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 .
DETAILED ACTION
The amendment after non-final office action filed November 10, 2025 is acknowledged. Claims 39-40, 43-49 and 54-56 were cancelled and claims 37-38, 41-42, 50-53 are pending.
Election/Restrictions
The restriction requirement was deemed proper and made FINAL in a previous office action.. Claim 38 remains withdrawn as being drawn to a non-elected invention/species.
Claims 37, 41-42, 50-53 are examined on the merits of this office action.
*After further review, a second Non-final follows due new rejection(s) under Double Patenting based on Amendment of the claims.
Maintained/Revised Rejections
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.
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) 37, 41-42, 50-53 are rejected under 35 U.S.C. 103 as being unpatentable over Chen (WO2012109561) in view of Patel (Curr Diabetes Rev 2014;10(4):238-50), Bhatt (HepatoBiliary Surg Nutr 2015;4(2):101-108) and Armstrong (Lancet 2016; 387: 679–90). *All references cited previously.
Chen teaches a method of treating obesity and metabolic syndrome in subjects comprising administering GGL (also referred to diapin, see Example 2, see abstract, claims 1-2). Chen teaches using animal models of obesity and diabetes (ob/ob and db/db). Chen specifically teaches that diapin stimulated GLP-1 secretion, insulin secretion and lowers blood glucose levels (see Figures 7-10). Chen teaches “The amount of the composition administered is therapeutically effective to achieve at least one of the following: reducing blood glucose levels, stimulating insulin secretion, stimulating GLP-1 secretion, reducing insulin resistance, and improving glycemic control” (see paragraph 0066).
Chen teaches administration of additional therapeutic agents for treatment of metabolic syndrome or diabetes (see paragraph 0075) and in particular a DPP4 inhibitor and TZD (see paragraph 0075, lines 10-11). Chen does not specifically provide an example of treating patients with fatty liver disease.
Bhatt teaches that insulin resistance appears to be a critical contributing factor to NAFLD (see page 103, left column, first paragraph). Bhatt teaches “ Elevated circulating free fatty acid levels, in part related to diminished suppression of adipose tissue lipolysis by insulin, result in increased delivery of free fatty acids to the liver. The synthesis of excess triglyceride in the liver is driven by this supply of fatty acids and the accumulation of excess liver fat is further exacerbated by impaired hepatic fatty acid oxidation secondary to insulin resistance. When glucose levels are elevated in the context of prediabetes or overt diabetes, this provides further substrate for triglyceride synthesis. Additionally, impaired very low density lipoprotein (VLDL) secretion, which commonly occurs with insulin resistance, further contributes to hepatic fat accumulation. Insulin resistance is not only a factor in obesity and diabetes, but also may be an underlying mechanism for NAFLD even in non-obese individuals without diabetes, as noted in a euglycemic insulin clamp study” (see page 103, left column). Bhatt teaches “A recent small study from Japan showed improved steatosis and NASH histology (lower NAS score) following liraglutide treatment in overweight or obese subjects with prediabetes (37). This was associated with improved glucose tolerance and a small decrease in BMI” (see GLP-1 analogs section).
Armstrong teaches use of Liraglutide (GLP-1 agonist) in patients with NASH and with or without diabetes (see Method, Abstract OC-016). Armstrong teaches that both patients with diabetes and without diabetes and NASH achieved the primary endpoint and resolution of NASH (see page 686, right column, second paragraph).
It would have been obvious before the effective filing date of the claimed invention to treat patients with fatty liver disease, including NAFLD and NASH, in non-diabetic subjects with the compositions of Chen. One of ordinary skill in the art would have been motivated to do so given that lowering glucose levels, improving glucose utilization, reducing insulin resistance and increasing GLP-1 secretion would be beneficial in treating patients with fatty liver disease regardless of diabetes status. Bhatt teaches that insulin resistance is a critical contributing factor to NAFLD, even in non-obese, non-diabetic individuals, and that improving insulin sensitivity ameliorates hepatic steatosis and fibrosis. Armstrong teaches that treatment with a GLP-1 agonist , liraglutide, improved NASH outcomes and achieved resolution of NASH in both diabetic and non-diabetic patients. Given that Chen’s GGL peptide stimulates GLP-1 secretion, improves insulin secretion, and reduces insulin resistance, a person of ordinary skill in the art would have had a reasonable expectation of success in using GGL or GGdL to treat NASH or NAFLD in non-diabetic subjects with similar beneficial results.
Regarding claim 53,Chen does not specifically provide an example using additional therapeutics (TZD or DPP4 inhibitor).
