DETAILED ACTION
All rejections and objections not mentioned below have been withdrawn.
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 .
Priority
A date of 5/20/2022 was used for priority.
While the applicants remarks (05/01/2026) mention providing the English translation of the priority documents no translated priority documents were provided.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 02/20/2024, 05/17/2024, 12/17/2024, 05/01/2026 are being considered by the examiner.
Claim Rejections - 35 USC § 103 – updated due to amendments
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.
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.
Claim(s) 16-19, 27-31, 33-34 is/are rejected under 35 U.S.C. 103 as being unpatentable over WENYUAN (WENYUAN et al., WO 2020244614 A1, 2020-12-10, IDS) in view of Egwuagu(Egwuagu et al., Therapeutic targeting of STAT pathwaysin CNS autoimmune diseases, JAK-STAT 2:1, e2413, 2013).
The reference WENYUAN teaches “The present invention relates to a pyrrolopyrimidine compound used as a JAK inhibitor, and the use thereof in the preparation of a drug for treating a JAK1- and/or JAK2-associated disease; and specifically relates to a compound represented by formula (I), an isomer thereof or a pharmaceutically acceptable salt thereof” (abstract) and “Janus kinases (JAKs) are cytoplasmic tyrosine kinases that can transmit cytokine signals. From membrane receptors to STAT transcription factors. The JAK family consists of four members, JAK1, JAK2, JAK3 and TYK2. The JAK-STAT pathway transmits extracellular signals from a variety of cytokines, growth factors and hormones to the nucleus, and is responsible for the expression of thousands of protein-coding genes. The JAK-STAT pathway involves several steps in converting extracellular signals into transcriptional responses: 1) When the cytokine receptors on the cell surface bind to their respective cytokine ligands, the conformation changes and the receptor molecules dimerize. This allows the JAK kinases coupled to the receptor to approach each other and activate through interactive tyrosine phosphorylation. 2) After JAK is activated, the tyrosine residues on the catalytic receptor undergo phosphorylation modification, and then these phosphorylated tyrosine sites and the surrounding amino acid sequence form a "docking site", which also contains the SH2 structure Domain STAT proteins are recruited to this "berthing site". 3) Finally, the kinase JAK catalyzes the phosphorylation modification of the STAT protein bound to the receptor. After the activated STAT protein leaves the receptor and forms a dimer, it is transferred to the nucleus to regulate the transcription of specific genes. JAK-STAT intracellular signal transduction serves interferons, most interleukins, and a variety of cytokines and endocrine factors, such as EPO, TPO, GH, OSM, LIF, CNTF, GM-CSF and PRL (Vainchenker WE Tal. (2008)”(page 1). The reference WENYUAN teaches the compound of instant formula I (reference claim 7, shown below). This helps to teach claims 16-18.
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The reference WENYUAN teaches “The term "pharmaceutically acceptable" used here refers to those compounds, materials, compositions and/or dosage forms that are within the scope of reliable medical judgment and are suitable for use in contact with human and animal tissues. , Without excessive toxicity, irritation, allergic reactions or other problems or complications, commensurate with a reasonable benefit/risk ratio. The term "pharmaceutically acceptable salt" refers to a salt of the compound of the present invention, which is prepared from a compound with specific substituents discovered in the present invention and a relatively non-toxic acid or base. When the compound of the present invention contains a relatively acidic functional group, a base addition salt can be obtained by contacting the compound with a sufficient amount of base in a pure solution or a suitable inert solvent… Examples of pharmaceutically acceptable acid addition salts include … such as acetic acid, propionic acid, isobutyric acid, maleic acid, malonic acid, benzoic acid, succinic acid, suberic acid, Similar acids such as fumaric acid, lactic acid, mandelic acid, phthalic acid, benzenesulfonic acid, p-toluenesulfonic acid, citric acid, tartaric acid and methanesulfonic acid; also include salts of amino acids (such as arginine, etc.) , …”[0034-0035] and “Test compounds 1-13 were dissolved in [5% DMSO, 95% (12% SBE) -β-CD), 0.5% MC)] In a mixed vehicle, and orally administered to female Lewis rats twice a day (the number of test animals in each dose group is 8). The administration was continued for two weeks, during which the state of the rats was observed, and the swelling of the foot volume was recorded and scored”.
