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 .
Application History
Claims 1-22 were originally presented on the filing of the instant application, 08/01/2023. Claims 1-22 were rejected in a non-final rejection mailed 01/14/2026. Applicant’s amendments to the claims and responses to the rejections were received on 04/07/2026.
Status of Claims
The amendments to the claims received on 04/07/2026 are acknowledged and entered. Claims 1-7, 9, 13-15, and 18-20 were canceled, claims 8, 12, 16-17, and 21 were amended, and claims 10-11, and 22 were maintained as originally presented.
The amendments affect the following changes. See Remarks received 04/07/2026, at 5 of 10:
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Remarks received 04/07/2026, at 5 of 10.
Accordingly, claims 8, 10-12, 16, 17, and 21-22 are pending.
Priority
As discussed in the non-final rejection mailed 01/14/2026, the instant application claims foreign priority to applications filed in the Republic of Korea, Korean Patent Application Nos. KR10-2022-0095425, filed on August 1, 2022, and KR10-2023-0059573, filed on May 9, 2023. Certified copies of the translations of the foreign applications have not been received. In leu of certified copies of the translations of the foreign applications, the effective filing date of the instant application is August 1, 2023, corresponding to filing date of the instant application, U.S. Patent Application No. 18/363,123.
Actives and Abbreviations
In effort to organize the following discussion, the following table provides the actives disclosed in the Specification and their associated names and abbreviations:
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Benzyl-decyl-methyl-amine, FMJ-G0, Chemical Formula 1-1, and/or BMDA
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128
400
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Benzyl-decyl-ethyl-amine, FMJ-G1, and/or Chemical Formula 1-3
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100
400
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Benzyl-dodecyl-methyl-amine, FMJ-G2, and/or Chemical Formula 1-4
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120
400
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(Decyl-4-fluoro-benzyl)-methyl-amine, FMJ-G3, and/or Chemical Formula 1-5
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138
400
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Decyl-(4-methoxy-benzyl)-methyl-amine, FMJ-G4, Chemical Formula 1-2, and/or DMMA
As discussed in the non-final rejection mailed 01/14/2026, and acknowledged in Remarks received 04/07/2026, at 6 of 10, Chemical Formula 1-1 (BMDA, found in garlic), and Chemical Formula 1-4 (FMJ-G2, found in propolis), are products of nature.
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.
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 8, 10-12, 16, 17, and 21-22 Obvious over KR’029 in view of Kaowinn 2018, Sisto 2021, Weissler 2021, and Atreya 2008, in further view of Topliss 1972, Njardarson 2022, and Edamatsu 1997
Claims 8, 10-12, 16, 17, and 21-22 are rejected under 35 U.S.C. 103 as being unpatentable over KR’029 in view of Kaowinn 2018, Sisto 2021, Weissler 2021, and Atreya 2008, in further view of Topliss 1972, Njardarson 2022, and Edamatsu 1997.1
Reference is made to the non-final rejection mailed 01/14/2026, sections of which are incorporated herein as explained below. The following rejections are effectively the same, with adjustments made due to the change of claim scope.
The amendments to the claims received 04/07/2026 generally remove BMDA and Chemical Formula 1-4 as active ingredients in the various compositions recited in the claims.
Chemical Formula 1-2 is now an embodiment of all pending claims.
As discussed, KR’029 discloses BMDA and the subject matter of original claims 1-18 and 20-22. See, e.g., non-final rejection mailed 01/14/2026, at 31-37.
As discussed, it was obvious at the time of filing to prepare an anti-inflammatory composition comprising Chemical Formula 1-2, the methoxy derivative of BMDA. See, e.g., non-final rejection mailed 01/14/2026, at 44-47. KR’029 in view of Kaowinn 2018 and Sisto 2021, in further view of Topliss 1972 and Njardarson 2022 were applied with respect to original claim 2, for Chemical Formula 1-2.
The knowledge at the time of filing established that BDMA administration inhibited TGF-β signalling both in vivo an in vitro. See, e.g., discussion of Kaowinn 2018, in non-final rejection mailed 01/14/2026, at 39-40. The knowledge at the time of filing established that BMDA administration blocked NF-κB P65 nuclear translocation. Id. Blocking NF-κB P65 nuclear translocation is synonymous with preventing NF-κB activation.
