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 .
Election/Restrictions and Claim Status
Applicant’s amendments and arguments filed 8/21/26 are acknowledged. Any objection or rejection from the 5/21/26 office action that is not addressed below is withdrawn based on the amendments.
Previously, compound 18 and short bowel syndrome were elected. Claim 15 recites additional features in addition to ‘short bowel syndrome’ and requires features in addition to the elected species. In order to advance prosecution, claim 15 is included in the instant examination. Claim 3 does not read on the elected species because a subject with short bowel syndrome would not necessarily have had a colostomy or ileostomy.
Claim 3 is withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected species, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 4/9/26.
Claims 11-12 and 16-17 have been canceled.
Claims 1-2, 4-10 and 13-15 are being examined.
Priority
The priority information is found in the filing receipt dated 8/14/24.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 8/21/26 has been considered by the examiner.
Claim Rejections - 35 USC § 103
The 103 rejection below is maintained from the previous office action.
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) 1-2, 4-10 and 13-15 is/are rejected under 35 U.S.C. 103 as being unpatentable over Due Larsen et al. (WO 2018/104561 as cited with IDS 1/5/24; ‘Larsen’) in view of Massironi et al. (cited C38 of IDS 1/5/24; ‘Massironi’).
Larsen teach compounds that have agonist activity at the GLP-1 and GLP-2 receptors for the treatment of intestinal damage (abstract). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen recognizes that beneficial effects of other GLP-2 analogues including for treating short bowel syndrome (page 60 lines 14-22). Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27) and inflammatory bowel disease (claim 57). Larsen teach methods of synthesizing the peptides (pages 65-68). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80). Larsen teach the stability of compound 18 (Table 4 page 79). Larsen teach that compound 18 was active at both GLP-1 and GLP-2 (Table 2 page 76). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15). Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph). Larsen teach the use of a therapeutically effective amount (page 58). Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph). Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
Larsen does not teach an example of administration to a patient who has undergone surgical resection of the bowel.
Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of Larsen because Larsen teach compounds that have agonist activity at the GLP-1 and GLP-2 receptors for the treatment of intestinal damage (abstract) and teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80) so one would have been motivated to use such compound. Since Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract) one would have been motivated to administer to such subjects based on the benefits disclosed by Larsen. Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20) so one would have been motivated to dose appropriately. One would have had a reasonable expectation of success because Larsen teach methods of synthesizing the peptides (pages 65-68) Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80).
In relation to the administration of claim 1, Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80).
In relation to the compound of claim 1, Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15).
In relation to the subject of claim 1, Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine (abstract).
In relation to claim 2, Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53).
In relation to the outcomes of claims 4-9, Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15) which is the same as the elected compound. Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph). Larsen teach the use of a therapeutically effective amount (page 58). Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph). Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
In relation to claim 10, Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
In relation to claim 13, Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph).
In relation to claim 14, Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph).
In relation to claim 15, Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27) and inflammatory bowel disease (claim 57). Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract).
Response to Arguments - 103
Applicant's arguments filed 8/11/26 have been fully considered but they are not persuasive.
Although applicants argue that the claims have been amended to specify treating diarrhea and/or incontinence, it is first noted that claim 1 still recites ‘treatment and/or prevention’. Further, the amended claims are addressed above. Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27)
Although applicants argue that Larsen teach 68 alternate compounds, MPEP 2123 recognizes that references are prior art for all that they contain.
Although applicants argue that compound 18 is not the best based on certain tables or examples, compound 18 was included in example 5 (pages 79-80) and Table 5 shows that compound 18 reduced fasting blood glucose and increased small intestine wet weight (page 80). There is nothing provided in the data to discredit the use of compound 18.
Although applicants argue that Larsen teach alternate ailments, MPEP 2123 recognizes that references are prior art for all that they contain. Claims 48-49, 52-53 and 57 of Larsen suggest specific methods including treatment of short bowel syndrome (claims 49, 53 and 57)
Although applicants argue that there is no motivation to combine Massironi, Larsen teach compounds that have agonist activity at the GLP-1 and GLP-2 receptors for the treatment of intestinal damage (abstract) and teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Since Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract) one would have been motivated to administer to such subjects based on the benefits disclosed by Larsen.
