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 .
Priority
Should applicant desire to obtain the benefit of foreign priority under 35 U.S.C. 119(a)-(d) prior to declaration of an interference, a certified English translation of the foreign application must be submitted in reply to this action. 37 CFR 41.154(b) and 41.202(e).
Failure to provide a certified translation may result in no benefit being accorded for the non-English application.
A date of 5/20/2022 was used for priority.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 02/20/2024, 05/17/2024, 12/17/2024 are being considered by the examiner.
Claim Interpretation
Claim 32 is a composition claim and thus does not depend on the use of the composition.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 6, 14-15 and 23-3 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while possibly being enabling for acute myelitis, or encephalomyelitis, does not reasonably provide enablement for purulent myelitis. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
[In re Sichert, 196 USPQ 209 (CCPA 1977)]
To be enabling, the specification of the patent must teach those skilled in the art how to make and use the full scope of the claimed invention without undue experimentation. In re Wright, 999 F.2d 1557, 1561 (Fed. Cir. 1993). Explaining what is meant by “undue experimentation,” the Federal Circuit has stated:
The test is not merely quantitative, since a considerable amount of experimentation is permissible, if it is merely , or if the specification in question provides a reasonable amount of guidance with respect to the direction in which the experimentation should proceed to enable the determination of how to practice a desired embodiment of the claimed invention. PPG v. Guardian, 75 F.3d 1558, 1564 (Fed. Cir. 1996).[1]
The factors that may be considered in determining whether a disclosure would require undue experimentation are set forth by In re Wands, 8 USPQ2d 1400 (CAFC 1988) at 1404 where the court set forth the eight factors to consider when assessing if a disclosure would have required undue experimentation. Citing Ex parte Forman, 230 USPQ 546 (BdApls 1986) at 547 the court recited eight factors:
1) the quantity of experimentation necessary,
2) the amount of direction or guidance provided,
3) the presence or absence of working examples,
4) the nature of the invention,
5) the state of the prior art,
6) the relative skill of those in the art,
7) the predictability of the art, and
8) the breadth of the claims.
These factors are always applied against the background understanding that scope of enablement varies inversely with the degree of unpredictability involved. In re Fisher, 57 CCPA 1099, 1108, 427 F.2d 833, 839, 166 USPQ 18, 24 (1970). Keeping that in mind, the Wands factors are relevant to the instant fact situation for the following reasons:
1. The nature of the invention, state and predictability of the art, and relative
skill level
The invention relates to a method for treating and/or preventing purulent myelitis, acute myelitis, or encephalomyelitis in a subject , comprising administering to the subject a therapeutically effective amount of a compound of formula I or a pharmaceutically acceptable salt thereof. The relative skill of those in the art is high, that of an MD or PHD. That factor is outweighed, however, by the unpredictable nature of the art. In fact, the courts have made a distinction between mechanical elements, which function the same in different circumstances, yielding predictable results, and chemical and biological compounds, which often react unpredictably under different circumstances. Nationwide Chem. Corp. v. Wright, 458 F. supp. 828, 839, 192 USPQ 95, 105(M.D. Fla. 1976); Aff’d 584 F.2d 714, 200 USPQ 257 (5th Cir. 1978); In re Fischer, 427 F.2d 833, 839, 166 USPQ 10, 24(CCPA 1970). Thus, the physiological activity of a chemical or biological compound is considered to be an unpredictable art. As illustrative of the state of the art, the examiner cites the fact that while Applicant demonstrated the use of compound of formula I for EAE in mice, spinal cord pathology scores in mice, STАТ3 phosphorylation levels, cell viability in NMO-IgG induced astrocyte injury model, nowhere in the specification did applicant demonstrate the use of a compound of formula I for bacteria that would cause purulent myelitis or purulent myelitis treatment. Since the state of the art teaches that a body’s immune system fights bacteria (Cleveland Clinic, Immune System, 2023) and Egwuagu(Egwuagu et al., Therapeutic targeting of STAT pathwaysin CNS autoimmune diseases, JAK-STAT 2:1, e2413, 2013) teaches that inhibiting the STAT pathway would shut down/ inhibit the immune defense then an inhibitor of STAT pathway would not be enabled for treating purulent myelitis based on the state of the art.
2. The breadth of the claims
The claims are thus very broad insofar as they recite a method for treating and/or preventing purulent myelitis, acute myelitis, or encephalomyelitis in a subject , comprising administering to the subject a therapeutically effective amount of a compound of formula I or a pharmaceutically acceptable salt thereof. Such “treatment” might theoretically be possible for treating acute myelitis, or encephalomyelitis utilizing formula I.
3. The amount of direction or guidance provided and the presence or absence of working examples
The specification provides no direction or guidance for the use of the compound of Formula I for purulent myelitis. No reasonably specific guidance is provided concerning useful therapeutic protocols for all of the disclosed compound of formula I, other than pages 10-32.
4. The quantity of experimentation necessary
Because of the known unpredictability of the art, and in the absence of experimental evidence, no one skilled in the art would accept the assertion that the claimed compound of formula I could be predictably used for the treatment of purulent myelitis as inferred by the claims and contemplated by the specification. Accordingly, the instant claims do not comply with the enablement requirement of §112, since to practice the invention claimed in the patent a person of ordinary skill in the art would have to engage in undue experimentation, with no assurance of success.