However, MPEP states “It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art.” In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) (citations omitted) (Claims to a process of preparing a spray-dried detergent by mixing together two conventional spray-dried detergents were held to be prima facie obvious.). See also In re Crockett, 279 F.2d 274, 126 USPQ 186 (CCPA 1960) (Claims directed to a method and material for treating cast iron using a mixture comprising calcium carbide and magnesium oxide were held unpatentable over prior art disclosures that the aforementioned components individually promote the formation of a nodular structure in cast iron.); and Ex parte Quadranti, 25 USPQ2d 1071 (Bd. Pat. App. & Inter. 1992) (mixture of two known herbicides held prima facie obvious). But see In re Geiger, 815 F.2d 686, 2 USPQ2d 1276 (Fed. Cir. 1987) (“Based upon the prior art and the fact that each of the three components of the composition used in the claimed method is conventionally employed in the art for treating cooling water systems, the board held that it would have been prima facie obvious, within the meaning of 35 U.S.C. 103, to employ these components in combination for their known functions and to optimize the amount of each additive....Appellant argues... hindsight reconstruction or at best,... obvious to try’.... We agree with appellant.”). One of ordinary skilled in the art would have been motivated to combine the two each known (DPP4 inhibitors, TZD) to be useful for the same purpose (treating diabetes, obesity, improving glucose utilization), with a reasonable expectation that at least here will be an additive effect.
Regarding the limitations of “decreases hepatic triglyceride levels” (claim 41); hepatic cholesterol (see claim 42); stabilization or reduction in NAFLD activity score (claim 50); slowing the progression of the steatosis component or inflammation of NAS, which is a SCORE (claim 51); wherein NAS is different by no less than 1.5 points…(claim 52); Claims 41, 42, 50, 51 and 52 simply express the intended results of the process step (administering the tripeptide) positively recited. MPEP 2111.04 (I).
Chen in view of Bhatt and Armstrong teach the same method of the instant claims including the same subject population and therapeutic and thus, these effects will inherently be achieved. Please note that the claims do not require that the patients have NASH or any specific NAS (NAFLD Score) which BRI, can be zero. Furthermore, Chen teaches administering the peptide which is the treatment. Claim 37 has no effective amount or mode of administration recited, so any dose or route of administration would result in the results claimed.
Response to Applicant’s Arguments
Applicant argues “The Applicant respectfully disagrees and notes that the combination of references cited by the Examiner does not render the claimed invention obvious because there was no reasonable expectation of success in substituting Chen's tripeptide into the therapeutic context described by Armstrong. Indeed, a person of skill reviewing Armstrong would necessarily note that it reports a controlled human study using liraglutide, a long-acting GLP- 1 receptor agonist administered by injection at pharmacologic doses. Chen, by contrast, teaches use of a much smaller peptide, Gly-Gly-Leu, given orally to improve glycemic control in diabetic and pre-diabetic animals through stimulation of endogenous GLP-1 and insulin release. Chen's disclosure is limited to glycemia-focused endpoints and does not demonstrate any effect on liver disease or on non-diabetic subjects. In fact, Chen shows that the peptide had no effect on fasting glucose in normal C57BL/6J mice, which would discourage a skilled artisan from expecting efficacy in non-diabetic liver disease. Even with Bhatt and Patel recognizing that NAFLD is metabolically linked to insulin resistance, it would not have been predictable that Chen's small tripeptide, never shown in a NASH setting or in human trials, would replicate the histologic improvements achieved with Armstrong's potent GLP-1 agonist. The structural and mechanistic differences between an injected long- acting agonist and an orally administered nutrient-like tripeptide create a clear uncertainty in outcome. The claimed method therefore would not have been obvious, and the obviousness
Applicant argues that Armstrong uses liraglutide, a long acting GLP-1 receptor agonist and Chen teaches a small oral tripeptide. The structural, pharmacological and administration differences create uncertainty in outcome. Therefore a person of ordinary skill would not expect Chens peptide to replicate Armstrong’s NASH improvements. Applicant’s argument has been fully considered but not found persuasive. The rejection is based on a shared biological mechanism, not structural identity. Chen teaches that Diapin stimulates endogenous GLP-1, increases insulin secretion, reduces insulin resistance and improves glucose utilization. Bhatt teaches insulin resistance is a central driver of NAFLD and NASH, including non-diabetic individuals. Armstrong teaches GLP-1 agonism improves NASH histology in both diabetic and non-diabetic patients. Thus, GLP-1 pathway modulation improved insulin sensitivity and improved NAFLD/NASH. The reasonable expectation of success arises from the shared pathway modulation not molecular similarity (see MPEP 243.02, “Obviousness does not require absolute predictability, but at least some degree of predictability is required”).
