisan would have been motivated to use a PRMT5 inhibitor to treat patients having a DNMT3A and FLT3-ITD mutation because Tarighat and Baiocchi teaches PRMT5 inhibition is capable of killing tumor cells with the single DNMT3A and FLT3-ITD mutations.
Response to Arguments - §103
Applicant argues that the claimed method is not obvious because Knudson does not teach known biomarkers for responding to PRMT5 inhibition and Tarighat fails to teach that patients with a DNMT3A mutation would be more likely to respond to PRMT5 inhibition (Remarks, pages 19-20). This argument has been fully considered but it is not persuasive because 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). The rejection is based on applying the general method of Knudson of measuring genetic biomarkers for determining the likelihood of drug response to the data shown in Tarighat that AML cells having the DNMT3A mutation respond to PRMT5 inhibitors in culture. As such, Applicant’s arguments are not directed to the merits of the rejection.
Applicant also argues that the obviousness rejection does not specifically indicate why the skilled artisan would only choose patients with a DNMT3a mutations (or those listed in claim 1) for treatment with a PRMT5 inhibitor (Remarks, page 19, ¶4). This argument has been fully considered but is not persuasive because it relies on features that are not recited in the rejected claim(s). Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993). The claims do not recite avoiding treatment of AML patients not having a DNMT3a mutation (or other mutation) with a PRMT5 inhibitor. Because Tarighat teaches that AML cells having a DNMT3a mutation are responsive to a PRMT5 inhibitor, it would have been obvious to treat patients having a DNMT3a mutation with the inhibitor with a reasonable expectation that the patient would be responsive to the inhibitor. Additionally, the new rejection of new claim 31 provides evidence that cancer cell lines and patient cells carrying the FLT3-ITD mutation are more responsive to PRMT5 inhibition than cells that do not carry the FLT3-ITD mutation, giving even more support that pre-clinical evidence provides predictable support for clinical application of the biomarker responsiveness method of Knudson.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1-2, 5-6, 8, 22-23, 25, 31 and 33 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 12,173,026 in view of Knudsen (US 20090023149 A1, of record) and Tarighat (Somayeh Tarighat Dissertation: Novel epigenetic role and therapeutic targeting of protein arginine methyltransferase 5 (PRMT5) in acute myeloid leukemia, (2014), Ohio State University). Claim 31 is further rejected in view of Baiocchi (US 20160046578 A1, published February 18, 2016). This is a maintained rejection and new rejections of new claims necessitated by amendment.
Patented claim 1 recites a compound of Formula I. Patented claim 16 recites the compound of claim 1… which is (2R,3R,3aS,6S,6aR)-6-((2-amino-3-bromoquinolin-7-yl)methyl)-2-(4-methyl-7H-pyrrolo[2,3-d] pyrimidin-7-yl) hexahydro-2H-cyclopenta[b] furan-3,3a-diol (i.e., a PRMT5 inhibitor). Patented claim 18 recites A method for treating cancer comprising administering to a patient in need thereof a compound of claim 1, or a pharmaceutically acceptable salt thereof.
The patented claims do not recite a method for treatment of an AML patient having a biomarker that is predictive of responsiveness to PRMT5 inhibition.
The teachings of Knudson are recited above in paragraph 14 and incorporated here.
The teachings of Tarighat are recited above in paragraphs 16 and 19 and incorporated here.
Regarding claims 1-2, 5-6, 8, 22-23, 25, 30 and 33, it would have been obvious to one of ordinary skill in the art to have amended the patented method of treatment by first detecting a mutation/biomarker in DNMT3A that is R288C as taught in Tarighat before treatment with the patented PRMT5 inhibitors in order to predict the response of the PRMT5 inhibitors according to Knudsen's method of identifying a patient for treatment optimization. It would have amounted to measuring a known biomarker that would be predicted to respond to PRMT5 inhibition and applying that biomarker into a known diagnostic and treatment pipeline. Because Tarighat teaches a cell line comprising a DNMT3A R288C mutation is sensitive to the C12 PRMT5 inhibitor, the skilled artisan would have predicted that an AML patient with the DNMT3A mutation would likewise respond to patented PRMT5 inhibitors. The skilled artisan would have been motivated to do so in order to predict the likelihood of response thereby avoiding treatment and the associated side effects in predicted non-responders.
Regarding new claim 31, the teachings of Baiocchi are recited above in paragraph 37.
It would have been obvious to one skilled in the art before the effective filing date of the claimed invention to have also detected the FLT3 gene status in the variant of the patented method rendered obvious above for claim 1. It would have amounted to measuring two known biomarkers that would be predicted to respond to PRMT5 inhibition and applying that biomarker into a known diagnostic and treatment pipeline. Because both Tarighat and Baiocchi teaches that AML cells having an FLT3-ITD mutation are sensitive to PRMT5 inhibition, the skilled artisan would have predicted that an AML patient with both the DNMT3A and FLT3-ITD mutations would respond to the patented PRMT5 inhibitor, similar to the cell culture results. The skilled artisan would have been motivated to use the patented PRMT5 inhibitor to treat patients having a DNMT3A and FLT3-ITD mutation because Tarighat and Baiocchi teaches PRMT5 inhibition is capable of killing tumor cells with the single DNMT3A and FLT3-ITD mutations.
Response to Arguments - NSDP
Applicant argues the claims are nonobvious over the patented methods for the reasons stated above in the §103 rejection traversal (Remarks, page 20, ¶5). This argument has been fully considered but is not persuasive for the reasons described in response to §103 rejection arguments in paragraphs 39 and 40 above.
Conclusion
No claims are allowable.
THIS ACTION IS MADE FINAL. 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.
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/CATHERINE KONOPKA/Examiner, Art Unit 1635
/ABIGAIL VANHORN/Primary Examiner, Art Unit 1636