Both modes of action were known to have an anti-inflammatory effect on certain inflammatory conditions. For example, the knowledge at the time of filing established that blocking TGF-β was a known method of treating acute and chronic rheumatoid arthritis symptoms. See, e.g., discussion of Sisto 2021, in non-final rejection mailed 01/14/2026, at 41-42, and 57. Further, the treatment nexus between TGF-β signalling inhibition, certain cancers, and certain inflammatory diseases, was known to those of ordinary skill in the art at the time of filing. See, e.g., Sisto 2021 at 3 of 26, first paragraph under the heading “TGF-β Activation and Signalling”.
The knowledge at the time of filing established that eliminating TGF-β was important to the resolution of atopic dermatitis. See, e.g., discussion of Weissler 2021, in non-final rejection mailed 01/14/2026, at 55-56.
The knowledge at the time of filing established that blocking NF-κB activation was a known method of treating IBD, which includes ulcerative colitis. See, e.g., discussion of Atreya 2008, in non-final rejection mailed 01/14/2026, at 56-57. Further, Atreya 2008 links NF-κB activation, cancer, and inflammation. See, e.g., Atreya 2008 at 595 citations 5 and 6.
The knowledge at the time of filing established that NF-κB activation was indispensable for the induction of the rat specific pro-inflammatory chemokine, CINC-3. See, e.g., discussion of Edamatsu 1997, in non-final rejection mailed 01/14/2026, at 61, and at 70-71.
Claims 8, 10 and 11 Obvious
Regarding claims 8, 10, and 11, to summarize the amendments received 04/07/2026, they remove the actives BMDA and Chemical Formula 1-4, and reflect the following changes:
Amended claim 8 is now generally directed to a cosmetic composition, comprising actives Chemical Formula 1-2, 1-3, “and/or” 1-5, with intended use for ameliorating atopic dermatitis. Claims 10 and 11 were not amended but the scope of the claims changed due to the removal of actives BMDA and Chemical Formula 1-4.
The examiner emphasizes that these are not method of treatment claims. Instead, they are claims generally directed to various compositions (e.g., lotions, creams).
As discussed, it was obvious to one of ordinary skill in the art at the time of filing to prepare a cosmetic composition for ameliorating atopic dermatitis containing an active ingredient represented by Chemical Formula 1-2, claim 8. See, e.g., non-final rejection mailed 01/14/2026, at 62-63.
Standard excipients for the cosmetic composition were obvious to one of ordinary skill in the art at the time of filing, claims 10 and 11. See, e.g., non-final rejection mailed 01/14/2026, at 63-64.
Accordingly, claims 8, 10, and 11 were obvious at the time of filing.
Claims 12, 16, 17, 21 and 22 Obvious
Regarding claims 12, 16, 17, 21 and 22, to summarize the amendments received 04/07/2026, they remove all actives (e.g., BMDA) except for Chemical Formula 1-2, and reflect the following changes:
Amended claim 12 is now generally directed to a pharmaceutical composition comprising Chemical Formula 1-2 (the methoxy derivative of BMDA), with an intended use for rheumatoid arthritis, administered orally. Amended claim 16 recites a dose of 15 to 25 mg/kg for the rheumatoid arthritis pharmaceutical composition.
Amended claim 17 is generally directed to a medicinal composition comprising Chemical Formula 1-2 (the methoxy derivative of BMDA), with an intended use for ulcerative colitis, administered by enema. Amended claim 21 recites a dose of 0.4 mg/kg or smaller for the ulcerative colitis medicinal composition administered by enema. Claim 22 was not amended, but its scope changed due to the removal of other actives (e.g., BMDA) from the parent claim 17.
The examiner emphasizes that these are not method of treatment claims. Instead, they are claims generally directed to various compositions (e.g., pills, liquid formulations, and enema solutions for rats).
Amended claims 12, 16, 17, 21 and 22 are just different variations of the pharmaceutical composition discussed in the non-final rejection mailed 01/14/2026, at 44-47 (i.e., same active, with minor variation how its prepared per the recited intended use). The claims are addressed collectively below.
As discussed, it was obvious to one of ordinary skill in the art at the time of filing to prepare a pharmaceutical composition for preventing or treating rheumatoid arthritis containing an active ingredient represented by Chemical Formula 1-2, original claim 12. See, e.g., non-final rejection mailed 01/14/2026, at 64-65.
