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
Applicant’s election of Group IV and species of bacterial which is a combination of Streptococcus Salivarius, Streptococcus parasanguinis, Haemophilus parainfluenzae, Ruminococcus albus, Ruminococcus Callidus, Ruminococcus bromii, Ruminococcus gnavus, and Bifidobacterium bifidum in the reply filed on 11/4/2025 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)).
All previous claims were cancelled and all currently pending claims ultimately depend from claim 13 and are drawn to the invention of Group IV.
Specification
The use of the terms on p. 67, second paragraph, Dynabeads and Microlab, each of which is a trade name or a mark used in commerce, has been noted in this application. The term should be accompanied by the generic terminology; furthermore the term should be capitalized wherever it appears or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the term.
Although the use of trade names and marks used in commerce (i.e., trademarks, service marks, certification marks, and collective marks) are permissible in patent applications, the proprietary nature of the marks should be respected and every effort made to prevent their use in any manner which might adversely affect their validity as commercial marks.
The disclosure is objected to because of the following informalities: On p. 72, line 23, in “a more rejection”, the “a” should be deleted or the phrase replaced by “greater”. On p. 73, line 2 and 4, “Fig. S1” and on line 6, “Fig. S2” are reference but there is no such figures. The specification lists (not in order) Tables 1, 3 and 5-11 but there is no Table 4. On p. 74, line 6 and 15, “Table 12 “is referenced but there is no such table. The legend of Table 10 (p. 83) says, “The top three bacteria species (*) are based…”, however, there are no asterisks in the Table.
Appropriate correction is required.
Claim Objections
Claims 47-49 are objected to because of the following informalities: In claims 47-49, lines 3, “lesser” should be --less--.
Claim Rejections - 35 USC § 112(b)
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 13, 37, 39-41, 45, 50 and dependent claims 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.
Claim 13 is indefinite because it recites in (ii) “identifying that the stool sample contains an increased or decreased level of the one or more candidate bacterial strains,…” Claim 13 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being incomplete for omitting essential steps, such omission amounting to a gap between the steps. See MPEP § 2172.01. The omitted steps are: determining whether the sample contains an increased verse a decreased level of candidate bacterial strain. That is, there is no step for that determination, for example, there is no comparison to a control-type level that would allow the skilled artisan to determine there is a difference representing an increase or decrease in the level in the stool sample from the patient. The terms “increased” or “decreased” are relative terms and without knowing what the bacterial strain(s) level is being compared to, the skilled artisan cannot determine if there is a change in level.
Claims 37 and 45 are indefinite because they recite at the end “who is not suffering from IBD or ulcerative colitis”. As stated in the specification on p. 1, lines 9-10, “Inflammatory bowel disease (IBD), which encompasses Crohn's disease and ulcerative colitis (UC),…” Therefore, if the patient is not suffering from IBD, then necessarily they are not suffering from UC. As a result, the current phrasing is confusing.
Claims 39-41 recites the limitation "the baseline bacterial level" in line 2. There is insufficient antecedent basis for this limitation in the claim.
Claim 50 is indefinite because it recites, “administering to the patient the TL1A antibody a plurality of induction doses”, which does not make sense. This rejection could be obviated by rephrasing such as ‘administering to the patient a plurality of induction doses of the TL1A antibody….’
Claim 50 is further indefinite because without knowing for the “plurality of doses” what the difference is between an induction dose and maintenance dose, by amount and interval, the metes and bounds of the claim is not clear.
Claim 50 is also indefinite because it recites “signs and symptoms” without more. For example, it is unclear what the difference is between a “sign” and a “symptom”. While the paragraph bridging pp. 48-49, p. 49, line 8-31, and p. 50, lines 3-13, present examples of “signs and symptoms”, and although a claim should be interpreted in light of the specification disclosure, it is generally considered improper to read limitations contained in the specification into the claims. See In re Prater, 415 F.2d 1393, 162 USPQ 541 (CCPA 1969) and In re Winkhaus, 527 F.2d 637, 188 USPQ 129 (CCPA 1975), which discuss the premise that one cannot rely on the specification to impart limitations to the claim that are not recited in the claim.