The reference WENYUAN teaches “Thirteen days after modeling, rats were divided into groups and given the corresponding test compounds. For example, different doses were given to rats (specific doses are shown in Table 4-2; test compounds 1-13 were dissolved in a mixed solvent of [5% DMSO, 95% (12% SBE-β-CD), 0.5% MC)] and administered orally to female Lewis rats twice daily (8 test animals in each dose group)”[0121] and “Conclusion: Compound 1-13 of the present invention exhibits significant therapeutic effects at doses (3 mg/kg and 10 mg/kg) (inhibition rate P<0.0001 compared with vehicle control group), and compound 1-13 of the present invention exhibits good results The positive correlation of the effect of dose (3mg/kg and 10mg/kg)”[0128]. "[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation." In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955.) This helps to teach claims 18-19, 29-30.
The reference WENYUAN has been discussed supra and does not disclose multiple sclerosis (claims 16-19, 27-31), or the specific STAT1, 3, 5 (claim 26).
The reference Egwuagu teaches “Therapeutic targeting of STAT pathways in CNS
autoimmune diseases”(title) and “Upon binding of the cytokine to its cognate receptor, JAKs are activated by transphosphorylation, providing docking sites for recruitment of specific members of the STAT family of transcription factors. STATs recruited to the receptor complex are phosphorylated at a critical tyrosine residue, form homo- or hetero-dimers and translocate into the nucleus where they bind to specific DNA sequences and activate gene transcription”(page 1). The reference also teaches “However, unbridled activation of STATs by pro-inflammatory cytokines or growth factors contributes to pathogenic autoimmunity”(abstract) and “Detection of IL-12 and IFN--y in MS lesions or vitreous of patients with active uveitis, together with reports of upregulated expression of pSTAT1, pSTAT4 and T-bet in PBMC of patients with relapsing-remitting multiple sclerosis, provided strong support for the role of Thl cells in MS and uveitis” (page 4). The reference also teaches “Uveitis and multiple sclerosis
are classical T cell mediated CNS autoimmune diseases that provide useful framework for understanding cross-talk between cytokines secreted by cells of the innate system (IL-12, IL-23 and IL-27) and cytokines produced by adaptive immune cells (IL-2, IL-17 and IFN--y) . The fact that these cytokines, as well as, neuronal-protective cytokines (CNTF, IGF-1, OSM and LIF) utilize STAT pathways, provides opportunity to study how aberrant regulation of ST AT pathways contribute to pathogenic autoimmunity and other neurodegenerative diseases”(page 2) and “As IL-12 is required for the development of Thl cells,
it was therefore expected that IL--12 administration would have disease-enhancing effects. Thus, Curcumin, a naturally occurring polyphenolic phytochemical was tested and shown to inhibit
EAE by blocking IL--12-induced activation of the STAT4 transcription factor”(page 5). This helps to teach claims 16-19, 27-31, 33-34.
The reference Egwuagu teaches “STAT4-deficient mice are defective in Thl differentiation and are highly resistant to the induction of EAE, suggesting that it may be beneficial to target STAT4 pathways in T cells as a treatment for EAE”(page 5) and “Experimental autoimmune encephalomyelitis (EAE), induced in various rodent models by immunization with spinal cord or brain homogenate in CFA, has provided valuable insights into immunopathogenic mechanisms of MS”(page 2). The reference also teaches “SOCSl-KIR (consisting of the kinase inhibitory region of SOCSl) and TKIP (complementary to the auto-phosphorylation site of JAK2) peptides inhibit STAT 1 activation/phosphorylation, and have been shown to be efficacious in the prevention and treatment of EAE”(table 1).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified WENYUAN with Egwuagu because both teach the relationship of the JAK/STAT pathway (including STAT1) and diseases associated with upregulation pSTAT (phosphorylated STAT) that are connected to that pathway. WENYUAN discloses that the compound of formula I can be used for treating and/or preventing diseases associated with JAK1 and/or JAK2. Moreover, JAK kinases are directly related to STAT phosphorylation, and WENYUAN also teaches the relationship between the two in the background art. Therefore, a person skilled in the art would have been motivated to use the compound disclosed in WENYUAN in the preparation of a STAT phosphorylation inhibitor with reasonable expectation of success because it is taught as a JAK inhibitor and the kinase JAK catalyzes the phosphorylation modification of the STAT protein bound to the receptor. Thus it would be obvious that inhibiting JAK kinases would manufacture a STAT phosphorylation inhibitor because it would reduce STAT phosphorylation. One would be motivated to do so to treat diseases associated with the JAK-STAT pathway. Egwuagu suggests that when treating multiple sclerosis it may be beneficial to target the STAT pathway; thus it would be obvious with a reasonable expectation of success to use inhibitors of that pathway as suggested and discussed by WENYUAN such as JAK inhibitors that will inhibit STAT to pSTAT (phosphorylated STAT), especially to decrease abnormal upregulation. One would be motivated to do so to treat multiple sclerosis as they are taught to be directly related to that pathway abnormal regulation. Furthermore, "[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation." In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955.)
