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 .
This is the second Office action on the merits of the claims.
All citations to the Manual of Patent Examining Procedure (MPEP) refer to Revision 01.2024, which was released in November 2024.
Status of the Claims
In the Amendment filed 05 June 2026, Applicant amended claims 1-2, 9-10, 17, and 21. Additionally, Applicant cancelled claims 18 and 20. Claims 1-17, 19, and 21-22 are pending.
Status of the Rejections and Objections
The objection to claims 21-22 is withdrawn in view of Applicant’s amendment to claim 21.
The rejection of claims 2 and 10 under 35 U.S.C. 112(a) is new and has been necessitated by Applicant’s recent amendments.
The rejection of claims 1-20 under 35 U.S.C. 112(b) set forth in the previous Office action (11 March 2026) is withdrawn in view of Applicant’s recent amendments.
The rejection of claim 8 under 35 U.S.C. 112(b) is new and has been necessitated by Applicant’s recent amendment to claim 1.
The rejection of claims 18 and 20 under 35 U.S.C. 112(d) set forth in the previous Office action is withdrawn in view of Applicant’s cancellation of both those claims.
The rejection of claims 3 and 17 under 35 U.S.C. 112(d) is new and has been necessitated by Applicant’s recent amendment to claim 1.
The rejection of claims 1-20 under 35 U.S.C. 102(a)(1) as being anticipated by Esser-Kahn (WO 2020/118159 A1) has been modified in view of Applicant’s recent amendments. Applicant’s arguments against this rejection are considered in paragraphs 44-45 of this Office action.
The rejection of claims 21-22 under 35 U.S.C. 102(a)(1) as being anticipated by Kimball (“Vanilloid receptor 1 antagonists attenuate disease severity in dextran sulphate sodium‐induced colitis in mice.” Neurogastroenterology & Motility 16.6 (2004): 811-818) is maintained. Applicant’s arguments against this rejection are considered in paragraphs 50-53 of this Office action.
Claim Rejections – 35 U.S.C. 112(a) – Written Description
The following is a quotation of 35 U.S.C. 112(a):
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.
Claims 2 and 10 are rejected under 35 U.S.C. 112(a) for failing to comply with the written description requirement.
Claims 2 and 10, as recently amended, now contains subject matter that was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventors, at the time the application was filed, had possession of the invention, as now claimed.
Specifically, the specification of the present application, as originally filed 24 August 2023 (WO 2022/182940), provides no support for the limitation now recited at the end of claims 2 and 10, respectively: “synthetic capsaicin analogues.” Emphasis added.
The word <capsaicin> appears only once in the specification. It is located in paragraph [0020], which states in relevant part: “Non-limiting examples of the TRPVI receptor agonists that can be used in the present invention include capsaicin, resiniferatoxin (RXT), eugenol, camphor, clotrimazole, arvanil….” (Emphasis added) Page 5. Neither of the following words appears in the specification: analog, analogue. Furthermore, the specification does not even support the selection of a derivative of capsaicin.
In sum, the specification does not support the selection of a “synthetic capsaicin analogue” as the TRPV1 receptor agonist or for any other purpose.
Given that none of Applicant’s claims, as originally filed, compensates for the deficiency in the specification identified above, the present application does not reasonably convey to persons skilled in the art that the inventors, at the time the application was filed, had possession of the following limitation: “synthetic capsaicin analogue.” Thus, claims 2 and 10 each recite new matter. 35 U.S.C. 132(a) (“No amendment shall introduce new matter into the disclosure of the invention.”); see also MPEP § 608.04. Accordingly, it is appropriate to reject claims 2 and 10 under 35 U.S.C. 112(a).
Claim Rejections - 35 U.S.C. 112(b)
The following is a quotation of 35 U.S.C. 112(b):
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.
Claim 8 is rejected under 35 U.S.C. 112(b) as being indefinite for failing to particularly point out and distinctly claim the subject matter that the inventors regard as the invention.
