DETAILED ACTION
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 28 April 2026 has been entered.
This Office Action is in response to Applicant’s Amendment and Remarks filed on 17 April 2026 in which claims 1, 11, and 21 were amended to change the scope and breadth of the claims.
Claims 1, 3, 4, 6, 8-11, 13, 14 and 18-21 are pending in the current application, and are examined on the merits herein.
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 .
Modified Rejections
The following are new ground(s) or modified rejections necessitated by Applicant's amendment. Therefore, rejections from the previous Office Action, dated 17 February 2026, have been modified and are listed below.
Response to Arguments
Applicant's arguments filed 17 April 2026 have been fully considered but they are not persuasive.
Applicant contends the claims have been amended to recite that the compound is provided at about 2.5 to 10 mg/kg. Applicant argues nothing in the combination of Acharya, Li and Jalan teaches the dosage amount claimed, with a reasonable expectation of success in achieving the claimed effect.
The above argument is not found persuasive. As noted in the modified rejection below, Acharya et al. teach at dose of 10 mg/kg, the compound decreased inflammatory cytokines and increased anti-inflammatory cytokines (para [0097]-[0098], and figures 26A-H). At 10 mg/kg, the compound decreased MIP-2, MCP-1, IL-17, IFN-Y, TNF-α, IL-1β, and IL-6 levels. And at 10 mg/kg, the compound increased IL-10 levels.
Thus, Acharya expressly teach a therapeutically effective concentration that lies within the range presently claimed, which simultaneously increases IL-10 and suppressed inflammation.
The rejection is hereby maintained.
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.
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) 1, 3, 4, 6, 8-11, 13, 14 and 18-21 are rejected under 35 U.S.C. 103 as being unpatentable over Acharya et al. (US Patent Application Publication No. 2020/0022995, cited in previous Office Action) in view of Li et al., (Chin. J. Integ. Med., 2019, vol. 25, no. 1, pp. 37-44, cited in previous Office Action) and further in view of Jalan et al. (WO2012/022939, cited in previous Office Action).
Acharya et al. teach a method of treating a subject in need of immunomodulation, comprising identifying a subject in need of immunomodulation; and providing the subject with an effective amount of a compound 8,
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(claims 3 and 18). At a dose of 10 mg/kg, the compound decreased inflammatory cytokines and increased anti-inflammatory cytokines (para [0097]-[0098], and figures 26A-H). At 10 mg/kg, the compound decreased MIP-2, MCP-1, IL-17, IFN-Y, TNF-α, IL-1β, and IL-6 levels. And at 10 mg/kg, the compound increased IL-10 levels.
The compound inhibits a TLR4 and TLR2 at 1-10 µM, inhibits TLR2 at 75-100 µM, and activates TLR4 at 75-10 µM (claim 3). The compound also modulates IL-10 at a concentration dependent manner (see fig. 7 and 8). Acharya et al. teach “reducing inflammation via activation of the anti-inflammatory cytokine IL-10 will be therapeutic for acute lung injury (ALI)….” (para [0037]). Achayra et al. teach simultaneously inhibiting TLR2 and TLR4 pathways and up-regulating IL-10 (para [0065]; [0111]). Acharya et al. teach compound 8 stimulates IL-10 production at 0.1-1.0 µM (para [0167]). The compound is formulated to treat sepsis (claim 22). The compound is formulated into a pharmaceutical composition adapted for pulmonary, parenteral, intravenous, enteral, or oral administration (para [0061]).
Acharya et al. do not expressly disclose treating acute glomerular kidney disease (present claims 1, 11, 17 and 21).