Double Patenting – updated due to amendments
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 16-19, 27-31, 33-34 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-17 of U.S. Patent No. 12351590 B2 in view of Egwuagu(Egwuagu et al., Therapeutic targeting of STAT pathways in CNS autoimmune diseases, JAK-STAT 2:1, e2413, 2013).
The patent ‘590 claims:
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The distinguishing feature of over patent ‘590 lies in that patent ‘590 does not multiple sclerosis (claims 16-19, 27-31, 33-34 ), or the specific STAT1, 3, 5 (claim 26).
The secondary references further teach that all needed changes would be obvious as outlined in the 103 rejection (which is incorporated herein by reference).
It would have been prima facie obvious to one of ordinary skill in the art to have modified patent ‘590 with Egwuagu because patent ‘590 teaches JAK inhibitors and Egwuagu teaches the relationship of the JAK/STAT pathway (including STAT1) and diseases associated with upregulation pSTAT (phosphorylated STAT) that are connected to that pathway. Egwuagu suggests that when treating multiple sclerosis it may be beneficial to target the STAT pathway; thus it would be obvious with a reasonable expectation of success to use inhibitors of that pathway as suggested and discussed by patent ‘590 such as JAK inhibitors that will inhibit STAT to pSTAT (phosphorylated STAT), especially to decrease abnormal upregulation. One would be motivated to do so to treat multiple sclerosis as it is taught to be directly related to that pathway abnormal regulation. Furthermore, "[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation." In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955.)
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified WENYUAN with Egwuagu because both teach the relationship of the JAK/STAT pathway (including STAT1) and diseases associated with upregulation pSTAT (phosphorylated STAT) that are connected to that pathway. WENYUAN discloses that the compound of formula I can be used for treating and/or preventing diseases associated with JAK1 and/or JAK2. Moreover, JAK kinases are directly related to STAT phosphorylation, and WENYUAN also teaches the relationship between the two in the background art. Therefore, a person skilled in the art would have been motivated to use the compound disclosed in WENYUAN in the preparation of a STAT phosphorylation inhibitor with reasonable expectation of success because it is taught as a JAK inhibitor and the kinase JAK catalyzes the phosphorylation modification of the STAT protein bound to the receptor. Thus it would be obvious that inhibiting JAK kinases would manufacture a STAT phosphorylation inhibitor because it would reduce STAT phosphorylation. One would be motivated to do so to treat diseases associated with the JAK-STAT pathway. Egwuagu suggests that when treating multiple sclerosis it may be beneficial to target the STAT pathway; thus it would be obvious with a reasonable expectation of success to use inhibitors of that pathway as suggested and discussed by WENYUAN such as JAK inhibitors that will inhibit STAT to pSTAT (phosphorylated STAT), especially to decrease abnormal upregulation. One would be motivated to do so to treat multiple sclerosis as they are taught to be directly related to that pathway abnormal regulation. Furthermore, "[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation." In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955.)
Claims 16-19, 27-31, 33-34 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3-9, and 11-19 of copending Application No. 18/254,186 in view of WENYUAN (WENYUAN et al., WO 2020244614 A1, 2020-12-10, IDS) in view of Egwuagu(Egwuagu et al., Therapeutic targeting of STAT pathways in CNS autoimmune diseases, JAK-STAT 2:1, e2413, 2013).
This is a provisional nonstatutory double patenting rejection.
The application ‘186 claims:
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The application ‘186 has does not disclose multiple sclerosis (claims 16-19, 27-31, 33-34 ), or the specific STAT1, 3, 5 (claim 26).
The secondary references further teach that all needed changes would be obvious as outlined in the 103 rejection (which is incorporated herein by reference).
It would have been prima facie obvious to one of ordinary skill in the art to have modified application ‘186 with WENYUAN to obtain instant claims because WENYUAN discloses the compound of formula I and so does application ‘186 and WENYUAN discloses it can be used for treating and/or preventing diseases associated with JAK1 and/or JAK2. Moreover, JAK kinases are directly related to STAT phosphorylation, and WENYUAN also teaches the relationship between the two in the background art. Therefore, a person skilled in the art would have been motivated to use the compound disclosed in WENYUAN in the preparation of a STAT phosphorylation inhibitor with reasonable expectation of success because it is taught as a JAK inhibitor and the kinase JAK catalyzes the phosphorylation modification of the STAT protein bound to the receptor. Thus it would be obvious that inhibiting JAK kinases would manufacture a STAT phosphorylation inhibitor because it would reduce STAT phosphorylation. One would be motivated to do so to treat diseases associated with the JAK-STAT pathway.