Claim Rejections - 35 USC § 112(a)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 13-15, 25, 26 and 36-53 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for wherein the candidate bacterial strain level in a stool sample from a patient with IBD is an increased level of Streptococcus salivarius, Streptococcus parasanguinis, and Haemophilus parainfluenzae and Ruminococcus gnavus and a decreased level of Ruminococcus albus, Ruminococcus callidus, Ruminococcus bromii and Bifidobacterium bifidum relative to the level in a stool sample from a healthy individual who is not suffering from IBD or, more specifically, ulcerative colitis, and for claims 39-41 and 47-48 wherein the fold increase or decrease is determined by metagenomics using DNA from a stool sample, does not reasonably provide enablement for wherein the level of R. gnavus is decreased in comparison to the level in a healthy individual or wherein the comparison of any candidate strain in an IBD patient stool sample is to the level in an individual who has IBD but is nonresponsive to anti-TL1A antibody therapy or wherein the comparison is in the patient before versus after treatment due to which strains are listed as increased/decreased in claims 14-15 or wherein the baseline is not determined from a stool sample or wherein the fold increase or decrease is measured by other than metagenomics, e.g., by protein level. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
First, it is acknowledged that as indicated under the rejection under 35 USC 112(b) above, it is unknown i) if the increase or decrease is determined before or after administration of an anti-TL1A antibody, ii) with the exception of claims 37-38 and 45-46, what the increase or decrease is compared to, e.g., to the patient prior to inflammatory bowel disease (IBD) onset or a healthy control or to the patient before or after treatment and iii) whether the patient is step (iii) of claim 13 is the same as in step (i) of the claim. Independent claim 13 has a step of determining the level of one or more candidate bacterial strains in a stool sample from a patient with IBD and identifying one or more strains that is increased or decreased. Claim 13 also has a step of administering a therapeutic dose of an anti-TL1A antibody to a patient. This is a separate independent step. It is not required that the patient in the administration step be the same patient from which the sample came. Nor is it required that even if it is the same patient, the administration is specifically before or after the stool sample is obtained. Further, it is not required for claims 38-39 and 45-46 that the baseline bacterial level be from a stool sample
Dependent claim 15 limits bacterial strains to those with “decreased” levels selected from one or more of R. albus, R. Callidus, R. Bromii, B. bifidum and R. gnavus. The instant specification used metagenomics to analyze bacterial abundance in stool samples before compared to after anti-TL1A antibody treatment (“Metagenomics sample collect and processing” section beginningp. 70, line 15). Table 10 shows levels before and after anti-TL1A inhibitor antibody therapy for a variety of bacterial strains, of which R. gnavus is not listed (see also paragraph bridging pp. 72-73). The only strains listed in Table 10 with a decrease in levels after treatment are R. champanelinsis and B. bifidium but no others. This is the same information shown in Fig. 6 of a post-filing reference by the instant inventors and others (Hassan-Zaharee et al., Inflamm. Bowel Dis. 28:434, 446, 2021). There is no data for levels in healthy compared to IBD patients prior to or after treatment. Nor is there data in the specification for pre- and post-treatment levels for patients of R. calidus or R. bromii. Glassner et al. (J. Allergy Clin. Immunol. 145(1):16-27, Jan. 2020) teaches, “R gnavus has a greatly increased abundance at the RNA level in both patients with UC and those with CD compared with healthy control subjects, with only a small increase in DNA abundance.88 This means that even small changes in R gnavus abundance at the DNA level can have greater effects in patients with IBD than expected. R gnavus produces a complex glucorhamnan polysaccharide that potently induces secretion of the inflammatory cytokine TNF-a by dendritic cells.89” Therefore, it is reasonable to speculate that after an IBD treatment effective to ameliorate IBD that levels of R. gnavus would decrease. The prior art teaches away from IBD patients having decreased levels of R. gnavus compared to healthy controls (see claims 37 and 45). This is supported by Willing et al. (Gastrenterol. 139(6):1844-54, 2010) which also found in a twin comparison that the twin with CD had relatively increased levels of R. gnavus as well as other unclassified Ruminococcaceae strains and Bifidobacterium (sentence bridging pp. 1847-1848, p. 1848, col. 1, second paragraph, and p. 1853, col. 1, third full paragraph). Therefore, the method for claim 13 is only enabled for wherein the decrease is compared to a baseline bacterial level for each of the listed strains for a healthy individual who is not suffering from IBD, including UC.