Applicant further argues that Chen is limited to glycemic endpoints and does not address liver disease. Applicant’s arguments have been fully considered but not found persuasive. It is the combination of Chen in view of Bhatt and Armstrong that render obvious the instant claims. Although Chen reports glycemic endpoints, these endpoints directly reflect sensitivity, GLP-1 signaling, substrate flux modulation. Bhatt explains that excess hepatic fat accumulation results from insulin resistance and impaired lipid handling. Thus, Chen’s biological effects are the upstream mechanisms implicated in both NAFLD and NAHS. A person of ordinary skill would recognize that improving insulin resistance improves hepatic steatosis.
Applicant argues that Chen does not demonstrate effect in non-diabetic subjects and Armstrong’s success in non-diabetic NASH cannot be extrapolated to Diapin.
Applicant relies on Chen (figures 9-12) showing no effect on fasting glucose in normal mice. However, NAFLD is driven by insulin resistance not normal baseline physiology. Applicant’s arguments have been fully considered but not found persuasive. Lack of effect in normoglycemic, insulin sensitive mice is expected. This does not criticize, discourage or discredit use in insulin resistance disease. Importantly, Figures 25-26 of Chen show that Diapin significantly reduces glucose excursion in a glucose challenge in control mice. Thus, there is no teaching away from use of Diapin in non-diabetic mice.
Applicant argues Chen lacks NASH and animal model data, histologic liver endpoints and there is no reasonable expectation of success.
Applicant’s arguments have been fully considered but not found persuasive. It is the combination of Chen in view of Bhatt and Armstrong that render obvious the instant claims with a reasonable expectation of success. Chen teaches that diapin modulates GLP-1 and insulin resistance, Bhatt links insulin resistance to NAFLD pathogenesis and Armstrong demonstrates GLP-1 agonism improves NASH. The mechanistic pathway is clear. The Examiner maintains that it would have been obvious before the effective filing date of the claimed invention to treat patients with fatty liver disease, including NAFLD and NASH, in non-diabetic subjects with the compositions of Chen. One of ordinary skill in the art would have been motivated to do so given that lowering glucose levels, improving glucose utilization, reducing insulin resistance and increasing GLP-1 secretion would be beneficial in treating patients with fatty liver disease regardless of diabetes status. Bhatt teaches that insulin resistance is a critical contributing factor to NAFLD, even in non-obese, non-diabetic individuals, and that improving insulin sensitivity ameliorates hepatic steatosis and fibrosis. Armstrong teaches that treatment with a GLP-1 agonist , liraglutide, improved NASH outcomes and achieved resolution of NASH in both diabetic and non-diabetic patients. Given that Chen’s GGL peptide stimulates GLP-1 secretion, improves insulin secretion, and reduces insulin resistance, a person of ordinary skill in the art would have had a reasonable expectation of success in using GGL or GGdL to treat NASH or NAFLD in non-diabetic subjects with similar beneficial results.
Applicant argues substituting Chens peptide into Armstrong’s therapeutic context is unpredictable and that the different mechanisms create uncertainty.
Applicant’s arguments have been fully considered but not found persuasive. Applicant asserts uncertainty but provides no evidence that GLP-1 stimulation would fail in NAFLD, insulin resistance reduction would not improve hepatic steatosis and that diapin acts through a contradictory mechanism. Speculative assertions of uncertainty are insufficient to overcome a prima facie case of obviousness. For all the reasons stated above, the rejection is maintained.
New Rejections
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 37, 41-42, 50-53 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 28, 30, 38-41 of co-pending Application No.18/163773 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because:.
The instant application claims A method for treating liver disease in a mammalian subject in need thereof comprising administering to the subject at least one tripeptide selected from Gly-Gly-Leu or Gly-Gly-dLeu, or a pharmaceutically acceptable salt thereof, wherein the mammalian subject does not have diabetes, and wherein the mammalian subject has liver disease and wherein the liver disease is fatty liver, steatohepatitis, non-alcoholic fatty liver disease (NAFLD), or non-alcoholic steatohepatitis (NASH).…” (claim 37). The co-pending application further claims reduction in TG (claim 41); decrease in hepatic cholesterol (claim 42); functional properties including reduction in NAS score (Claims 50-52), an additional therapeutic including GLP-1 (claim 53 ) treatment for the prevention delay or reduction in arteriosclerosis (which Applicants claim as a complication of atherosclerosis).
