DETAILED ACTION
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 05/13/2026 has been entered.
Status of the Application
Receipt is acknowledged of Applicants’ amendment, filed on 05/13/2026, in which claim 1 is amended and claims 15 and 24-31 are cancelled. Claims 1-14, 16-23, and 32-48 are pending.
Claims 16-23 and 32-48 are withdrawn from consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim in the office action of 05/28/2025.
Claims 1-14 are examined on the merits herein.
Priority
The instant application is a 371 of PCT/CA2020/050447 filed on 04/03/2020, which claims foreign priority to United Kingdom 1904758.8 filed on 04/04/2019.
Rejections Withdrawn
Applicant’s amendment and remarks, filed 05/13/2026, with respect that claims 1-10 are rejected under 35 U.S.C. 103 as being unpatentable over Friend in view of Larsbrink and Periasamy has been fully considered and is withdrawn in favor of the new rejection below. This rejection has been withdrawn.
Applicant’s amendment and remarks, filed 05/13/2026, with respect that claims 11-14 are rejected under 35 U.S.C. 103 as being unpatentable over Friend in view of Larsbrink and Periasamy as applied to claims 1-10 further in view of Berry and Accetto has been fully considered and is withdrawn in favor of the new rejection below. This rejection has been withdrawn.
The following are new grounds of rejection.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 1-10 are rejected under 35 U.S.C. 103 as being unpatentable over Nakamura (US 2007/0173461 A1; IDS 04/26/2023) in view of Larsbrink et al. (Nature, 2014; PTO-892 10/28/2024) and Periasamy et al. (Journal of Functional Foods, 2018; PTO-892 10/28/2024).
Nakamura teaches that 5-Aminosalicylic acid (5-ASA) is useful for treating inflammatory bowel diseases including ulcerative colitis and Crohn's disease [0004]. However, orally administered 5-ASA is rapidly and completely absorbed in the upper part of the small intestine, and little 5-ASA, which exhibits its effect by the local action on the inflammatory site, is delivered to the large intestine of the affected site [0005]. Nakamura teaches that prodrugs of 5-ASA have thus been studied in order to deliver 5-ASA to the large intestine [0006].
Nakamura discloses a therapeutic agent for ulcerative colitis which allows 5-aminosalicylic acid (5-ASA) to be efficiently delivered to the large intestine almost without being absorbed or metabolized in the stomach or the upper part of the small intestine and is safe and can be administered over a long term. This compound is degraded by the intestinal bacterial flora, whereby 5-ASA as the active ingredient can be produced in the large intestine (abstract). Compounds of Nakamura are shown below ([0001] and [0003]), which show glycoside prodrugs of 5-ASA connected by a β-glycosidic bond to glucose or galactose.
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307
1411
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Greyscale
Nakamura further teaches that the compound may be administered as an oral tablet [0047] formulated using an excipient [0051].
The teachings of Nakamura differ from that of the instantly claimed invention in that Nakamura does not teach that the prodrug comprises xyloglucan.
Larsbrink discloses a study of xyloglucan (XyG) metabolism in human gut Bacteroidetes and demonstrates that a single, complex gene locus confers XyG catabolism in in Bacteroides ovatus, a common colonic symbiont (page 498, paragraph 1). Larsbrink teaches that the vanguard role in XyG utilization by B. ovatus is performed by the versatile endo-xyloglucanase BoGH5A (paragraph bridging pages 499-500). Chromogenic XyGO aryl β-glycoside substrates were used to determine enzyme activity, which indicated that the enzyme productively harnesses the Xylα(1→6) side chains for catalysis (page 506, paragraph 3). The 2-chloro-4-nitrophenol
glycoside substrates GGGG-β-CNP, XXXG-β-CNP and XLLG-β-CNP were synthesized, (methods, page 2, paragraph 1). Assays using these CNP-glycosides were monitored continuously by spectrophotometer for the release of 2-chloro-4-nitrophenolate (methods, page 2, paragraph 13). Larsbrink teaches that these compounds, including XXXG-β-CNP, are substrates for the enzyme BoGH5A (Extended data table 1). Larsbrink teaches that tamarind kernel xyloglucan is cleaved by BoGH5A (page 499, paragraph 1), and includes XXXG xyloglucans (Figure 1).
Periasamy discusses the mucoadhesive role of Tamarind xyloglucan, which attenuates inflammation via the TLR4/NF-κB signaling pathway (abstract). Periasamy teaches that xyloglucan extracted from tamarind seed (section 2.2 on page 3) decreases inflammation of the colon and enhances the healing of ulcerative colitis (paragraph 1 of section 4 on page 3), and that it is not digested by small intestinal enzymes, but rather reaches the colon unaltered (paragraph 2 found on page 2).
A person of ordinary skill in the art before the effective filing date of the invention would have been motivated to exchange the glucose or galactose in the 5-ASA glycoside prodrug of Nakamura with the tamarind seed XXXG xyloglucan of Larsbrink in order to achieve a prodrug with the additional benefit of enhances the healing of ulcerative colitis because Periasamy teaches that tamarind seed xyloglucan decreases inflammation of the colon. One of ordinary skill in the art would have a reasonable expectation of success because Nakamura teaches a β-glycosidic prodrug degraded by the intestinal bacterial flora, whereby 5-ASA as the active ingredient can be produced in the large intestine, Larsbrink teaches that XXXG β-glycoside substrates are cleaved by the endo-xyloglucanase BoGH5A of a common colonic symbiont, and Periasamy teaches that xyloglucan reaches the colon unaltered.
