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 .
*Notice to Applicant*
The Examiner notes that the instant Office Action supersedes the Office Action mailed 31 December 2025. The time for reply restarts with the mailing of the instant Office Action.
Foreign Priority
The present application claims priority to the following applications: KR 10-2021-0044583
and PCT/KR2022/004621, with effective filing dates of 6 April 2021 and 31 March 2022, respectively.
Claim Status
This Office Action is in response to Applicant’s Amendment filed, 5 October 2023, wherein the Applicant canceled claims 1-14 and added new claims 15-21.
Claims 15-21 are pending.
Information Disclosure Statement
The Information Disclosure Statement filed 5 October 2023 and the references cited therein have been considered, unless indicated otherwise.
Specification
The specification (including the abstract and claims), and any amendments for applications, except as provided for in 37 CFR 1.821 through 1.825, must have text written plainly and legibly either by a typewriter or machine printer in a nonscript type font (e.g., Arial, Times Roman, or Courier, preferably a font size of 12) lettering style having capital letters which should be at least 0.3175 cm. (0.125 inch) high, but may be no smaller than 0.21 cm. (0.08 inch) high (e.g., a font size of 6) in portrait orientation and presented in a form having sufficient clarity and contrast between the paper and the writing thereon to permit the direct reproduction of readily legible copies in any number by use of photographic, electrostatic, photo-offset, and microfilming processes and electronic capture by use of digital imaging and optical character recognition; and only a single column of text. See 37 CFR 1.52(a) and (b).
1. The application papers are objected to because Tables 2-8 are unclear and thus illegible. A legible substitute specification in compliance with 37 CFR 1.52(a) and (b) and 1.125 is required.
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.
2. Claims 15 and 17 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for treating, does not reasonably provide enablement for preventing a kidney disease, wherein the kidney disease comprises one or more selected from the group consisting of acute kidney injury, end-stage kidney disease, renal failure, systemic lupus erythematosus, diabetic renal disease, IgA nephritis, HIV-related nephropathy, chronic kidney disease, focal segmental glomerulosclerosis, minimal change nephrotic syndrome, and xanthine oxidase deficiency or treating xanthine oxidase deficiency. 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.
The criteria for enablement set out in the In re Wands, MPEP § 2164.01(a), considers the
following factors:
Breadth of the Claims
The instant claims are directed to a method of preventing or treating a kidney disease comprising administering (R)-4-{(R)-1-[7-(3,4,5-trimethoxy-phenyl)-[1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one. Thus, encompassing any kidney disease, and in particular, acute kidney injury, end-stage kidney disease, renal failure, systemic lupus erythematosus, diabetic renal disease, IgA nephritis, HIV-related nephropathy, chronic kidney disease, focal segmental glomerulosclerosis, minimal change nephrotic syndrome, and xanthine oxidase deficiency.
As such, the breadth of the claims is great.
Level of Skill in the Art
The level of skill in the art is a clinician or an artisan with a PhD.
State of the Art
Hoffmann (U.S. Patent No. 8,969,568, issued 3 Mar 2015) specifically teaches (R)-4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one:
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, which has (R,R) stereochemistry and activity against the kinase, Syk (Example 35, column 163; column 2, lines 19-22). However, Hoffman is silent to utilizing R)-4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one to treat kidney disease.
Lee (U.S. Patent No. 10,174,000, issued 8 Jan 2019) teaches compounds of a similar structure:
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, with activity against the kinase, IRAK4 (column 14 lines 60). Further, Zarrin (Nature Reviews: Drug Discovery, 2021, 20, 39-63) teaches that selective inhibition of kinases remains challenging, because most kinase inhibitors are aimed to bind to the kinase pocket to compete with the ATP-binding site, which is highly conserved across the kinome (page 43, column 1, paragraph 2). Additionally, Lee teaches a method of treating acute kidney injury, IgA nephropathy, HIV associated nephropathy, diabetic nephropathy, focal segmental glomerulosclerosis, and systemic lupus erythematosus via their substituted 1,6-napthyridine compounds (column 25, lines 14-29; column 23, lines 27-29).