Regarding claim 8, there no longer is an antecedent basis for the following limitation: “the immunogenic-specific vaccine.” This ambiguity renders the claim indefinite, especially considering that claim 1 does not even require a nexus between (i) the vaccine that was previously administered to the subject (thereby yielding the “vaccinated subject”) and (ii) the immunogen-specific antibody. For example, the antigen in the vaccine could be specific for SARS-CoV-2 (a coronavirus), while the antibody is specific for an influenza virus. Applicant is referred to MPEP § 2173.05(e) (lack of antecedent basis).
Claim Rejections - 35 U.S.C. 112(d)
The following is a quotation of 35 U.S.C. 112(d):
[A] claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claims 3 and 17 are rejected under 35 U.S.C. 112(d) as being of improper dependent form.
Claim 3 recites that “the TRPV1 receptor agonist is administered concurrently with the vaccine.” Emphasis added. However, claim 3 depends on claim 1, which implicitly requires that the subjected is vaccinated before the TRPV1 receptor agonist is administered. See claim 1 (requiring administration of the TRPV1 receptor agonist to a “vaccinated subject”). Thus, claim 3 conflicts with claim 1 and, consequently, fails to comply with 35 U.S.C. 112(d).
Claim 17 recites that “the TRPV1 receptor agonist is administered after the subject is vaccinated.” Emphasis added. However, claim 17 depends on claim 1, which already implicitly requires that the subjected is vaccinated before the TRPV1 receptor agonist is administered. See claim 1 (requiring administration of the TRPV1 receptor agonist to a “vaccinated subject”). Thus, claim 17 does not further limit claim 1 and, consequently, fails to comply with 35 U.S.C. 112(d).
Applicant may cancel the claims, amend the claims to place the claims in proper dependent form, rewrite the claims in independent form, or present a sufficient showing that the dependent claims comply with the statutory requirements.
Claim Rejections - 35 U.S.C. 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale or otherwise available to the public before the effective filing date of the claimed invention.
Claims 1-17 and 19 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Esser-Kahn (WO 2020/118159 A1).
Esser-Kahn is directed to the use of NFkB inhibitors as innnune potentiators in vaccine compositions. Abstract.
Esser-Khan identifies capsaicin as a preferred NFkB inhibitor. Page 3 at lines 15-16 (“In some
embodiments, the NFkB inhibitor comprises capsaicin.”); see also page 67 at para. [0168] (“Of the molecules tested, honokiol and capsaicin proved to be effective at both limiting inflammation and potentiating the protective response.”).
Esser-Kahn discloses: “The primary in vivo target for capsaicin is the transient receptor potential cation channel subfamily V member 1 (TRPV1). TRPV1 modulates the immune response in a variety of ways, and importantly, has been implicated in dampening systemic inflammation associated with sepsis. However, it has never been explored in a vaccine setting. To understand how activation of TRPV1 may be modulating the effects of the adjuvant, the inventors compared the immediate inflammatory response of the vaccination in wild type mice (WT) and TRPV1 knockout mice. The inventors vaccinated WT and TRPV1 KO mice with 100 μg OVA and: 50μg CpG, 50 μg CpG + 20 μg capsaicin or PBS.” Page 69 at para. [0173] (emphasis added). In the interest of clarity, the examiner notes that OVA (ovalbumin) is a model antigen that is widely used in immunology and allergy research.
Esser-Kahn discloses: “Interestingly, the inventors found that anti-OVA antibody levels were increased in groups with capsaicin + CpG in both WT and KO mice. This implies that the antibody-boosting activity of capsaicin is separate from TRPV1-dependent decrease in inflammatory cytokines. This result demonstrates both that the decrease in inflammation is not responsible for the antibody-boosting activity of the NF-kB inhibitor a result that the inventors demonstrated previously, and also that the enhancement of the adaptive response is TRPV1 independent.” Page 70 at para. [0173] (emphasis added).
Esser-Kahn discloses: “In summary, the inventors present that select small molecule inhibitors of NF-kB can decrease the inflammatory effects of adjuvanted vaccination - potentially enabling safer vaccination while also acting as immune potentiators and increasing the antibody level. The inventors identified two such immune potentiators, honokiol and capsaicin that effectively decrease inflammation while increasing the adaptive response.” Page 71 at para. [0176] (emphasis added). Applicant is additionally referred to claims 1-3, 9, and 22 of Esser-Kahn, located on pages 79 and 81. Referring to claim 22 of Esser-Kahn, “at least 12 mg” of capsaicin (NFkB inhibitor) qualifies as “an amount sufficient to increase antibody production” (Applicant’s claim 1, as recently amended). MPEP § 2111 (“During patent examination, the pending claims must be ‘given their broadest reasonable interpretation consistent with the specification.’”).