Although applicants argue that Massironi alone does not teach the invention, the instant rejection is a multiple reference 103 rejection and as such any single reference does not necessarily anticipate the claim.
Although applicants argue that Massironi does not discuss GLP-1/GLP-2 agonists compared to teduglutide, the instant claims are not drawn to methods of comparing to teduglutide.
Although applicants argue that the application provides data to confirm the ability of compound 18 to treat, it is noted that there is no current enablement or scope of enablement rejection. A mere confirmation of an ability to treat is not necessarily enough to overcome a prima facie base of obviousness.
Double Patenting
The double patenting rejections below are maintained from the previous office action.
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, 4-10 and 13-15 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-4 and 7-16 of copending Application No. 17906888 (888) in view of Due Larsen et al. (WO 2018/104561 as cited with IDS 1/5/24; ‘Larsen’) in view of Massironi et al. (cited C38 of IDS 1/5/24; ‘Massironi’).
This is a provisional nonstatutory double patenting rejection.
888 recites methods of administering compound 18 and refer to ameliorating a loss of intestinal mass (claim 1) and refers to a patient with short bowel syndrome (claim 2). 888 recites a pharmaceutical composition (claim 9) and particular doses (claims 10 and 16).
888 does not recite surgical resection or a period of days of the doses.
Larsen teach compounds that have agonist activity at the GLP-1 and GLP-2 receptors for the treatment of intestinal damage (abstract). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen recognizes that beneficial effects of other GLP-2 analogues including for treating short bowel syndrome (page 60 lines 14-22). Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27) and inflammatory bowel disease (claim 57). Larsen teach methods of synthesizing the peptides (pages 65-68). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80). Larsen teach the stability of compound 18 (Table 4 page 79). Larsen teach that compound 18 was active at both GLP-1 and GLP-2 (Table 2 page 76). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15). Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph). Larsen teach the use of a therapeutically effective amount (page 58). Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph). Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 888 because Larsen teach the same compound (compound 18). Thus one would have been motivated to use known methods and conditions. Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20) so one would have been motivated to dose appropriately. Since Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract) one would have been motivated to administer to such subjects based on the benefits disclosed by Larsen. One would have had a reasonable expectation of success because Larsen teach methods of synthesizing the peptides (pages 65-68) Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80). Further, 888 recites for ameliorating certain effects (claim 1).
In relation to the administration of claim 1, 888 teach administration (claim 1). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80).
In relation to the compound of claim 1, 888 teach compound 18 (claim 1). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15).
In relation to the subject of claim 1, 888 teach short bowel syndrome (claim 2). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine (abstract).
In relation to claim 2, 888 teach short bowel syndrome (claim 2). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53).
In relation to the outcomes of claims 4-9, 888 teach compound 18 (claim 1). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15) which is the same as the elected compound. Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph). Larsen teach the use of a therapeutically effective amount (page 58). Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph). Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
In relation to claim 10, Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
In relation to claim 13, Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph).
In relation to claim 14, Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph).
In relation to claim 15, Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27) and inflammatory bowel disease (claim 57). Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract).
Claims 1-2, 4-10 and 13-15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-45 of U.S. Patent No. 11,395,847 (as cited with IDS 1/5/24; ‘847’) in view of Due Larsen et al. (WO 2018/104561 as cited with IDS 1/5/24; ‘Larsen’) in view of Massironi et al. (cited C38 of IDS 1/5/24; ‘Massironi’).
847 recites a method of increasing intestinal mass by administering a dual agonist (claim 44). 847 recites compound 18 (claim 41).
847 does not recite surgical resection or short bowel syndrome or a period of days of the doses.