[1] As pointed out by the court in In re Angstadt, 537 F.2d 498 at 504 (CCPA 1976), the key word is “undue”, not “experimentation”.
Claim Rejections - 35 USC § 102
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 the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claim(s) 20-22 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by WENYUAN (WENYUAN et al., WO 2020244614 A1, 2020-12-10, IDS).
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).
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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”.
WENYUAN teaches a JAK inhibitor that is also used as a STAT phosphorylation inhibitor. This property is inherent to the compound and one of ordinary skill based on the background of the reference would understand that when it was used to inhibit the JAK/STAT pathway it would also be inhibiting STAT phosphorylation. “Products of identical chemical composition cannot have mutually exclusive properties.” Therefore, if the prior art teaches the identical chemical structure, the properties applicant discloses and/or claims are necessarily present. In re Spada, 911 F. 2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990). 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. This anticipates claims 20-22.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
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) 6, 14-19, 23-31is/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 6, 14-18.
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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”. This helps to teach claims 15, 25.
The reference WENYUAN has been discussed supra and does not disclose purulent myelitis, acute myelitis, or encephalomyelitis (claims 6, 14-15, 23-26) or CNS, autoimmune diseases and 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, 23-31 6.
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). This helps to teach claims 6, 14-15, and 23-26.
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 encephalomyelitis, CNS autoimmune diseases, and 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 encephalomyelitis, autoimmune diseases, and 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.)
Claim(s) 32 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 Chaudhari (Chaudhari et al., Pharmaceutical Excipients: A review IJAPBC – Vol. 1(1), Jan- Mar, 2012).
The WENYUAN reference has been discussed supra and does not disclose pharmaceutical excipients (claim 32).
The reference Chaudhari teaches “Excipients play an important role in formulating a dosage form. These are the ingredients which along with Active Pharmaceutical Ingredients make up the dosage forms. Excipients act as protective agents, bulking agents and can also be used to improve bioavailability of drugs in some instances…”(abstract). This helps to teach claim 32.
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 Chaudhari because WENYUAN teaches pharmaceutically acceptable dosage forms and Chaudhari teaches dosage forms can contain excipients. One would have a reasonable expectation of success because excipients can be as simple as adding a non-toxic solvent such as water for better administration and one would be motivated to do so because excipients have many benefits including easier administration, acting as protective agents and improving bioavailability of drugs.
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 6, 14-32 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) and in view of Chaudhari (Chaudhari et al., Pharmaceutical Excipients: A review IJAPBC – Vol. 1(1), Jan- Mar, 2012).
The patent ‘590 claims:
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The distinguishing feature of claim 20-22 over patent ‘590 lies in that patent ‘590 does not explicitly disclose that the compound is used as a STAT phosphorylation inhibitor. The patent ‘590 has does not disclose The reference WENYUAN has been discussed supra and does not disclose purulent myelitis, acute myelitis, or encephalomyelitis (claims 6, 14-15, 23-26) or CNS, autoimmune diseases and multiple sclerosis (claims 16-19, 27-31), or the specific STAT1, 3, 5 (claim 26).. The patent ‘590 has been discussed supra and does not disclose pharmaceutical excipients (claim 32).
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 encephalomyelitis, CNS autoimmune diseases, and 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 encephalomyelitis, autoimmune diseases, and 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.)
It would have been prima facie obvious to one of ordinary skill in the art to have modified patent ‘590 with Chaudhari because patent ‘590 teaches pharmaceutically acceptable dosage forms and Chaudhari teaches dosage forms can contain excipients. One would have a reasonable expectation of success because excipients can be as simple as adding a non-toxic solvent such as water for better administration and one would be motivated to do so because excipients have many benefits including easier administration, acting as protective agents and improving bioavailability of drugs.
Claims 6, 14-32 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-19 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) and in view of Chaudhari (Chaudhari et al., Pharmaceutical Excipients: A review IJAPBC – Vol. 1(1), Jan- Mar, 2012).
This is a provisional nonstatutory double patenting rejection.
The application ‘186 claims:
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The distinguishing feature of claim 20-22 over application ‘186 lies in that application ‘186 does not explicitly disclose that the compound is used as a STAT phosphorylation inhibitor. The application ‘186 has does not disclose purulent myelitis, acute myelitis, or encephalomyelitis (claims 6, 14-15, 23-26) or CNS autoimmune diseases and multiple sclerosis (claims 16-19, 27-31), or the specific STAT1, 3, 5 (claim 26). The application ‘186 has been discussed supra and does not disclose pharmaceutical excipients (claim 32).
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 20-22 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 encephalomyelitis, CNS autoimmune diseases, and 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 encephalomyelitis, autoimmune diseases, and 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.)
It would have been prima facie obvious to one of ordinary skill in the art to have modified application ‘186 and WENYUAN with Chaudhari because WENYUAN teaches pharmaceutically acceptable dosage forms and Chaudhari teaches dosage forms can contain excipients. One would have a reasonable expectation of success because excipients can be as simple as adding a non-toxic solvent such as water for better administration and one would be motivated to do so because excipients have many benefits including easier administration, acting as protective agents and improving bioavailability of drugs.
Conclusion
Claims 6 and 14-32are rejected.
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/A.A.S./ Examiner, Art Unit 1627
/Kortney L. Klinkel/ Supervisory Patent Examiner, Art Unit 1627