Further, it was obvious to one of ordinary skill in the art at the time of filing to prepare a pharmaceutical composition for preventing or treating rheumatoid arthritis containing an active ingredient BMDA, wherein the pharmaceutical composition is formulated in a unit dosage form suitable for oral administration at a dose of 15 to 25 mg/kg, original claim 16 (dependent upon original claim 12). See, e.g., non-final rejection mailed 01/14/2026, at 66-67.
The prior rejection did not expressly reject original claim 16 with respect to Chemical Formula 1-2.
Further, as discussed, it was obvious to one of ordinary skill in the art at the time of filing to prepare a medicinal composition for treatment of ulcerative colitis containing an active ingredient represented by Chemical Formula 1-2, original claim 17. See, e.g., non-final rejection mailed 01/14/2026, at 67-68.
Further, as discussed, it was obvious to one of ordinary skill in the art at the time of filing to prepare a medicinal composition for treatment of ulcerative colitis containing an active ingredient BMDA, wherein the medicinal composition is administered directly to an ulcerative colitis patient in the enema manner at 0.4 mg/kg or smaller as an effective dosage per day (original claim 21, dependent upon original claims 20 and 17). See, e.g., non-final rejection mailed 01/14/2026, at 68-70.
Further, as discussed, it was obvious to one of ordinary skill in the art at the time of filing to prepare a medicinal composition for treatment of ulcerative colitis containing an active ingredient BMDA, wherein the administration of the medicinal composition in an enema manner suppresses production of chemokine CINC-3. See, e.g., non-final rejection mailed 01/14/2026, at 70-71 (original claim 22, dependent upon original claim 17).
The prior rejection did not expressly reject original claim 21 with respect to Chemical Formula 1-2.
However, Topliss 1972 (see non-final rejection mailed 01/14/2026, at 44-46) teaches that the methoxy group has a minimal impact on the lipophilic properties of a lead compound. Generally, this means the membrane permeability remains relatively the same. Further, it teaches that the methoxy group improves solubility, which generally makes the preparation of pharmaceutical compositions easier. While it would take only routine experimentation to prepare different pharmaceutical/medicinal compositions comprising the methoxy derivative of BMDA, one of ordinary skill in the art at the time of filing would have the entire teachings of the same BMDA pharmaceutical compositions to base its experimentation on. That ordinary chemist would have a reasonable expectation of success in using the same compositions taught for BMDA (e.g., amounts, excipients for routes of administration) for the methoxy derivative because the inventors of BMDA already worked out optimal conditions for its pharmaceutical compositions. A reasonable chemist would start from the teachings for BMDA compositions because of the shared structural similarity. Moreover, Topliss 1972 suggests that it would be even easier to prepare the pharmaceutical compositions because of the expected increase in solubility.
Accordingly, while the non-final rejection mailed 01/14/2026 may not have expressly rejected original claims 12, 16, 17, 21 and 22 with respect to amounts of Chemical Formula 1-2 and routes of administration for this methoxy derivative of BMDA, the same references applied in the non-final rejection render the claims obvious at the time of filing.
Therefore, claims 12, 16, 17, 21 and 22 were obvious at the time of filing.
Response to Arguments
The examiner has fully considered Applicant’s Remarks received 04/07/2026. Applicant’s positions are addressed below.
Claim Rejections under 35 USC 112(b)
Applicant’s arguments, see Remarks received 04/07/2026, at 5 of 10, with respect to rejections of claims 3-7 under 35 USC 112(b) have been fully considered. The rejections of claims 3-7 under 35 USC 112(b) have been withdrawn, in view of the claims being canceled.
Claim Rejections under 35 USC 101
Applicant’s arguments, see Remarks received 04/07/2026, at 6 of 10, with respect to rejections of claims 1-9, 12-18, and 20-22 under 35 USC 101 have been fully considered. The rejections of claims 1-9, 12-18, and 20-22 under 35 USC 101 have been withdrawn. In particular, the products of nature, Chemical Formula 1-1 (BMDA, found in garlic), and Chemical Formula 1-4 (FMJ-G2, found in propolis), were amended out of the claims. Accordingly, the 35 USC 101 rejections are now moot.
Claim Rejections under 35 USC 102
Applicant’s arguments, see Remarks received 04/07/2026, at 6-7 of 10, with respect to rejections of claims 1-18 and 20-22 under 35 USC 102 have been fully considered. The rejections of claims 1-18 and 20-22 under 35 USC 102 have been withdrawn. In particular, Chemical Formula 1-1 (BMDA), disclosed in KR’029, was amended out of the claims, in view of the 35 USC 101 rejections. Accordingly, the 35 USC 102 rejections are now moot.