In further regard to Applicant’s recent amendment to claim 1, which now requires administration of capsaicin or other TRPV1 receptor agonist to a “vaccinated subject,” Applicant is referred to paragraph [0016] of Esser-Kahn, which discloses in relevant part:
In some embodiments, the NFkB inhibitor is administered after the antigen. In some embodiments, the NFkB inhibitor is administered at least or at most 0.5, 1, 2, 3, 4, 5, or 10 hours or 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, or l4, days before or after (or any derivable range therein) the adjuvant and/or antigen.
Page 7, lines 27-31 (emphasis added).
By way of review, the antigen has long been recognized by those skilled in the art as the essential, active core component of a vaccine. The antigen is a substance — such as a protein, sugar, or genetic blueprint like mRNA — that mimics a real pathogen to train the immune system to recognize and fight a specific disease. Persons having ordinary skill in the art — following a review of paragraph [0016] of Esser-Kahn —would have readily envisaged administering the NFkB inhibitor after a vaccine because that paragraph discloses administering the NFkB inhibitor after an antigen. MPEP § 2131.02(III) (“A reference disclosure can anticipate a claim when the reference describes the limitations but ‘d[oes] not expressly spell out’ the limitations as arranged or combined as in the claim, if a person of skill in the art, reading the reference, would ‘at once envisage’ the claimed arrangement or combination.”), quoting Kennametal, Inc. v. Ingersoll Cutting Tool Co., 780 F.3d 1376, 1381 (Fed. Cir. 2015).
On the basis of the foregoing disclosure, claims 1-3, 7, 9-11, and 16 are anticipated by Esser-Kahn.
Regarding claims 4 and 12, Esser-Khan discloses “topical” administration on page 11 at paragraph [0025] and specifies that “[i]n some embodiments, NFkB inhibitor, the adjuvant, and/or the antigen are administered locally to the same site in the subject.” Page 8 at para. [0016]; see also page 81 at claims 20-21.
Regarding claims 5 and 13, Esser-Khan discloses systemic administration in paragraph [0173]. Applicant is additionally referred to paragraph [0016] of Esser-Khan, which discloses that “[i]n some embodiments, the NFkB inhibitor, antigen, and/or adjuvant is administered by intramucosal, intramuscular, parenteral, or subcutaneous administration.” See also page 81 at claim 16.
Regarding claims 6 and 15, Applicant is referred to claim 23 of Esser-Khan, which is on page 81. See also page 8 at para. [0018] (“In some embodiments, the subject is a human.”).
Regarding claims 8 and 14, Applicant is referred to claims 10-11 of Esser-Khan, which are on page 81. See also page 7 at para. [0015] (“In some embodiments, the method further comprises administration of inactivated virus, live attenuated virus, or antigenic fragments thereof. In some embodiments, the virus comprises influenza, dengue, or HIV.”).
Regarding claims 17 and 19, Applicant is referred to claim 18 of Esser-Khan, which is on page 81. See also page 7 at para. [0016] (“In some embodiments, the NFkB inhibitor is administered prior to the antigen. … In some embodiments, the NFkB inhibitor is administered after the antigen.”). Applicant is additionally referred above to paragraphs 36-37 of this Office action.
Response to Applicant’s Argument
The following brief remarks are provided in reply to the arguments raised by Applicant on page 8 of the Reply filed 05 June 2026, to the extent they have not already been addressed above in the modified §102 rejection:
Applicant’s argument relies, in significant part, on the fact that capsaicin is identified in the claims as a TRPVI receptor agonist, in contrast to Esser-Khan, which identifies it as an NFkB inhibitor. That distinction is irrelevant in the context of anticipation because a chemical compound and its properties are inseparable. MPEP § 2112.01(II) (if the composition is physically the same, it must have the same properties). In other words, you can call it what you want, but it is what it is. Furthermore, Applicant’s argument overlooks that Esser-Khan discloses that administration of capsaicin increases antibody levels. See, e.g., Esser-Khan at pages 70-71. In closing, Applicant is reminded that “[t]he question [of] whether a reference ‘teaches away’ from the invention is inapplicable to an anticipation analysis.” MPEP § 2131.05.