However, Sebesta (“Hereditary xanthinuria,” Orphanet, 2012, < www.orpha.net/en/disease/detail/3467>, accessed 21 Jan 2026) teaches xanthinuria (xanthine oxidase deficiency) is a rare disease, characterized by failure to degrade hypoxanthine and xanthine to uric acid, leading to accumulation of xanthine (page 1, paragraph 1; page 2, paragraph 3). Currently, there is no curative treatment for xanthine oxidase deficiency (page 3, paragraph 3). Conversely, Higgins (Cardiovascular Psychiatry and Neurology, 2009, 282059, 1-9) teaches that xanthine oxidase inhibitors are common and used to treat gout, nephropathy, and renal stone disease (page 1, column 1, paragraph 1). Further, Higgins teaches that xanthine oxidase metabolizes xanthine to uric acid and that uric acid crystals induce inflammation and are linked to gout and proinflammatory cytokines (page 1, column 1, paragraph 3; page 1, column 2, paragraph 1; page 2, column 2, paragraph 2). Thus, xanthine oxidase deficiency results from too little uric acid, but xanthine oxidase inhibition is a treatment of too much uric acid.
Predictability in the Art
Regarding treating a kidney disease, Lee teaches acute kidney injury, IgA nephropathy, HIV associated nephropathy, diabetic nephropathy, focal segmental glomerulosclerosis, and systemic lupus erythematosus via their substituted 1,6-napthyridine compounds (column 25, lines 14-29; column 23, lines 27-29).
Regarding xanthine oxidase deficiency, there is no known cure, underscoring the unpredictability of the art (Sebesta, page 3, paragraph 3).
Regarding preventing a kidney disease, while there are methods to prevent the progression of a kidney disease, there are currently no known methods of administering a small molecule to prevent onset of a kidney disease (page 2, paragraph 2; Broad Institute of MIT and Harvard, "New compound stops progressive kidney disease in its tracks," ScienceDaily, 2017, http://www.sciencedaily.com/releases/2017/12/171207141711>, accessed 21 Jan 2026).
Working Examples
While the instant specification teaches administration of (R)-4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one to treat mice with diabetic renal diseases as compared to the control group (page 32, lines 4-14), the instant specification does not teach treating xanthine oxidase deficiency via administration of (R)-4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one, nor prevention of a kidney disease, in particular a kidney disease, wherein the kidney disease comprises one or more selected from the group consisting of acute kidney injury, end-stage kidney disease, renal failure, systemic lupus erythematosus, diabetic renal disease, IgA nephritis, HIV-related nephropathy, chronic kidney disease, focal segmental glomerulosclerosis, minimal change nephrotic syndrome, and xanthine oxidase deficiency.
Thus, it is not possible to determine all the kidney diseases that can be prevented by (R)-4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one nor all the methods to treat xanthine oxidase deficiency.
Quality of Experimentation
The amount of experimentation required to determine which kidney disease to prevent, how to prevent any kidney disease, how to treat xanthine oxidase deficiency, in what amounts, what order, would be astronomical. A skilled artisan would be required to start with proof -of-concept and proceed through all levels of lead identification and optimization, which is invention and not development; this is undue amount of experimentation.
As such, while the specification is enabling for a method of treating a kidney disease via administration of (R)-4-{(R)-1-[7-(3,4,5-trimethoxy-phenyl)-[1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one, wherein the kidney disease comprises one or more selected from the group consisting of acute kidney injury, end-stage kidney disease, renal failure, systemic lupus erythematosus, diabetic renal disease, IgA nephritis, HIV-related nephropathy, chronic kidney disease, focal segmental glomerulosclerosis, and minimal change nephrotic syndrome, it does not reasonably provide enablement for preventing a kidney disease, wherein the kidney disease comprises one or more selected from the group consisting of acute kidney injury, end-stage kidney disease, renal failure, systemic lupus erythematosus, diabetic renal disease, IgA nephritis, HIV-related nephropathy, chronic kidney disease, focal segmental glomerulosclerosis, minimal change nephrotic syndrome, and xanthine oxidase deficiency or treating xanthine oxidase deficiency.
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
3. Claim 16 is rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Claim 15 recites a method of treating a kidney disease via administrating the stereoisomer: (R)-4-{(R)-1-[7-(3,4,5-trimethoxy-phenyl)-[1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one. However, claim 16 specifies the structure:
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, which is racemic. Thus, claim 16 expands the scope of the claim upon which it depends.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
4. Claims 15-18 and 21 are rejected under 35 U.S.C. 103 as being unpatentable over Hoffmann (U.S. Patent No. 8,969,568, issued 3 Mar 2015) in view of Lee (U.S. Patent No. 10,174,000, issued 8 Jan 2019), as evidenced by Zarrin (Nature Reviews: Drug Discovery, 2021, 20, 39-63).