Claim Rejections under 35 USC 103
Applicant's arguments, see Remarks received on 04/07/2026 at 7-10 of 10, with respect to rejections of claims 1-22 under 35 USC 103 have been fully considered but they are not persuasive.
Applicant’s position generally rests upon an incorrect assertion that there was no known link between BDMA administration and its anti-inflammatory effects at the time of filing. The position is based on the prior art disclosing a cancer indication for BDMA, and not expressly reporting that the prior administrations of BDMA had an anti-inflammatory effect. Applicant brushes aside the knowledge at the time of filing that established BDMA administration inhibited TGF-β signalling both in vivo an in vitro, and that inhibition of TGF-β signalling was a known method of treating certain inflammatory conditions that share a TGF-β nexus. More remarkably, despite the instant Specification expressly acknowledging that NF-κB was a well-known key mediator of inflammation, Applicant entirely disregards the knowledge at the time of filing that established BMDA administration blocked NF-κB P65 nuclear translocation. Blocking NF-κB P65 nuclear translocation is synonymous with preventing NF-κB activation, which in turn, draws down inflammation.
Applicant does not appear to contest that the structural modifications to BMDA were obvious to one of ordinary skill in the art at the time of filing seeking to optimize the pharmaceutical properties of BMDA in general.
Applicant summarizes its position in Remarks received on 04/07/2026 at 8 of 10, excerpted below. See last sentence of the excerpt for Applicant’s general position, and note that the quoted phrases in in the first sentence of the excerpt do not appear expressly in the non-final rejection, and mischaracterize the rejections:
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Remarks received on 04/07/2026 at 8 of 10.
In response to Applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
Here, the knowledge at the time of filing established that BDMA administration inhibited TGF-β signalling both in vivo an in vitro. See, e.g., discussion of Kaowinn 2018, in non-final rejection mailed 01/14/2026, at 39-40. The knowledge at the time of filing established that BMDA administration blocked NF-κB P65 nuclear translocation. Id.
Both modes of action were known to have an anti-inflammatory effect on certain inflammatory conditions. For example, the knowledge at the time of filing established that blocking TGF-β was a known method of treating acute and chronic rheumatoid arthritis symptoms. See, e.g., discussion of Sisto 2021, in non-final rejection mailed 01/14/2026, at 41-42, and 57. Further, the treatment nexus between TGF-β signalling inhibition, certain cancers, and certain inflammatory diseases, was known to those of ordinary skill in the art at the time of filing. See, e.g., Sisto 2021 at 3 of 26, under the heading “TGF-β Activation and Signalling”.
The knowledge at the time of filing established that eliminating TGF-β was important to the resolution of atopic dermatitis. See, e.g., discussion of Weissler 2021, in non-final rejection mailed 01/14/2026, at 55-56.
The knowledge at the time of filing established that blocking NF-κB activation was a known method of treating IBD, which includes ulcerative colitis. See, e.g., discussion of Atreya 2008, in non-final rejection mailed 01/14/2026, at 56-57. Further, Atreya 2008 links NF-κB activation, cancer, and inflammation. See, e.g., Atreya 2008 at 595 citations 5 and 6.
Therefore, Applicant’s position that “no reference establishes that BMDA or its derivatives have anti-inflammatory activity” is inconsistent with the knowledge at the time of filing that established BMDA’s modes of action with known anti-inflammatory treatment protocols of rheumatoid arthritis, atopic dermatitis, and ulcerative colitis.
Moreover, Applicant’s position that “no reference establishes that BMDA or its derivatives have anti-inflammatory activity” is inconsistent with Kaowinn 2018 itself and Applicant’s own statements in the instant Specification.
Applicant’s key finding in the current Application appears to be that BMDA administration inhibited NF-KB.
See, e.g., Specification at 15, paragraph [00117], where it states that NF-KB inactivation occurred after BMDA administration (“It was identified that BMDA (FMJ-G0) and a derivative thereof DMMA (FMJ-G4) according to the present disclosure as a low molecular substance inhibited the activity of the transcription factor NF-KB, and inhibited NF-KB expression and migration in the nucleus (FIG. 2D).”) (emphases added).
