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 election with traverse of compound 18 and short bowel syndrome in the reply filed on 4/9/26 is acknowledged. The traversal is on the ground(s) that a patient with short bowel syndrome may have had a colostomy. This is not found persuasive because instant claim 1 generically recites ‘surgical resection’. Claim 15 is evidence that claim 1 is generic with respect to the surgical resection. MPEP 808.01(a) expressly recognizes that where there is no disclosure of a relationship between species they are independent. In the instant case, there is no disclosure of a relationship of all the species (such as those recited in claim 15) nor is there any indication that they are obvious variants. An argument that some type of condition ‘may’ occur is not a disclosure that it necessarily occurs or that there is a relationship of all the species.
The requirement is still deemed proper and is therefore made FINAL.
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Claim 3 is withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected species, there being no allowable generic or linking claim.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 statements (IDS) submitted on 1/5/24, 1/26/24, 4/9/24, 7/23/24, 1/13/25, 6/30/25, 7/17/25, 11/12/25, 12/30/25 and 4/9/26 have been considered by the examiner.
Specification
The disclosure is objected to because of the following informalities:
37 CFR 1.821(d) states that each occurrence of a sequence should include the corresponding sequence identifier. In the instant case, pages 26-31 of the specification recite sequences but do not recite the corresponding sequence identifiers.
Appropriate correction is required.
Claim Objections
Claim 1 is objected to because of the following informalities:
37 CFR 1.821(d) states that each occurrence of a sequence should include the corresponding sequence identifier. In the instant case, claim 1 recites a sequence but does not recite the corresponding sequence identifier.
Appropriate correction is required.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 1-2, 4-10 and 13-15 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Instant claim 1 refers to an agonist that comprises “[17-carboxy-heptadecanoyl]-isoGlu”. The instant specification refers to “[17-carboxy-heptadecanoyl]-isoGlu” and depicts (page 17 first paragraph):
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The structure as required by claim 1 is unclear. The structure in the specification shown above for “[17-carboxy-heptadecanoyl]-isoGlu” does not depict any nitrogens or oxygens and does not even show all of the molecules connected together. It is unclear if applicants are intending to be their own lexicographer and redefine certain terms known in the art. None of the dependent claims clarify the claim scope.
Claim 1 lines 1-2 refer to “loose”, “high” and “urgency”. Although the specification further describes certain terms (page 3) the scope of such terms remains subjective. The terms are relative terms which renders the claim indefinite. The terms are not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention. None of the dependent claims clarify the claim scope. Instant claim 8 refers to a score which is described on page 5 but such scale is also based on subjective determinations.
Regarding claim 14, the phrase "preferably" renders the claim indefinite because it is unclear whether the limitation(s) following the phrase are part of the claimed invention. See MPEP § 2173.05(d). MPEP § 2173.05(d) states that preferences are properly set forth in the specification rather than the claims.
Regarding claim 15, the phrase "for example" (which appears in lines 4 and 8) renders the claim indefinite because it is unclear whether the limitation(s) following the phrase are part of the claimed invention. See MPEP § 2173.05(d).
Claim 15 recites “small intestine damage Crohn’s disease”. The meaning of such phrase is unclear. It is unclear if multiple conditions are required or if a comma is missing. The last recited options in claim 15 are not separated by ‘and’ or ‘or’. It is unclear if the list is open ended or closed.
Although unclear, the claims have been given the broadest reasonable interpretation consistent with the specification. With respect to “[17-carboxy-heptadecanoyl]-isoGlu” such term has been interpreted consistent with the prior art teachings.
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) 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).
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1-2, 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).
Conclusion
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RONALD T. NIEBAUER
Primary Examiner
Art Unit 1658
/RONALD T NIEBAUER/Examiner, Art Unit 1658
Prosecution Insights