Further, Hassan-Zaharee et al. (supra, p. 442, sentence bridging cols. 1-2) states in reference to anti-TL1A antibody treatment, “[T]here was no evidence of a difference in bacterial species between responders and nonresponders using species-level data (data not shown).” This is pertinent to claims 38 and 46, wherein the level of one or more bacterial strains is compared against a baseline bacterial level base on an estimated level of those bacterial strains for individuals who are non-responsive to anti-TL1A antibody treatment. There is no related information in the specification and Hassan-Zaharee et al. teach away from any such difference. Therefore, there is no reasonable expectation that there is a difference in candidate bacterial strain levels between anti-TL1A antibody responders and nonresponders, so that one could not use the method of claims 38 and 46 or any method relying on this comparison to detect a difference, e.g., those encompassed by claim 13 with the generic determination step.
The specification states Streptococcus subspecies and Haemophilus parainfluenzae bacterial strains (listed in claim 14) are associated with IBD, with increased H. parainfluenzae found in patients with active IBD, potentially contributing to inflammation, and “Haemophilus … and Streptococcus subspecies showing increased colonization during IBD….” (p. 24, lines 17-23). These bacterial strains are in contrast to levels of Ruminoccocus and Bifidobacterium, which are associated with intestinal health (p. 24, lines 23-25), with the exception of R. gnavus. IBD patients in remission after treatment with anti-IL23 antibody ustekinumab showed high levels of Ruminoccocaceae (p. 24, lines 25-29).
As the claims are written, the sample from which the bacterial strains are detected need not be the same for the sample from the IBD patient and from the control sample (claims 37-38 and 45-46). Nor does the method of detection need to be the same, e.g., protein detection by, for example, ELISA, or encoding DNA or mRNA. As to the sample, Gevers et al. (Cell Host Microbe, 15:382–392, March 12, 2014, p. 484, paragraph bridging cols. 1-2) teaches that levels of bacterial markers in stool at the onset of CD was significantly different compared to mucosal tissue samples. Glassner et al., supra, p. 22, first full paragraph) explain, “The functional activity and potential of an organism do not always correlate. For example, R gnavus has a greatly increased abundance at the RNA level in both patients with UC and those with CD compared with healthy control subjects, with only a small increase in DNA abundance.88” The instant application used only metagenomics with DNA analysis in stool samples (p. 70-71 and paragraph bridging pp. 72-73). Detection as recited in the claims is not commensurate in scope with the disclosed invention.
The relationship of gut bacteria to IBD is complex and difficult to predict for those bacterial strains for which there is no data in the specification or prior art. For the reasons discussed above, it reasonably appears that compared to a level of the bacterial strain in a healthy individual, the skilled artisan would have reasonably expected for a patient with IBD an increased level of Streptococcus salivarius, Streptococcus parasanguinis, and Haemophilus parainfluenzae and Ruminococcus gnavus and a decreased level of Ruminococcus albus, Ruminococcus callidus, Ruminococcus bromii and Bifidobacterium bifidum. No difference would have been expected where the comparison is between levels in a patient nonresponsive to anti-TL1A antibody treatment and a patient responsive to treatment. It is noted that if the comparison of bacterial strain levels was between that of the patient with IBD and that of the patient who responded positively to anti-TL1A antibody therapy, then those strains indicated as increased above would instead be reasonably expected to decrease and vice versa for those indicated as decreased above. Additionally, if the comparison was from a stool sample from an IBD patient and, for example, a saliva or blood sample from a healthy individual, this would not support the findings of the instant application. Instead, the samples must be from the same source (see claims 38-39 and 45-46).
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.
Claim Rejections - 35 USC § 103
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) 13-15, 25, 26 and 36-53 is/are rejected under 35 U.S.C. 103 as being unpatentable over US 11,806,372 B2 (Hall) in view of 9,683,998 B2 (Arch) and Berinstein et al. (Inflammatory Bowel Disease:A Practical Approach, Series #106, Practical Gatroenterol. April 2019).