It would have been prima facie obvious to one of ordinary skill in the art to have modified application ‘186 and WENYUAN with Egwuagu because WENYUAN teaches JAK inhibitors and Egwuagu teaches the relationship of the JAK/STAT pathway (including STAT1) and diseases associated with upregulation pSTAT (phosphorylated STAT) that are connected to that pathway. Egwuagu suggests that when treating multiple sclerosis it may be beneficial to target the STAT pathway; thus it would be obvious with a reasonable expectation of success to use inhibitors of that pathway as suggested and discussed by WENYUAN such as JAK inhibitors that will inhibit STAT to pSTAT (phosphorylated STAT), especially to decrease abnormal upregulation. One would be motivated to do so to treat multiple sclerosis as it is taught to be directly related to that pathway abnormal regulation. Furthermore, "[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation." In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955.)
Allowable Subject Matter
Claims 6, 14-15, 23-26 allowed.
Applicant’s arguments, see page 11, point (b), filed 05/01/2026, with respect to Claims 6, 14-15, 23-26 have been fully considered and are persuasive. The rejection of claims 6, 14-15, 23-26 from the previous office action has been withdrawn.
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Response to Arguments
Applicant's arguments filed 05/01/2026 have been fully considered but they are not persuasive.
The applicant argues that:
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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).
In response to the excellent technical effect argument or in other words unexpected results argument, these arguments are not persuasive because one would expect the compound to treat multiple sclerosis as suggested by Egwuagu so this is not unexpected and additionally unexpected results must be commensurate in scope to the instant claims. The data in the examples are only shown for certain concentrations and thus are not commensurate in scope with the claims. Additionally, table 10 indicates that the ‘unexpected’ activity of the compound is a concentration dependent property as several concentrations allow for compound I to produce basically the same outcome as the control drug and thus does not give unexpected results under all conditions claimed. Whether the unexpected results are the result of unexpectedly improved results or a property not taught by the prior art, the "objective evidence of nonobviousness must be commensurate in scope with the claims which the evidence is offered to support." In other words, the showing of unexpected results must be reviewed to see if the results occur over the entire claimed range. In re Clemens, 622 F.2d 1029, 1036, 206 USPQ 289, 296 (CCPA 1980) (Claims were directed to a process for removing corrosion at "elevated temperatures" using a certain ion exchange resin (with the exception of claim 8 which recited a temperature in excess of 100C). See also In re Peterson, 315 F.3d 1325, 1329-31, 65 USPQ2d 1379, 1382-85 (Fed. Cir. 2003) (data showing improved alloy strength with the addition of 2% rhenium did not evidence unexpected results for the entire claimed range of about 1-3% rhenium); In re Grasselli, 713 F .2d 731,741,218 USPQ 769, 777 (Fed. Cir. 1983) (Claims were directed to certain catalysts containing an alkali metal. Evidence presented to rebut an obviousness rejection compared catalysts containing sodium with the prior art. The court held this evidence insufficient to rebut the prima facie case because experiments limited to sodium were not commensurate in scope with the claims.). To establish unexpected results over a claimed range, applicants should compare a sufficient number of tests both inside and outside the claimed range to show the criticality of the claimed range. In re Hill, 284 F.2d 955, 128 USPQ 197 (CCPA 1960).
The applicant argues that:
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This argument is not persuasive for two reasons first Egwuagu does suggest multiple sclerosis and the combination does suggest using formula I for the treatment of MS as pointed out in the 103 above. Secondly, Attachments 1-2 are not persevere because no where in the references does it mention that the compound of formula I work as a TNF-blocking agent and thus would not be presumed to have the same issues as a TNF-blocking agent.
The applicant argues that:
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This argument is not persuasive because Egwuagu suggests that when treating multiple sclerosis it may be beneficial to target the STAT pathway; thus it would be obvious with a reasonable expectation of success to use inhibitors of that pathway as suggested and discussed by WENYUAN such as JAK inhibitors that will inhibit STAT to pSTAT (phosphorylated STAT), especially to decrease abnormal upregulation. "Obviousness does not require absolute predictability of success.” Id. at 903, 7 USPQ2d at 1681". Thus given the suggestion to treat that condition based on the STAT pathway one would have had a reasonable expectation but not a guarantee of success.
Conclusion
Claims 16-19, 27-31, 33-34 are rejected.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/A.A.H./ Examiner, Art Unit 1627
/Kortney L. Klinkel/ Supervisory Patent Examiner, Art Unit 1627
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