Claims 11-14 are rejected under 35 U.S.C. 103 as being unpatentable over Nakamura (US 2007/0173461 A1; IDS 04/26/2023) in view of Larsbrink et al. (Nature, 2014; PTO-892 10/28/2024) and Periasamy et al. (Journal of Functional Foods, 2018; PTO-892 10/28/2024) as applied to claim 9 above, further in view of Berry et al. (US 9610307 B2; PTO-892 10/28/2024) and Accetto (Systematic and Applied Microbiology, 2019; PTO-892 10/28/2024).
The combined teachings of Nakamura, Larsbrink, and Periasamy are as above.
The combined teachings of Nakamura, Larsbrink, and Periasamy differ from that of the instantly claimed invention in that they do not teach a composition which further comprises a probiotic or a pre-biotic polysaccharide.
Berry provides compositions containing microbial entities that me be used to treat disorders of the local or systemic microbiome (abstract). The therapeutic compositions contain probiotic, non-pathogenic bacterial populations for the treatment of diseases, in particular immune and inflammatory diseases (col. 2, lines 6-11). These compositions may be used to treat patients suffering from, among others, Crohn’s disease, inflammatory bowel disease, and ulcerative colitis (col. 19, lines 4-8). Berry teaches that the probiotic bacterial species may include, among others, Bacteroides ovatus (col. 30, lines 17-18). Berry further teaches that the bacteria may be Prevotella sp. bacteria (Table 1 on beginning at col. 101, including Prevotella copri (Table 1 at col. 103). The compositions may further comprise prebiotics in conjunction with microbial populations (col. 2, lines 11-14). Prebiotics can include complex carbohydrates, amino acids, peptides, or other nutritional components useful for the survival of the bacterial composition. The prebiotic may be, among others, xylooligosaccharides (co. 53, lines 17-24).
Accetto discusses the polysaccharide utilization loci of Prevotella bacteria in mammalian rumen and hindgut (abstract). Accetto teaches that Prevotella species have been routinely shown to degrade xyloglucan (page 112, paragraph 3), this includes Prevotella copri (Table 1) which is found in the human microbiome (page 112, paragraph 1).
It would have been prima facie obvious before the effective filing date of the claimed invention for a person of ordinary skill in the art to combine the xyloglucan glycoside suggested by the combined teachings of Nakamura, Larsbrink, and Periasamy, with a composition comprising a probiotic bacterial such as Prevotella copri and a pre-biotic polysaccharide such as xylooligosaccharide to obtain the predictable result of a composition for treating inflammatory bowel disease such as ulcerative colitis, because both compositions are suggested as being useful for the same purpose of treating an inflammatory bowel disease. One of ordinary skill in the art would have a reasonable expectation of success because Accetto teaches that Prevotella copri is a xyloglucan degrading bacteria found in the human microbiome and Berry teaches that the prebiotic may be a nutritional component useful for the survival of the bacterial composition.
Response to Arguments
Applicant's arguments filed 05/13/2026 have been fully considered but they are not persuasive.
Insofar as Applicant’s arguments are applicable to the current rejections, Applicant argues that the prior art does not teach methodology for attaching an XXXG oligosaccharide to a drug aglycone via a β-glycosidic bond (remarks, page 11, paragraph 1). This is not persuasive.
As discussed in the above grounds of rejections, Larsbrink teaches the formation of β-glycosides which comprise a bond between an XXXG oligosaccharide and an aryl compound that is cleaved to give the phenolate. Nakamura teaches prodrugs comprising a β-glycosidic bond between a glycone and 5-aminosalicylic acid. Thus the 5-ASA comprises a similar phenol core structure to that of the aglycones of Larsbrink such that one of ordinary skill in the art would have had a reasonable expectation of success in synthesizing the suggested compound using the methodology of Larsbrink to synthesize an XXXG-β-5-ASA compound. Furthermore, the instant claims are drawn to prodrug compounds comprising xyloglucan rather than methods of synthesizing and thus do not require a particular synthetic route.
Applicant argues that the prior art does not suggest that the prodrug will be cleaved by an endo-xyloglucanase (Remarks, page 12, paragraph 2). This is not persuasive.
As discussed in the above grounds of rejection, the glycosides of Larsbrink including XXXG-β-CNP are taught as being cleaved by the endo-xylogluconase BoGH5A to give the 2-chloro-4-nitrophenolate, which is cleavage of the β-glycosidic bond to release the aglycone. Thus one of ordinary skill in the art would have expected that the suggested compound would be cleaved by the endo-xylogluconase BoGH5A.
Applicant further argues that to prior art does not suggest a xylose-containing prodrug and does not provide an expectation of success in the use of complex branched oligosaccharides (Remarks, page 132, paragraph 3). This is not persuasive.
MPEP 2123(I) states that "The use of patents as references is not limited to what the patentees describe as their own inventions or to the problems with which they are concerned. They are part of the literature of the art, relevant for all they contain...A reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill in the art. MPEP2123(II) states that "Disclosed examples and preferred embodiments do not constitute a teaching away from a broader disclosure or nonpreferred embodiments." The teachings of Nakamura as a whole suggest a 5-ASA glycoside prodrug which is degraded by the intestinal bacterial flora such that the 5-ASA is delivered to provide local action on the inflammatory site in the large intestine. One of ordinary skill in the art would have had a reasonable expectation of success in substituting the glucose or galactose sugars of Nakamura with the XXXG of Larsbrink to achieve the predictable result of a colon targeting 5-ASA prodrug because Larsbrink teaches that XXXG β-glycoside substrates are cleaved by the endo-xyloglucanase BoGH5A of a common colonic symbiont, and Periasamy teaches that xyloglucan reaches the colon unaltered. Thus the teachings of the prior art as a whole render prima facie obvious the instantly claimed invention.
Conclusion
No claims are allowed.
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/S.G.H./Examiner, Art Unit 1693
/SCARLETT Y GOON/Supervisory Patent Examiner
Art Unit 1693
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