See also, Specification at 23, paragraph [00164], where the Specification admits that NF-KB activity was known to be related to inflammation (“When the activity of signaling proteins that affect the transcription of these proteins was investigated using immunoblotting, BMDA or DMMA (FMJ-G0/G4) treatments significantly lowered the phosphorylation level of JNK, p38MAPK and NF-KB which are related to inflammation, as supported by the previous results, compared to the control group (FIG. 11D).”) (emphasis added).
See also, original claim 5, which Applicant cancelled, that further links the known association between NF-KB and inflammation.
5. The anti-inflammatory composition of claim 1, wherein the anti-inflammatory composition inhibits production of a pro-inflammatory cytokine selected from TNF-α, IL-1β or IL-6, and inhibits activity of a transcription factor NF-KB.
Original claim 5 (emphasis added).
However, it was already known from Kaowinn 2018 itself that BMDA administration inactivated NF-KB.
The authors of Kaowinn 2018, which include the current inventor, expressly acknowledge that BMDA administration blocked NF-κB P65 nuclear translocation (i.e., the administration blocked NF-κB activation). The result was significant enough that despite focusing on endpoints relating to cancer and apoptosis, the authors repeatedly discuss the finding that BMDA administration blocked NF-κB activation. The non-final rejection mailed 01/14/2026, at 39-40, highlighted several of these sections. See, e.g., Kaowinn 2018 at 22 (“Furthermore, the treatment with BMDA significantly reduced the level of NF-κB P65 in A549-CUG2 cells, but it moderately decreased their levels in A549-Vec cells (Fig. 2B).”). In the sentence immediately following that statement, the authors explain that CUG2 activates NF-κB, and that administration of BDMA blocked the process. The same result occurred in A549-Vec cells (i.e., non-CUG2 cells), see the next sentence. The same result occurred in HCT116 colon cancer cells and SKBR3 breast cancer cells. See second last sentence, same paragraph.
The mice of Kaowinn 2018 felt the same effect caused by blocking both TGF-B signalling and NF-κB activation that Applicant instantly reports and originally claimed in claim 5. The mice of Kaowinn 2018 received thrice-weekly i.p. injections of BMDA at 40 mg/kg body weight, see id. at 24, Fig. 4 caption for the cite to dose administered. While this route of administration was local, the authors differentiated it from direct injection into tumor tissues. See Kaowinn 2018 at 25 (“The in vivo experiment revealed that the i.p. injection of BMDA significantly inhibited tumor development to a level that was comparable with the direct injection of BMDA into tumor sites.”). Therefore, mice cells in general, and not just cancer cells implanted into mice, received treatment with BMDA in Kaowinn 2018. In the following sentences, the authors indicate that other systemic routes of administration, such as i.v. or oral, should work.
Therefore, Applicant’s position that “no reference establishes that BMDA or its derivatives have anti-inflammatory activity” is inconsistent with Kaowinn 2018 itself, and Applicant’s own statements in the instant Specification.
Accordingly, Applicant’s position that “no reference establishes that BMDA or its derivatives have anti-inflammatory activity” is not persuasive.
Applicant’s further positions in Remarks received on 04/07/2026 at 9 of 10 do not advance its position argued on page 8. The main gist of the positions on this page are pointing to references not mentioning BMDA. In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
Last, the authors of Kaowinn 2018 point directly to another related small molecule NF-κB inhibitor derived from garlic that shows autoinflammatory and anti-cancer properties. See discussion of diallyl trisulfide in Kaowinn 2018 at 841, and citation to Shigemi et al., 2016, which is attached hereto as supplemental reading.2 Shigemi 2016 teaches the same general experiment discussed in the instant Specification at 9, paragraph [0086] (administration of a small molecule NF-κB inhibitor inhibited LPS induced inflammation), see, e.g., Shigemi 2016 at 294 (left column, discussion of inflammation NF-κB, LPS, and inflammation suppression), at 300, Figure 5., and at 302-303, Figures 7 and 8 (each showing aspects of anti-cancer and anti-inflammation activity through NF-κB suppression mechanisms). Later work on diallyl trisulfide established its use for treating other inflammatory conditions. See, e.g, Zhang 2023,3 attached hereto as supplemental reading (teaching the indication for ulcerative colitis).
Turning to Applicant’s positions regarding dosing for administration of the actives, Remarks received on 04/07/2026 at 10 of 10, Applicant’s position is that the non-final rejection mailed 01/14/2026 did not specifically “identif[y] any reference teaching these routes or dosages for inflammatory disease treatment with BMDA derivatives.”