Larsen teach compounds that have agonist activity at the GLP-1 and GLP-2 receptors for the treatment of intestinal damage (abstract). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen recognizes that beneficial effects of other GLP-2 analogues including for treating short bowel syndrome (page 60 lines 14-22). Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27) and inflammatory bowel disease (claim 57). Larsen teach methods of synthesizing the peptides (pages 65-68). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80). Larsen teach the stability of compound 18 (Table 4 page 79). Larsen teach that compound 18 was active at both GLP-1 and GLP-2 (Table 2 page 76). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15). Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph). Larsen teach the use of a therapeutically effective amount (page 58). Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph). Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 847 because Larsen teach the same compound (compound 18) and also teach for improving the intestine. Thus one would have been motivated to use known methods and conditions. Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20) so one would have been motivated to dose appropriately. Since Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract) one would have been motivated to administer to such subjects based on the benefits disclosed by Larsen. One would have had a reasonable expectation of success because Larsen teach methods of synthesizing the peptides (pages 65-68) Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80).
In relation to the administration of claim 1, 847 teach administration (claim 44). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80).
In relation to the compound of claim 1, 847 teach compound 18 (claim 41). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15).
In relation to the subject of claim 1, Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine (abstract).
In relation to claim 2, Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53).
In relation to the outcomes of claims 4-9, Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15) which is the same as the elected compound. Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph). Larsen teach the use of a therapeutically effective amount (page 58). Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph). Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
In relation to claim 10, Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
In relation to claim 13, Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph).
In relation to claim 14, Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph).
In relation to claim 15, Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27) and inflammatory bowel disease (claim 57). Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract).
Claims 1-2, 4-10 and 13-15 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-32 of copending Application No. 17834062 (062) in view of in view of Due Larsen et al. (WO 2018/104561 as cited with IDS 1/5/24; ‘Larsen’) in view of Massironi et al. (cited C38 of IDS 1/5/24; ‘Massironi’).
This is a provisional nonstatutory double patenting rejection.
062 recites methods of treating short bowel syndrome comprising administering compound 18 (claim 32).
062 does not recite surgical resection or a period of days of the doses.
Larsen teach compounds that have agonist activity at the GLP-1 and GLP-2 receptors for the treatment of intestinal damage (abstract). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen recognizes that beneficial effects of other GLP-2 analogues including for treating short bowel syndrome (page 60 lines 14-22). Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27) and inflammatory bowel disease (claim 57). Larsen teach methods of synthesizing the peptides (pages 65-68). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80). Larsen teach the stability of compound 18 (Table 4 page 79). Larsen teach that compound 18 was active at both GLP-1 and GLP-2 (Table 2 page 76). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15). Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph). Larsen teach the use of a therapeutically effective amount (page 58). Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph). Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 062 because Larsen teach the same compound (compound 18). Thus one would have been motivated to use known methods and conditions. Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20) so one would have been motivated to dose appropriately. Since Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract) one would have been motivated to administer to such subjects based on the benefits disclosed by Larsen. One would have had a reasonable expectation of success because Larsen teach methods of synthesizing the peptides (pages 65-68) Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80).
In relation to the administration of claim 1, 062 teach administration (claim 32). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80).
In relation to the compound of claim 1, 062 teach compound 18 (claim 32). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15).
In relation to the subject of claim 1, 062 teach short bowel syndrome (claim 32). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine (abstract).
In relation to claim 2, 062 teach short bowel syndrome (claim 32). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53).
In relation to the outcomes of claims 4-9, 062 teach compound 18 (claim 32). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15) which is the same as the elected compound. Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph). Larsen teach the use of a therapeutically effective amount (page 58). Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph). Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
In relation to claim 10, Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
In relation to claim 13, Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph).
In relation to claim 14, Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph).
In relation to claim 15, Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27) and inflammatory bowel disease (claim 57). Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract).
Claims 1-2, 4-10 and 13-15 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2, 7-9, 11-13, 15, 20, 22, 30-32 and 37-42 of copending Application No. 19236746 (746) in view of in view of Due Larsen et al. (WO 2018/104561 as cited with IDS 1/5/24; ‘Larsen’) in view of Massironi et al. (cited C38 of IDS 1/5/24; ‘Massironi’).
This is a provisional nonstatutory double patenting rejection.
