CTNF 18/700,884 CTNF 101891 DETAILED ACTION Notice of Pre-AIA or AIA Status 07-03-aia AIA 15-10-aia The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA. Status of the Claims Claims 9-22 are currently pending and under examination. Priority 02-27 AIA Acknowledgment is made of applicant’s claim for foreign priority under 35 U.S.C. 119 (a)-(d). The certified copy has been filed in parent Application No. KR10-2021-0138372 , filed on October 18 2021 . Information Disclosure Statement 06-52 The information disclosure statement (IDS) submitted on 04/12/2024 and 01/06/2025. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner. Claim Rejections - 35 USC § 102 07-06 AIA 15-10-15 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. 07-07-aia AIA 07-07 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 – 07-12-aia AIA (a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention. 07-15-03-aia AIA Claim s 9-11, 13-16 and 19-20 are rejected under 35 U.S.C. 102(a)(2) as being anticipated by Yea et al. (WO2007007982A2) . Yea et al. teaches a glucose uptake modulator which comprises a compound selected from the group consisting of lysophosphatidylcholine(LPC), lysophosphatidylserine(LPS), lysophosphatidic acid(LPA), and urocortin(UCN) (See e.g. p. 37, line 2 claim 1). Yea et al. further teaches a method for treating diabetes or diabetic complications in a mammal in need thereof, which comprises administering to said mammal an effective amount of a glucose uptake modulator selected from the group consisting of lysophosphatidylcholine, lysophosphatidylserine, lysophosphatidic acid, or urocortin(See e.g. p. 4 line 24). Because LPC is a lysophospholipid, Yea et al. teaches administering a composition comprising a lysophospholipid to treat a metabolic disease, as required by claim 9. Yea et al further teaches diabetic complication is obesity, hyperlipidemia, arteriosclerosis, hypertension or heart disease(See e.g. p. 5 line 2). Thus, Yea et al. teaches the limitation of claim 10 at least insofar as the metabolic disease is selected from diabetes, obesity, hyperlipidemia, hypertension, and arteriosclerosis (Claims 13-16, 19). Yea et al. also teaches the limitation of claim 11 because the disclosed lysophospholipid may be lysophosphatidylcholine (LPC), which falls within the claimed “lysophosphatidylcholine (LPC) and/or lysophosphatidylethanolamine (LPE)” (See e.g. p. 37, line 2 claim 1) . Accordingly, treatment of diabetes by administration of LPLs, as taught by Yea et al., results in improvement or treatment of such associated metabolic disorders, such as fatty liver(claim 20), the claimed therapeutic effects are inherent to the disclosed method because fatty liver arise from the same metabolic pathways, including lipid metabolism and glucose homeostasis. Therefore, Yea et al. anticipates the instantly claimed invention . Claim Rejections - 35 USC § 103 07-06 AIA 15-10-15 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. 07-20-aia AIA 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. 07-103 AIA The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action. 07-23-aia AIA 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. 07-21-aia AIA Claim s 9–22 are rejected under 35 U.S.C. § 103 as being unpatentable over Yea et al. (J. Bio. Chem. 2009, 284(49) 33833) in view of Soga et al. (BBRC 2005, 326, 744), and further in view of Overton et al. (British J. Pharmacology 2007 153 S76), as evidenced by Bahirat et.al. (Eur. J Pharmacology 2017, 801:35), Hoem et al. (WO2019123015A1), Yamada et al.(Adv Ther. 2018 Mar;35(3):367-381), Tadaki et al. (Clin Exp Pharmacol Physiol. 2019 46(10):910-919) and Watanabe et al. ( J Cardiovasc Pharmacol. 2002;39(3):449-59) . Regarding claims 9-11 and 14, Yea et al. teaches lysophosphatidylcholine activates adipocyte glucose uptake and lowers Blood glucose Levels in murine models of diabetes(See e.g. p. 33833 title), LPC improves blood glucose levels in mouse models of type 1 and 2 diabetes (see e.g. p. 33833 col. 1 line 19). These results suggest that an understanding of the mode of action of LPC may provide a new perspective of glucose homeostasis. Yea et al. teaches that an understanding of the mechanism responsible for the metabolic effects of LPC could lead to the development of a novel means of treating diabetes(see e.g. p. 33833 col. 2 line 46). Yea et al. does not expressly teach the broader claimed LPL genus, including LPE, or the broader set of recited metabolic