Hoffmann teaches substituted naphthyridines and their use as medicaments (abstract).
Hoffmann specifically teaches (R)-4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one:
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, which has (R,R) stereochemistry and activity against the kinase, Syk (Example 35, column 163; column 2, lines 19-22).
Regarding claim 1, Hoffmann fails to teach the use of compound 35 for treating or preventing kidney disease.
Lee teaches a method of treating a subject with compounds containing a 1,6- naphthyridine core with a pyrrolidone-substituted ether at the 5-position that can be used for treating renal/kidney disease (column 23, lines 10-12; column 14, line 60; column 23, lines 22; column 25, lines 14-29).
Lee specifically teaches compounds of Formula IIc:
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, with activity against the kinase, IRAK4 (column 14 lines
60). Kinases are known to be promiscuous, as evidenced by Zarrin (Nature Reviews: Drug Discovery, 2021, 20, 39-63). Zarrin teaches that selective inhibition of kinases remains challenging, because most kinase inhibitors are aimed to bind to the kinase pocket to compete with the ATP-binding site, which is highly conserved across the kinome (page 43, column 1, paragraph 2). Zarrin also teaches that IRAK4 and Syk are two kinases that affect autoimmune and inflammatory diseases (abstract).
It would have been obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention to select the compound of Hoffmann and the methods of treating of Lee to arrive at instant claim 15. One of ordinary skill in the art would have been motivated to make such a selection, with a reasonable expectation of success, because:
-Hoffmann teaches 1,6-naphthyridine compounds that have activity against the protein kinase Syk,
-Lee teaches compounds containing a 1,6-naphthyridine core with a pyrrolidone- substituted ether at the 5-position (i.e. similar structures) that can be used for treating renal/kidney disease,
-Lee teaches protein kinases are families of enzymes that catalyze phosphorylation of highly conserved, specific residues in proteins and that dysregulation of kinases is believed to underlie the causes of many diseases (as evidenced by Zarrin), and
-Lee teaches targeting the innate immune system with small molecule inhibitors (column 1, lines 26-28).
As such, an artisan having ordinary skill in the art would have been motivated to make such a selection to predictably arrive at a method of preventing or treating kidney disease via (R)- 4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one.
Regarding claim 16, Hoffmann teaches compound 35:
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, (Example 35, column 163).
Regarding claim 17, Lee teaches a method of treating acute kidney injury, IgA nephropathy, HIV associated nephropathy, diabetic nephropathy, focal segmental glomerulosclerosis, and systemic lupus erythematosus via their substituted 1,6-napthyridine compounds (column 25, lines 14-29; column 23, lines 27-29).
Regarding claim 18, Lee teaches the kidney disease is diabetic nephropathy (column 25, lines 21-22).
Regarding claim 21, Lee teaches that the compound is administered with the following therapeutic agent: cromolyn (column 31, lines 16-18 and 30).
5. Claim 19 is rejected under 35 U.S.C. 103 as being unpatentable over Hoffmann (U.S. Patent No. 8,969,568, issued 3 Mar 2015) and Lee (U.S. Patent No. 10,174,000, issued 8 Jan 2019), as evidenced by Zarrin (Nature Reviews: Drug Discovery, 2021, 20, 39-63), as applied to claims 15-18 and 21 above, and further in view of Havasi (Kidney International, 2011, 80, 29-40).
Hoffmann (U.S. Patent No. 8,969,568, issued 3 Mar 2015) and Lee (U.S. Patent No. 10,174,000, issued 8 Jan 2019) are applied as discussed in the 35 U.S.C. 103 rejection above.
Regarding claim 19, while the combination of Hoffmann and Lee teach a method of treating kidney disease via (R)-4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]- ethyl}pyrrolidin-2-one, they differ from that of the instantly claimed invention in that they do not explicitly teach a method of treating a subject requiring inhibiting apoptosis of the renal medulla.
It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to exemplify the compound of Hoffmann and method of treating of Lee with the method of treating kidney disease via inhibiting apoptosis of the renal medulla, as taught by Havasi, to arrive at the instantly claimed invention (page 32, column 1, paragraph 1).