746 recites methods of treating short bowel syndrome and increasing intestinal mass comprising administering compound CPD1OH (claim 37).
746 does not recite surgical resection or a period of days of the doses.
Larsen teach compounds that have agonist activity at the GLP-1 and GLP-2 receptors for the treatment of intestinal damage (abstract). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen recognizes that beneficial effects of other GLP-2 analogues including for treating short bowel syndrome (page 60 lines 14-22). Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27) and inflammatory bowel disease (claim 57). Larsen teach methods of synthesizing the peptides (pages 65-68). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80). Larsen teach the stability of compound 18 (Table 4 page 79). Larsen teach that compound 18 was active at both GLP-1 and GLP-2 (Table 2 page 76). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15). Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph). Larsen teach the use of a therapeutically effective amount (page 58). Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph). Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 746 because Larsen teach the same compound (compound 18 is the same as CPD1OH). Thus one would have been motivated to use known methods and conditions. Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20) so one would have been motivated to dose appropriately. Since Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract) one would have been motivated to administer to such subjects based on the benefits disclosed by Larsen. One would have had a reasonable expectation of success because Larsen teach methods of synthesizing the peptides (pages 65-68) Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80).
In relation to the administration of claim 1, 746 teach administration (claim 37). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80).
In relation to the compound of claim 1, 746 teach compound CPD1OH (claim 1). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15).
In relation to the subject of claim 1, 746 teach short bowel syndrome (claim 37). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine (abstract).
In relation to claim 2, 746 teach short bowel syndrome (claim 37). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53).
In relation to the outcomes of claims 4-9, 746 teach compound CPD1OH (claim 1). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15) which is the same as the elected compound. Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph). Larsen teach the use of a therapeutically effective amount (page 58). Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph). Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
In relation to claim 10, Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
In relation to claim 13, Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph).
In relation to claim 14, Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph).
In relation to claim 15, Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27) and inflammatory bowel disease (claim 57). Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract).
Claims 1-2, 4-10 and 13-15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-25 of U.S. Patent No. 12576025 (025) in view of Due Larsen et al. (WO 2018/104561 as cited with IDS 1/5/24; ‘Larsen’) in view of Massironi et al. (cited C38 of IDS 1/5/24; ‘Massironi’).
025 recites a method of treating short bowel syndrome by administering a composition (claim 23) that contains CPD10H (claim 1).
025 does not recite surgical resection or a period of days of the doses.
Larsen teach compounds that have agonist activity at the GLP-1 and GLP-2 receptors for the treatment of intestinal damage (abstract). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen recognizes that beneficial effects of other GLP-2 analogues including for treating short bowel syndrome (page 60 lines 14-22). Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27) and inflammatory bowel disease (claim 57). Larsen teach methods of synthesizing the peptides (pages 65-68). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80). Larsen teach the stability of compound 18 (Table 4 page 79). Larsen teach that compound 18 was active at both GLP-1 and GLP-2 (Table 2 page 76). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15). Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph). Larsen teach the use of a therapeutically effective amount (page 58). Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph). Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 025 because Larsen teach the same compound (compound 18 is the same as CPD1OH). Thus one would have been motivated to use known methods and conditions. Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20) so one would have been motivated to dose appropriately. Since Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract) one would have been motivated to administer to such subjects based on the benefits disclosed by Larsen. One would have had a reasonable expectation of success because Larsen teach methods of synthesizing the peptides (pages 65-68) Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80).
In relation to the administration of claim 1, 025 teach administration (claim 23). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80).
In relation to the compound of claim 1, 025 teach compound CPD1OH (claim 1). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15).
In relation to the subject of claim 1, 025 teach short bowel syndrome (claim 23). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine (abstract).
In relation to claim 2, 025 teach short bowel syndrome (claim 23). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53).
In relation to the outcomes of claims 4-9, 025 teach compound CPD1OH (claim 1). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15) which is the same as the elected compound. Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph). Larsen teach the use of a therapeutically effective amount (page 58). Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph). Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
In relation to claim 10, Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
In relation to claim 13, Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph).
In relation to claim 14, Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph).