diseases. Regarding claims 10-12 and 19, Soga et al teaches a lysophospholipid series including LPC and LPE, and further identifies specific LPC species including 16:0, 18:0, and 18:1(See e.g. p 748 Fig. 3). Soga et al. also teaches that LPC plays an etiological role in atherosclerosis, thereby suggesting use of LPLs in relation to arteriosclerosis( See e.g. p. 744 col. 2 line 1), and teaches that LPLs, including LPC, act through GPR119 as endogenous mediators( See e.g. p. 744 col. 2 line 7). These teachings would have suggested to a person of ordinary skill in the art that Yea’s beneficial metabolic findings with LPC were not limited to diabetes alone, but were part of a broader LPL/GPR119 metabolic pathway. Accordingly, it would have been obvious to expand Yea’s LPC-based metabolic treatment method to the related LPLs taught by Soga et al., including LPE. Regarding claims 13-18, Overton et al. teaches that GPR119 is a target for treatment of type 2 diabetes and obesity(See e.g. p S76 title), and that GPR119 agonists improve glucose homeostasis, promote glucose-stimulated insulin secretion, stimulate GLP-1 and GIP release, suppress food intake, reduce weight gain, and lower plasma triglyceride levels(See e.g. p S78 col. 2 line 1). Overton et al. also states that GPR119 agonists could be valuable agents for treatment of type 2 diabetes and obesity by improving glucose homeostasis while concurrently limiting food intake and body weight gain, and describes oral dosing as a therapeutic approach(See e.g. p. S79 col. 1 line 12). Overton et al. teaches certain lysophospholipids, including LPC species, LPE, and LPI, produced elevated cAMP in GPR119-expressing cells(See e.g. p S78 col. 1 line 5). Soga et al. teaches that LPC acts through GPR119. Overton et al. further teaches that multiple lysophospholipids, including oleoyl-, stearoyl-, and palmitoyl-LPC, lysophosphatidylethanolamine, and lysophosphatidylinositol, produced elevated cAMP levels in GPR119-expressing cells, thereby evidencing that certain lysophospholipids function as GPR119 agonists(See e.g. p S78 col. 1 line 5). Because Soga et al. teaches LPLs, including LPC and LPE, as GPR119 agonists/endogenous mediators, and Overton et al. teaches the therapeutic utility of GPR119 agonism for diabetes, obesity, glycemic control, and weight-related metabolic disorders, it would have been obvious to use the LPLs taught by Soga et al., including LPC and LPE, in Yea et al.’s metabolic treatment method for obesity, diabetes, hyperlipidemia, hyperinsulinemia, and related metabolic disorders. Regarding claim 16, Watanabe et al. teaches Lysophosphatidylcholine is a major contributor to the synergistic effect of mildly oxidized low-density lipoprotein with endothelin-1 on vascular smooth muscle cell proliferation(See e. g. p 449, title). Because endo Endothelin-1 (ET-1) and oxidized low-density lipoprotein (ox-LDL) are associated with atherosclerosis and essential hypertension (See e. g. p 449, Abstract). Watanabe et al. would have suggested to one of ordinary skill in the art that LPC was relevant to hypertension-associated vascular disease. Regarding claim 17, Yamada et al. teaches that the GPR119 agonist DS-8500a significantly reduced total cholesterol and LDL-cholesterol(See e.g. p. 368 col. 1 line 11). Regarding claim 18, Tadaki et al. teaches that chronic treatment with the GPR119 agonist JTP-109192 improved insulin sensitivity in Zucker Fatty rats( See e.g. p. 910 title, abstract), thereby supporting treatment of hyperinsulinemia-associated metabolic abnormality. Regarding claim 15, 20, Bahirat teaches that APD668, a GPR119 agonist, inhibits intestinal triglyceride absorption after acute fat load, increases incretin secretion, improves fat tolerance, and, upon oral administration in a high-trans-fat diet steatohepatitis model, ameliorates hepatic endpoints including liver weight and steatosis(See e.g. p36 col. 2 line 17). Bahirat further states that these findings suggest GPR119 agonists may represent a promising therapeutic strategy for treatment of dyslipidemia and non-alcoholic steatohepatitis(See e.g. p. 35 Abstract). In view of Soga’s teaching that LPC/LPE-type LPL signaling acts through GPR119, and Overton’s teaching that GPR119 agonist is useful for metabolic disease treatment, Bahirat et al. would have provided additional motivation and reasonable expectation of success to employ such LPL/GPR119 agonist therapy for fatty liver. Regarding