Hall teaches that R. gnavus shows disproportionate growth in IBD, while Bifidobacterium is found in the small intestine of healthy humans (col. 9., lines 16-29). Table 2 shows that Streptococcus parasanguinis and salivarius as well as Haemophilus parainfluenzae are increased in patients with IBD, while Ruminococcus bromii decreased in IBD (see also Table 3 describing results of Lewis et al.). IBD and UC may be diagnosis by identification of increased R. gnavus (col. 31, lines 14-27, and col. 32, line 54, through col. 33, line 15, and claims 1-5). The claims (claim 3) are drawn to “A method of diagnosing IBD in a human subject comprising a. determining from a gut microbiome sample whether the gut microbiome comprises Ruminococcus gnavus, b. determining relative abundance of R. gnavus, and if the relative abundance of R. gnavus is at least 5%, c. diagnosing the subject as having IBD,…” (claim 1). The IBD may be Crohn’s disease or ulcerative colitis (claim 4). It was found that the relative abundance in controls was 1.06-2.44%, whereas it went up to over 41-69% in IBD individuals (col. 24, lines 1-17). Claim 17 specifies the gut microbiome sample from which R. gnavus is identified comes from a stool sample. It also teaches a number of IBD therapies, including an immune system suppressor which is a TNF-alpha inhibitor, including an anti-TNF-alpha antibody (col. 35, lines 20-21, 33-36. 50-57). Hall does not teach treatment with an anti-TL1A antibody.
Arch teaches that in studies using mouse models of IBD, asthma, multiple sclerosis and arthritis, treatment with anti-TL1A antibodies showed the involvement of the TL1A pathway with these diseases (col. 1, lines 57-62). TL1A is also known as TNFRSF15 (col. 1, lines 35-37). Evidence supports a role for the pathway in enhancing effector cell functions, inflammatory cell expansion and cytokine secretion (col. 1, lines 45-48). “Moreover, significant literature from studies involving nonclinical species and humans implicates TL1A most prominently in the pathophysiology of inflammatory bowel disease (IBD), such as, ulcerative colitis (UC) and Crohn's Disease (CD).” (col. 1, lines 63-67) “Additionally, human inflamed IBD tissues show high levels of TL1A and DR3 expression and several independent laboratories have demonstrated that antibody blockade of TL1A prevents or attenuates established gut inflammation in a number of murine IBD models (Bamias et al, 2003, J Immunol 171(9):4868-4874; Prehn et al, 2004; Bamias et al, 2006, Proc Natl Acad Sci USA 103(22):8441-8446; Takedatsu et al, 2008, Gastroenterology 135(2):552-567; Shih et al, 2009; Kamada et al, 2010, Inflamm Bowel Dis 16(4):568-575; Meylan et al, 2011, Immunol Rev 244(1):188-196; Taraban et al, 2011, Mucosal Immunol 4(2):186-196; Bamias et al, 2012, Dig Liver Dis. 44(1):30-36).” (col. 2, lines 8-20) It is stated that the present invention meets the need for a therapy to treat IBD, including UC and DC (col. 2, lines 29-33). Administration of the antibody may be by intravenous injection (col. 119, lines 61-66). The administration may be a plurality of doses administered every 1, 2, 3, 5, 10, 15 days or 3 months (col. 123, lines 48-42). Claims 1-3 teach an anti-TL1A antibody comprising the variable heavy and variable light chain regions (VH and VL, respectively) of SEQ ID NO:226 and 102, respectively, and CDRs thereof.