One of ordinary skill in the art would have been motivated to make a method of treating kidney disease that inhibits apoptosis with a reasonable expectation of success, because Havasi teaches methods of reducing apoptosis in the proximal tubule in the cortex and outer medulla to improve renal function after ischemia (page 32, column 1, paragraph 1). Havasi specifically teaches that inhibiting apoptosis appears to be critical, because circulating factors released by the injured kidney induce apoptosis and inflammation in distant organs, including the heart, lung, liver, and brain, contributing to the high morbidity and mortality associated with acute kidney injury (abstract). Thus, one of ordinary skill in the art would have been motivated to make such a selection, to predictably arrive at instant claim 19: a method of treating a subject requiring inhibiting apoptosis of the renal medulla.
6. Claim 20 is rejected under 35 U.S.C. 103 as being unpatentable over Hoffmann (U.S. Patent No. 8,969,568, issued 3 Mar 2015) and Lee (U.S. Patent No. 10,174,000, issued 8 Jan 2019), as evidenced by Zarrin (Nature Reviews: Drug Discovery, 2021, 20, 39-63), as applied to claima 15-18 and 21 above, and further in view of Kletzmayr (ACS Pharmacology & Translational Science, 2020, 3, 1339-1351).
Hoffmann (U.S. Patent No. 8,969,568, issued 3 Mar 2015) and Lee (U.S. Patent No. 10,174,000, issued 8 Jan 2019) are applied as discussed in the 35 U.S.C. 103 rejection above.
Regarding claim 20, while the combination of Hoffmann and Lee teach a method of treating kidney disease via (R)-4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]- ethyl}pyrrolidin-2-one, they differ from that of the instantly claimed invention in that they do not explicitly teach a method of treating a subject requiring inhibiting calcification of the renal medulla.
It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to exemplify the compound of Hoffmann and method of treating of Lee with the method of treating kidney disease via inhibiting calcification of the renal medulla, as taught by Kletzmayr, to arrive at the instantly claimed invention (page 1340, column 2, paragraph 2; page 1347, column 1, paragraph 5; page 1349, column 2, paragraph 1).
One of ordinary skill in the art would have been motivated to make a method of treating kidney disease that inhibits calcification with a reasonable expectation of success, because Kletzmayr teaches methods of inhibiting calcification in chronic kidney disease via small molecule, (OEG2)2-IP4 in a dose-dependent fashion (page 1347, column 1, paragraph 5).
Additionally, Kletzmayr teaches precipitation and growth of calcium phosphate in renal tubules causes tissue damage and increased risk of chronic kidney disease; further, Kletzmayr discloses concerns about animal kidney calcification models accurately recapitulating human disease progression, which further impedes inhibitor development (page 1339, column 1, paragraph 1; page 1339, column 2, paragraph 1). Kletzmayr then teaches that the translational value of their developed calcification profiling platform, which evaluated the cortex and cortico-medullary junction separately (page 1340, column 2, paragraph 2; column 1349, column 2, paragraph 1).
Thus, one of ordinary skill in the art would have been motivated to make such a selection, to predictably arrive at instant claim 20: a method of treating a subject requiring inhibiting calcification of the renal medulla.
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.
7. Claims 15-18 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 7, and 10 of copending Application No. 18/286,068 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
U.S. Application No. 18/286,068 claims a method for treating diabetes and reducing kidney damage, comprising administering (R)-4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one (claims 1, 2, and 7 of ‘068). Further, ‘068 teaches a pharmaceutical composition for treating diabetic peripheral neuropathy via administering (R)-4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one (claim 10 of ‘068).
Regarding claim 15, ‘068 teaches a method of treating kidney damage (i.e. a kidney disease) via administering (R)-4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one (claims 1, 2, and 7 of ‘068).
Regarding claim 16, ‘068 teaches administering (R)-4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one (claims 1, 2, and 7 of ‘068).
Regarding claim 17, ‘068 teaches administering (R)-4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one to treat diabetic neuropathy (claim 10 of ‘068), which is a diabetic renal disease (as defined by claim 18 of the instant claims).
Regarding claim 18, ‘068 teaches administering (R)-4- {(R)- 1-[7-(3 ,4,5-trimethoxy-phenyl)-[ 1,6] naphthyridin-5-yloxy]-ethyl}pyrrolidin-2-one to treat diabetic neuropathy (claim 10 of ‘068).
Conclusion
No claim is allowed.
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/MADELINE M. DEKARSKE/Examiner, Art Unit 1622
/JAMES H ALSTRUM-ACEVEDO/Supervisory Patent Examiner, Art Unit 1622