However, as discussed in the non-final rejection mailed 01/14/2026, at 66-67, and at 36, the dosage of 15 to 25 mg/kg was taught for BMDA (claim 16). Further, the dosage of 0.4 mg/kg or smaller and enema route (claim 21), was taught for BMDA. See non-final rejection mailed 01/14/2026, at 69-70, and at 37.
As discussed in the non-final rejection mailed 01/14/2026, at 44-47, it was obvious to one of ordinary skill in the art at the time of filing to prepare an anti-inflammatory pharmaceutical composition comprising Chemical Formula 1-2.
Amended claims 12, 16, 17, 21 and 22 are just different variations of the pharmaceutical composition discussed in the non-final rejection mailed 01/14/2026, at 44-47 (i.e., same active, with minor variation how its prepared per the recited intended use).
Topliss 1972 (see non-final rejection mailed 01/14/2026, at 44-46) teaches that the methoxy group has a minimal impact on the lipophilic properties of a lead compound. Generally, this means the membrane permeability remains relatively the same. Further, it teaches that the methoxy group improves solubility, which generally makes the preparation of pharmaceutical compositions easier. While it would take only routine experimentation to prepare different pharmaceutical/medicinal compositions comprising the methoxy derivative of BMDA, one of ordinary skill in the art at the time of filing would have the entire teachings of the same BMDA pharmaceutical compositions to base its experimentation on. That ordinary chemist would have a reasonable expectation of success in using the same compositions taught for BMDA (e.g., amounts, excipients for routes of administration) for the methoxy derivative because the inventors of BMDA already worked out optimal conditions for BMDA’s pharmaceutical compositions. Topliss 1972 suggests that it would be even easier to prepare the pharmaceutical compositions because of the expected increase in solubility.
Accordingly, while the non-final rejection mailed 01/14/2026 may not have expressly rejected original claims 12, 16, 17, 21 and 22 with respect to exact dosing for the methoxy derivative of BMDA, the same references applied in the non-final rejection render the claims obvious at the time of filing.
Prior art Cited but not Applied
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
Chung, C. Y., et al. "Rice prolamin extract ameliorates acute murine colitis by inhibiting nuclear factor-kappa B and modulating intestinal apoptosis and cell proliferation." Clinical & Experimental Immunology 178.3 (2014): 537-547.
Teaches generally the same concept. Rice prolamin extract used to treat LPS-induced colitis in mice. Rice prolamin extract was known to inhibit NF-κB signalling. Administration of the NF-κB signalling inhibitor prevented LPS-induced colitis.
Seetharaman, Rajasekar, et al. "Activity-guided Purification of N-benzyl-N-methyldecan-1-amine from Garlic and Its Antitumor Activity against CT-26 Colorectal Carcinoma in BALB/C Mice." Journal of Life Science, 29.10 (2019): 1062-1070.
Teaches oral administration of BMDA to mice.
Kim, Ji Eun, et al. "N-benzyl-N-methyldecan-1-amine and its derivative mitigate 2, 4-dinitrobenzenesulfonic acid-induced colitis and collagen-induced rheumatoid arthritis." Frontiers in Pharmacology 14 (19 April 2023): article 1095955.
Discloses many of the results from the instant application. It is unclear if inventorship should be corrected at some stage given the number of authors on this manuscript, compared to the sole inventor named in this Application.
Conclusion
No claims 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 Christopher Evan Redwood whose telephone number is (571) 272-8882. The examiner can normally be reached Monday - Friday 6:15 AM - 4:45 PM.
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/C.E.R./ Examiner, Art Unit 1629
/JEFFREY S LUNDGREN/ Supervisory Patent Examiner, Art Unit 1629
1 Full citations to the references were provided in the non-final rejection mailed 01/14/2026. Copies of the references were annexed to the non-final rejection.
2 Shigemi, Zenpei, et al. "Diallyl trisulfide induces apoptosis by suppressing NF-κB signaling through destabilization of TRAF6 in primary effusion lymphoma." International journal of oncology 48.1 (2016): 293-304, hereinafter “Shigemi 2016”.
3 Zhang, Yajing, et al. "Diallyl trisulfide, a major bioactive constituent of garlic, promotes colonic mucosal healing in ulcerative colitis through accelerating focal adhesion assembly and consequent epithelial cell migration via the Rab21‐integrin β1‐Fak pathway." Molecular Nutrition & Food Research, vol. 67, no. 12 (2023), pp. 1-14, article 2200784, hereinafter “Zhang 2023”.
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