Li et al. evaluated the efficacy of a tablet comprising a mixture of plant extracts (SHT tablet) on targeting multiple toll-like receptor (TLR) pathways to treat renal ischemia-reperfusion injury (IRI), (title, abstract). Li et al. teach the active ingredients of Chinese medicine produce “multi-targeted therapeutic effects”, making it a promising pathway for designing new treatments (p.43, second para). Acute kidney injury (AKI) often results from insults to ischemia, toxic substance and septicemia, wherein renal-IRI is one of the primary causes of AKI (p.42, Discussion). Increasing evidence demonstrates ischemia-induced inflammatory responses are primarily stimulated via TLRs, including TLR2 and TLR4 (Li et al., p.42). Li et al. further found protein and mRNA expression levels of TLR2 and TLR4 exhibited synchronized uptrend after surgery-induced ischemia in a rat-animal model (p.43, third para). High doses of SHT had a protective effect on renal-IRI, wherein TLR2 and TLR4 were much lower than the model group. Li et al. conclude SHT’s protective effect on renal function may relate to the regulation of renal TLR2 and TLR4 expression, for the clinical prevention and treatment of ischemic AKI (p.43-44, bridging para).
Jalan et al. teach the use of a TLR4 inhibitor for treating an individual suffering from kidney disease (claim 1). These patients include those suffering from acute kidney injury (examples 3 and 4). Jalan teaches treating an individual suffering from renal dysfunction and/or renal failure (claim 4). The patient suffering from kidney failure also has glomerular damage (p.28, line 17 to p.29). Jalan et al. teach a method of identifying a patient suitable for treatment of renal dysfunction and/or renal failure, the method comprising measuring and comparing the level of TLR4 in the patient’s urine with a control patient not suffering from the disease (claim 10).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to administer p-nitrophenyl-N-acetyl-β-D-glucosamine at a dose of 10 mg/kg to treat a patient suffering from acute glomerular renal disease.
One having ordinary skill in the art would have been motivated to provide the compound at a dose of 10 mg/kg to treat the acute glomerular renal disease, because this specific dose was found to decrease inflammatory cytokines and increase anti-inflammatory cytokines. The concentration taught by Acharya et al. lies within the range claimed.
The recitation “wherein the compound simultaneously increases IL-10 and suppresses kidney inflammation” in claim 1, will necessarily occur upon performing the positively recited steps.
Nonetheless, the ordinary artisan would have had a reasonable expectation of success in increasing IL-10 and suppressing kidney inflammation. Acharya et al. teach the presently claimed compound acts as both a TLR4 and TLR2 activator and inhibitor. The ordinary artisan would have also known from Acharya et al., that these effects are concentration dependent. And, the ordinary artisan would have known the compound can be formulated at a concentration to inhibit TLR4 and increase the anti-inflammatory cytokine, IL-10. Acharya et al. teach the compound will reduce inflammation and treat acute lung injury. More specifically, Acharya et al. found a 10 mg/kg dose increased IL-10 levels and reduced inflammation.
One having ordinary skill in the art would have been motivated to administer p-nitrophenyl-N-acetyl-β-D-glucosamine to treat a patient suffering from acute glomerular renal disease because it inhibits TLR4 inhibitor, where Jalan et al. found TLR4 inhibitors are useful for the treatment of acute kidney injury including those suffering from glomerular damage. As discussed above, p-nitrophenyl-N-acetyl-β-D-glucosamine inhibits both TLR2 and TLR4. Furthermore, Li et al. teach targeting multiple receptors is expected to be advantageous. More specifically Li et al. found targeting TLR2 and TLR4 had a renal protective effect in an IRI-animal model, for the treatment of acute kidney injury.
The ordinary artisan would have had a reasonable expectation of success because p-nitrophenyl-N-acetyl-β-D-glucosamine is recognized as targeting both TLR2 and TLR4, wherein targeting both receptors was an effective means for treating renal-IRI for the treatment of kidney disease, and further supported by Jalan et al. which teach inhibiting TLR4 for treating kidney disease.
Thus, the claimed invention as a whole is prima facie obvious over the combined teaching of the prior art.
Conclusion
In view of the rejections to the pending claims set forth above, 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 BAHAR A CRAIGO whose telephone number is (571)270-1326. The examiner can normally be reached M-F: Noon-8pm ET.
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/BAHAR CRAIGO/
Primary Examiner
Art Unit 1699
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