In relation to claim 15, Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27) and inflammatory bowel disease (claim 57). Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract).
Claims 1-2, 4-10 and 13-15 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4-6 and 11-18 of copending Application No. 17906871 (871) in view of in view of Due Larsen et al. (WO 2018/104561 as cited with IDS 1/5/24; ‘Larsen’) in view of Massironi et al. (cited C38 of IDS 1/5/24; ‘Massironi’).
This is a provisional nonstatutory double patenting rejection.
871 recites methods of administering compound 18 to subjects who have undergone surgical resection of the bowel (claim 1) and who have short bowel syndrome (claim 6) that is secondary to inflammatory bowel disease (claim 14). 871 recites specific amounts (claim 17) and a pharmaceutical composition (claim 16).
871 does not recite a period of days of the doses.
Larsen teach compounds that have agonist activity at the GLP-1 and GLP-2 receptors for the treatment of intestinal damage (abstract). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen recognizes that beneficial effects of other GLP-2 analogues including for treating short bowel syndrome (page 60 lines 14-22). Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27) and inflammatory bowel disease (claim 57). Larsen teach methods of synthesizing the peptides (pages 65-68). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80). Larsen teach the stability of compound 18 (Table 4 page 79). Larsen teach that compound 18 was active at both GLP-1 and GLP-2 (Table 2 page 76). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15). Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph). Larsen teach the use of a therapeutically effective amount (page 58). Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph). Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 871 because Larsen teach the same compound (compound 18). Thus one would have been motivated to use known methods and conditions. Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20) so one would have been motivated to dose appropriately. Since Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract) one would have been motivated to administer to such subjects based on the benefits disclosed by Larsen. One would have had a reasonable expectation of success because Larsen teach methods of synthesizing the peptides (pages 65-68) Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80).
In relation to the administration of claim 1, 871 teach administration (claim 1). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Larsen teach that 100 nmol/kg was administered daily to mice and that administration of compound 18 results in small intestinal weight gain (example 5 and Table 5 pages 79-80).
In relation to the compound of claim 1, 871 teach compound 18 (claim 1). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15).
In relation to the subject of claim 1, 871 teach short bowel syndrome (claim 14). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53). Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine (abstract).
In relation to claim 2, 871 teach short bowel syndrome (claim 14). Larsen teach methods of treating short bowel syndrome comprising administering a compound (page 18 lines 15-19, page 19 lines 9-23, page 61 lines 16-20 and claims 49 and 53).
In relation to the outcomes of claims 4-9, 871 teach compound 18 (claim 1). Larsen teach the sequence of compound 18 as Hy-H[Aib]EGSFTSELATILD[K([17-carboxy-heptadecanoyl]isoGlu)]QAARDFIAWLIQHKITD-OH (page 15) which is the same as the elected compound. Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph). Larsen teach the use of a therapeutically effective amount (page 58). Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph). Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
In relation to claim 10, Larsen teach the use of an appropriate dosing regimen and refers to maintenance doses (page 59 lines 10-20).
In relation to claim 13, Larsen teach the composition as a pharmaceutical composition (page 18 first paragraph).
In relation to claim 14, Larsen specifically teach between 50 pmol/kg and 0.1 umol/kg body weight (page 59 first paragraph).
In relation to claim 15, Larsen teach applications for treating diarrhea (page 61 lines 16-24 and page 62 lines 21-27) and inflammatory bowel disease (claim 57). Massironi teach that short bowel syndrome is a result of the loss of bowel mass mostly secondary to surgical resection of the small intestine and other causes include inflammatory bowel disease (abstract).
Response to Arguments – double patenting
Applicant's arguments filed 8/11/26 have been fully considered but they are not persuasive.
Although applicants argue that the claims are amended, the amended claims are addressed above.
Although applicants refer to arguments above, those arguments are addressed above and are not found persuasive.
Conclusion
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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RONALD T. NIEBAUER
Primary Examiner
Art Unit 1658
/RONALD T NIEBAUER/Examiner, Art Unit 1658
Prosecution Insights