Berinstein et al. teaches IBD therapeutics, including treatment with interleukin inhibitors, saying (p. 25, col. 2, first paragraph):
Perhaps the most promising target interleukin is IL23 with or without concomitant inhibition of IL12. IL23 and IL12 are critical mediators of T cell differentiation and function.5 While the exact role of IL12 and IL23 in the pathogenesis of Crohn’s disease is unclear, IL23 in particular is thought to be important in the pathogenesis of CD through induction of IL22 expression.6 Ustekinumab (Stelara) (Janssen) is an inhibitor of IL12 and IL23 through direct action on P40, a subunit of both interleukins.5 In 2016 ustekinumab became the only approved IL12/23 inhibitor in inflammatory bowel disease (CD), and a recent phase III long-term extension trial demonstrated reduction in the incidence of CD related hospitalization, surgery, and alternative biologic therapy at two years in patients treated with ustekinumab compared to placebo.7 There are several specific IL23 inhibitors currently in clinical trials.
Additionally, several other IL-23-specific inhibitors are entering clinical trials for CD and UC (p. 26, col. 1, second paragraph). Further, the selective inhibition of IL-23 without interaction with IL-12 may increase therapeutic safety, since IL-12 plays a role in defense against intracellular pathogens (p. 26, col. 1, third paragraph). Also (p. 27, col. 1, second paragraph), “An additional cytokine modulator in the pipeline is PF-06480605 (Pfizer). This therapy is also an inhibitor of a cytokine, a blocker of the TNF ligand known as TNFSF15 (TNF super family 15). A phase II trial for patients with UC has reportedly completed enrollment, however no data on efficacy has been published yet (NCT02840721).14”
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have determined the relative level of R. gnavus in a stool sample of a patient suspected of having IBD, wherein detection of a relative increase in the level of the bacteria compared to in a stool sample of a healthy control indicated the patient had IBD. Alternatively or additionally, it would have been obvious to determine the relative amount of Streptococcus parasanguinis, S. salivarius and/or Haemophilus parainfluenzae in a stool sample from a patient suspected of having IBD, wherein detection of a relative increase in the level of one or more of these bacterial strains compared to in a stool sample of a healthy control indicated the patient had IBD because Hall teaches patients with IBD have increased levels of these bacterial strains. It further would have been obvious to administer to the patient with IBD the anti-TL1A antibody of Arch with a reasonable expectation of treating the IBD, including UC, due to the prior art showing of the involvement of TL1A in inflammation and cytokine secretion as well as the preclinical treatment of IBD and clinical trial using an anti-TL1A antibody to treat IBD. It would have been obvious wherein the antibody was administered intravenously every several days or weeks as determined by routine optimization as within the ranges set forth by Arch. Depending on the dose and frequency, the artisan of ordinary skill would have reasonably expected improvement of IBD to some extent after 12 weeks, absent evidence to the contrary. It would have also been obvious after treatment with the anti-TL1A antibody of Arch to test or retest a stool sample from the IBD patient for R. gvanus levels, a decrease in which would reasonably be expected to indicate the patient is responsive to treatment. SEQ ID NO:226 and 102 of Arch are identical respectively to instant SEQ ID NO:3 and 4. It would have been obvious wherein in addition to treatment with the anti-TL1A antibody, an IL-23 antagonist was also administered because Berinstein et al. taught one such agent was already approved for IBD treatment and others were in or about to go into clinical trials. Note there is nothing in the claims to distinguish an “induction dose” from a “maintenance dose”, except for the reasonable interpretation that the induction dose comes before the maintenance dose.
Prior Art
The prior art made of record and not relied upon is considered pertinent to Applicant's disclosure.
US 20150132311 A1, cited in the IDS filed 4/22/02026, is the pregrant publication from which US Patent 9,683,998 B2 (Arch, relied on above) issued.
Danese et al. (J. Crohn's Colitis, 14(Supplement_1): S108–S11, January 2020) shares some inventors with the instant application and teaches results of a phase 2a clinical trial with the antibody of the instant claims, PF-06480605, for treatment of CD and UC. Treatment was with 7 doses of 500 mg Q2W. Neither the sequence of the antibody nor examination of bacteria in stools is discussed.
WO2018/081074 (cited in the IDS filed 4/22/2026) teaches a method of treating IBD with an anti-TL1A antibody (Example 5 and 7 and claims 24-28 and 30). It is cited to show this method of treatment using different anti-TL1A antibodies was known before the effective filing date of the instant invention.
Conclusion
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Claire Kaufman
/Claire Kaufman/
Primary Examiner, Art Unit 1674
July 2, 2026
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