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Claims 21-22 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Kimball (“Vanilloid receptor 1 antagonists attenuate disease severity in dextran sulphate sodium‐induced colitis in mice.” Neurogastroenterology & Motility 16.6 (2004): 811-818).
Kimball discloses: “Neurogenic mechanisms have been implicated in the induction of inflammatory bowel disease (IBD). Vanilloid receptor type 1 (TRPV1) has been visualized on nerve terminals of intrinsic and extrinsic afferent neurones innervating the gastrointestinal tract and local administration of a TRPV1 antagonist, capsazepine, reduces the severity of dextran sulphate sodium (DSS)-induced colitis in rats (Gut 2003; 52: 713–91). Our aim was to test whether systemically or orally administered TRPV1 antagonists attenuate experimental colitis induced by 5% DSS in Balb/c mice. Intraperitoneal capsazepine (2.5 mg kg-1, bid), significantly reduced the overall macroscopic damage severity compared with vehicle-treated animals (80% inhibition, P < 0.05); however, there was no effect on myeloperoxidase (MPO) levels. An experimental TRPV1 antagonist given orally was tested against DSS-induced colitis, and shown to reverse the macroscopic damage score at doses of 0.5 and 5.0 mg kg-1. Epithelial damage assessed microscopically was significantly reduced. MPO levels were attenuated by approximately 50%, and diarrhoea scores were reduced by as much as 70%. These results suggest that pharmacological modulation of TRPV1 attenuates indices of experimental colitis in mice, and that development of orally active TRPV1 antagonists might have therapeutic potential for the treatment of IBD.” (Emphasis added) Abstract.
The examiner notes that colitis and other IBDs (inflammatory bowel diseases) are defined as “autoimmune disorders” on page 7 of the specification of the present application (WO 2022/182940), as originally filed.
On the basis of the foregoing disclosure, claims 21-22 are anticipated by Kimball.
Response to Applicant’s Argument
The following remarks are provided in reply to the arguments raised by Applicant on pages 9-10 of the Reply filed 05 June 2026:
Applicant’s arguments overlook that Kimball discloses: “The levels of TRPV1 are elevated in colonic tissues from patients with both Crohn’s disease and ulcerative pancolitis, and there is a marked increase in TRPV1-immunoreactive fibres in the submucosal plexus of diseased tissue. Experimental data suggest a protective role of TRPV1 antagonists in acute experimental colitis.” Page 811, right column (emphasis added).
Kimball additionally discloses: “Inflammatory bowel diseases (IBD) such as ulcerative colitis, Crohn’s disease and celiac disease are characterized by diminished intestinal barrier function, erosive loss of intestinal mucosa, inflammatory infiltrates in the submucosa and mucosa, and dysregulated cytokine and T-helper cell profiles.” Id. (emphasis added). In the context of Kimball, the foregoing diseases are autoimmune disorders, which is consistent with (i) the general consensus among skilled medical practitioners and (ii) the specification of the present application, as originally filed (see page 7 at para. [0025]).
The foregoing §102 rejection is maintained. Applicant is strongly encouraged to narrow claims 21 and 22 to advance prosecution.
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Conclusion
Claims 1-17, 19, and 21-22 are rejected.
No claim is allowed.
Applicant’s amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to PETER ANTHOPOLOS whose telephone number is 571-270-5989. The examiner can normally be reached on Monday – Friday (9:00 am – 5:00 pm). If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Bethany P. Barham, can be reached on Monday – Friday (9:00 am – 5:00 pm) at 571-272-6175. The fax number for the organization where this application or proceeding is assigned is 571-273-8300.
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/P.A./
05 August 2026
/BETHANY P BARHAM/Supervisory Patent Examiner, Art Unit 1611
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