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 .
Claim Status
Applicant’s remarks and amendments, filed 8 September 2025 in response to the non-final rejection mailed 28 July 2025, are acknowledged and have been fully considered. Applicant’s amendments to the claims are acknowledged. The listing of claims filed 8 September 2025 replaces all prior versions and listings of the claims.
Claims 1-3 and 26-27 are pending. Claims 4-25 are canceled by Applicant’s amendment. Claims 1-3 and 26 are amended. Claims 1-3 and 26-27 are being examined on the merits.
Response to Amendment
Any previous rejection or objection not mentioned herein is withdrawn.
Applicant’s arguments and amendments, on pages 4-8 of the reply filed 8 September 2025 with respect to the rejection of Claims 1-3 and 26-27 under 35 USC § 103 as being unpatentable over Nagashima et al. in view of Carhalho et al. and Kiguchi et al. have been fully considered. The rejections of Claims 1-3 and 26-27 are rendered moot by amendment of Claims 1-3.
Claim Rejections - 35 USC § 103
(grounds modified as necessitated by amendment)
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 text of those sections of Title 35, U.S. Code not included in this action can be found in prior Office actions.
Claim 1-3, 26, and 27 are rejected under 35 U.S.C. 103 as being unpatentable over Kaneda et al. (US 8,697,148 B2) in view of Jing et al. (Brit J Nutr, 2014, 170-182), Kiguchi et al. (Cytokine, 2013, 666-672), and Akhter et al. (J Diab Metabol Disord, 2018, 77-84).
The instant claims are as of record, drawn to methods of suppressing lipopolysaccharide-induced inflammation in intestinal cells of poultry, pigs, or ruminants comprising administering cashew nut shell liquid or heated cashew nutshell liquid wherein administration suppresses production of TNF-α, IL-6, and MCP-1.
Kaneda et al. teach a method of improving milk yield comprising administering cashew nut shell liquid to a ruminant (non-human animal) which may be administered in combination with a feed (e.g., feed mixed with the cashew nut shell liquid; Kaneda et al., col. 3, lines 64-67; as required for instant Claims 1-3). The cashew nut shell liquid is present in the feed additive based upon dry matter of the feed to which it is added is 5 to 500,000 mass ppm (Kaneda et al., col. 10, lines 8-15) and is administered at a dose of 0.1 to 500 g per head per day (Kaneda et al., col. 10, lines37-47; as required for instant Claims 3 and 26). The cashew nut shell liquid, when heated, contains 0-10 mass% anacardic acid, 55-80 mass% cardanol, and 5-30 mass% cardol (Kaneda et al., col. , lines 50-55; as required for instant Claim 27).
Kaneda et al. do not teach wherein the method is for suppression of LPS-induced intestinal cell inflammation and inflammatory cytokine production.
Jing et al., however, teach that dairy cattle (e.g., the milk-producing ruminants of Kaneda et al.) are fed a high concentrate diet in order to improve milk production that can result in a shift in ruminal bacterial populations, ultimately leading to rises in LPS concentration in the rumen (Jing et al., col. 1, page 170). This increase in LPS stimulates an intense host inflammatory response that results in altered gastrointestinal digestibility, digesta passage rate, and modifies gut microbial composition (Jing et al., col. 2, page 170). Additionally, when mimicking this bacterial-induced infection, jugular vein infusion is use, resulting in a systemic inflammatory response – broadly, the increase in LPS as a result of the high concentrate diet of dairy cattle leads to intestinal cell inflammation (Jing et al., Discussion, col. 1, page 177; as required for instant Claims 1-3).
Kiguchi et al. teach that anacardic acid suppresses upregulation of CCL-2 (MCP-1) in mice (Kiguchi et al., Figure 8 and Discussion, page 671; as required for instant Claims 1-3).
Akhter et al. teach that a high fat diet alters permeability of the intestinal mucosa for LPS, thereby leading to higher LPS endotoxin levels. The LPS binds to TLR-4, activating a proinflammatory signaling cascade which includes CCL-2 (MCP-1), TNF-α, and IL-6 (Akhter et al., Introduction, page 77; Discussion, page 81 as required for instant Claims 1-3).
It would have been obvious to a person of ordinary skill in the art prior to the effective filing date of the instant application to combine the teachings of Kaneda et al., Jing et al., and Akhter et al. in order to arrive at the instantly claimed invention. A skilled artisan would know from the teachings of Kaneda et al. that administration of cashew nut shell liquid to a ruminant, either alone or in a feed, results in improved milk production and also know from Jing et al. that dairy cattle are often fed high concentrate diets that result in LPS-induced inflammation. It would therefore be obvious to a skilled artisan that the dairy cows of Kaneda et al. would also have the LPS-induced inflammation of Jing et al. operating through the known proinflammatory signaling cascade of Akhter et al. because of the positive teaching of Kiguchi et al. that anacardic acid is capable of suppressing CCL-2 and thus all of the molecules downstream in the signaling cascade. A skilled artisan could therefore provide the composition of Kaneda et al. and expect to suppress LPS-induced inflammation in intestinal cells with a reasonable expectation of success.
From the teachings of the references, it is apparent that one of ordinary skill in the art would have had a reasonable expectation of success in producing the claimed invention. Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the time the invention was made, as evidenced by the references, especially in the absence of evidence to the contrary.
Response to Arguments
Applicant's arguments filed 8 September 2025 have been fully considered but they are not persuasive.
Applicant argues that anacardic acid suppression of CCL-2 by anacardic acid in a mouse model of neuropathic pain as taught by Kiguchi et al. is fundamentally different from an inflammatory model in the intestine (Remarks, pages 6-7) because the cell type and overall pathologic processes are distinct and thus extrapolation from one model to another is not possible due to differences in physiology, metabolism, and immunology between organisms, however the examiner respectfully disagrees. As previously stated, mice are a well-known and commonly used model organism in the biological sciences and that extrapolation of mechanisms of action of a given chemical in not only different organisms but also different cell types is well within the skillset of a person of ordinary skill in the art. It is additionally noted that the applicant utilizes porcine intestinal epithelial cells ([0032], page 14) to extrapolate the mechanism of action and effect of administration of cashew nut shell liquid to ruminants and poultry at an organismal level. Overall, taken together, these references indicate that anti-inflammatory effects in intestinal cells via the mechanism of suppression of TNF-a, IL-6, and MCP-1 is expected and obvious absent evidence to the contrary.
Please note that discovery of a new feature of a composition administered at the same dose in the same manner (e.g., as a feed) to the same organisms encompassing the same patient population (e.g., animals fed high fat/concentrate diets that lead to increased LPS) does not exclude reference silent features (e.g., suppression of LPS-induced inflammation). See MPEP 2112.02. Additionally, the specification indicates that suppression encompasses prevention ([0012], lines 21-25), and therefore administration of the composition to any chicken, pig, or ruminant at risk of LPS-induced inflammation (e.g., those fed a high fat/concentrate diet) encompasses the intended patient population.
Applicant’s additional arguments (e.g., lung inflammation, necrotic enteritis) with respect to claims 1-3 and 26-27 have been considered but are moot because the new ground of rejection does not rely on any reference applied in the prior rejection of record for any teaching or matter specifically challenged in the argument.
Conclusion
No claims are 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.
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/J.L.C./Examiner, Art Unit 1655
/AARON J KOSAR/Primary Examiner, Art Unit 1655
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