claims 21 and 22, Hoem et al. teaches marine lysophosphatidylcholine compositions for use in pharmaceuticals, nutraceuticals, and functional foods(See e.g. p. 1 line 4); teaches a pharmaceutical or nutraceutical composition comprising LPC and a physiologically acceptable carrier(See e.g. p. 59 claims 22, 23, 28); and teaches oral delivery vehicles and formulation for human consumption(See e.g. p. 59 claims 24). Hoem also reinforces claim 12 to the extent it teaches LPC compositions containing EPA and/or DHA(See e.g. p. 57 claims 1), thereby further supporting at least some claimed species selections within the recited lipid class. Once the art suggested administering LPC and/or LPE compositions to treat metabolic disease, formulating the active LPL in a pharmaceutical composition with a pharmaceutically acceptable carrier, excipient, or diluent, as recited in claim 21, would have been an obvious and routine formulation choice for a person of ordinary skill in the art. Similarly, because the cited art treats these lipids as endogenous metabolic mediators and Overton discusses oral dosing for improved glycemic control and weight loss, incorporating the LPL into a health functional food, as recited in claim 22, would have been an obvious alternative delivery format for the same known metabolic purpose. it would have been obvious to one of ordinary skill in the art before the effective date to modify Yea et al.’s method of administering LPC for diabetes in view of Soga et al.’s teachings that the relevant bioactive LPC and LPE, including specific LPC species, and that such lipids function through GPR119-related signaling, and further in view of Overton et al.’s teachings that GPR119 agonists are useful for improving glucose homeostasis, enhancing glucose-stimulated insulin secretion, stimulating incretin release, reducing food intake, limiting weight gain, and treating diabetes, obesity, and related metabolic disorders. A person of ordinary skill in the art would have been motivated to combine these teachings because the references are directed to the same field of metabolic-disease therapy and collectively suggest that modulation of the same biological pathway would predictably provide benefit across related metabolic conditions rather than only a single disease state. Bahirat et al. further evidences that GPR119 agonist is useful in improving fat tolerance and attenuating fatty liver, thereby reinforcing the reasonable expectation that extending the known LPC/LPE-GPR119 metabolic pathway to fatty liver and other recited metabolic disorders would have been a predictable use of prior-art elements according to their established functions. Moreover, Noem et al. teaches lysophosphatidylcholine compositions for in pharmaceutical, functional food products, including compositions containing physiologically acceptable carriers and excipients for oral consumption, selecting among the disclosed lysophospholipids, including LPC and LPE, selecting known lipid species within that class, and formulating such agents in a pharmaceutical composition or health functional food would have constituted no more than routine optimization of known result-effective variables and implementation of known delivery formats for known metabolic benefits. Accordingly, the claimed methods of claims 9–22 would have been the product of ordinary skill and common sense, supported by a reasonable expectation of success, rather than of inventive effective. Conclusion No claims are allowed. Any inquiry concerning this communication or earlier communications from the examiner should be directed to GENBIN SHI whose telephone number is (571)272-8796. 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If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000. /GENBIN SHI/Examiner, Art Unit 1628 /AMY L CLARK/Supervisory Patent Examiner, Art Unit 1628 Application/Control Number: 18/700,884 Page 2 Art Unit: 1628 Application/Control Number: 18/700,884 Page 3 Art Unit: 1628 Application/Control Number: 18/700,884 Page 4 Art Unit: 1628 Application/Control Number: 18/700,884 Page 5 Art Unit: 1628 Application/Control Number: 18/700,884 Page 6 Art Unit: 1628 Application/Control Number: 18/700,884 Page 7 Art Unit: 1628 Application/Control Number: 18/700,884 Page 8 Art Unit: 1628 Application/Control Number: 18/700,884 Page 9 Art Unit: 1628 Application/Control Number: 18/700,884 Page 10 Art Unit: 1628
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