The copending application claims “A method of treating atherosclerosis, the method comprising administering to a subject in need thereof, a therapeutically effective amount of a glycine-containing tripeptide molecule Gly-Gly-Leu or Gly-Gly-dLeu, or a pharmaceutically acceptable salt thereof, wherein the subject has atherosclerosis and does not have diabetes, wherein the administering increases hepatic expression of fatty acid oxidation genes…..wherein the administering reduces atherosclerotic plaque burden in the aorta, wherein the administering reduces plasma LDL cholesterol levels, wherein the administering reduces hepatic triglyceride content and hepatic total cholesterol levels in the subject.”. The copending application further claims wherein the subject has CKD, stroke, atherosclerosis, PAD, CAD or aneurysm (see claim 3); and administering an additional therapeutic such as a GLP-1 or variant thereof (see claim 38). The co-pending application doesn’t specifically claim treating liver disease (NASH, NAFLD or steatopheptitis).
It would have been an obvious variant of the invention claimed in the co-pending application to treat liver disease including fatty liver disease and NAFLD. The co-pending application claims recite administering the same compound for reducing plasma LDL cholesterol levels, reducing hepatic total cholesterol and triglyceride content, all of which would have been beneficial in treating fatty liver disease, including NAFLD, in non-diabetic subjects. A person of ordinary skill would have reasonably expected that a therapy capable of reducing liver triglycerides, LDL and hepatic total cholesterol would be beneficial at treating fatty liver disease. Accordingly, the present claims do no define a patentably distinct use of the same peptide. The properties of instant claims 50-52 would inherently occur as a result of practicing the method of Co-pending Application No.18/163773 (same patient population, fatty liver disease (NAFLD) and administering the same drug.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 37, 41-42, 50-53 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 14, 53-64 of co-pending Application No.18/020908 (reference application) in view of Armstrong (see above reference). Although the claims at issue are not identical, they are not patentably distinct from each other because:.
The instant application claims A method for treating liver disease in a mammalian subject in need thereof comprising administering to the subject at least one tripeptide selected from Gly-Gly-Leu or Gly-Gly-dLeu, or a pharmaceutically acceptable salt thereof, wherein the mammalian subject does not have diabetes, and wherein the mammalian subject has liver disease and wherein the liver disease is fatty liver, steatohepatitis, non-alcoholic fatty liver disease (NAFLD), or non-alcoholic steatohepatitis (NASH).…” (claim 37). The co-pending application further claims reduction in TG (claim 41); decrease in hepatic cholesterol (claim 42); functional properties including reduction in NAS score (Claims 50-52), an additional therapeutic including GLP-1 (claim 53 ) treatment for the prevention delay or reduction in arteriosclerosis (which Applicants claim as a complication of atherosclerosis).
The copending application claims “A method of treating steatohepatitis in a subject, comprising administering a pharmaceutically effective amount of at least one N-acyl amino acid product to the subject, wherein the N-acyl amino acid product has a fatty acid component and an amino acid component” (see claim 14). The copending application further claims wherein the amino acid component is glycine- glycine-leucine or glycine-glycine-D-leucine (which is the peptide of the instant claims) (claim 58); wherein the steatohepatitis is non-alcoholic steatohepatitis, alcoholic liver disease or alcoholic steatohepatitis (claim 62); wherein the treating results in the subject in decreased liver fat, decreased inflammatory status, decreased injured hepatocytes and decreased atherosclerotic plaques (see claim 62). The properties of instant claims 41-42, 50-52 would inherently occur as a result of practicing the method of Co-pending Application No. 18/020908 (same patient population, fatty liver disease (NAFLD) and administering the same drug. Co-pending Application No.18/020908 is silent to including an additional therapeutic. However, Armstrong teaches use of Liraglutide (GLP-1 agonist) in patients with NASH and with or without diabetes (see Method, Abstract OC-016). Armstrong teaches that both patients with diabetes and without diabetes and NASH achieved the primary endpoint and resolution of NASH (see page 686, right column, second paragraph).
MPEP states “It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art.” In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) (citations omitted) (Claims to a process of preparing a spray-dried detergent by mixing together two conventional spray-dried detergents were held to be prima facie obvious.). See also In re Crockett, 279 F.2d 274, 126 USPQ 186 (CCPA 1960) (Claims directed to a method and material for treating cast iron using a mixture comprising calcium carbide and magnesium oxide were held unpatentable over prior art disclosures that the aforementioned components individually promote the formation of a nodular structure in cast iron.); and Ex parte Quadranti, 25 USPQ2d 1071 (Bd. Pat. App. & Inter. 1992) (mixture of two known herbicides held prima facie obvious). But see In re Geiger, 815 F.2d 686, 2 USPQ2d 1276 (Fed. Cir. 1987) (“Based upon the prior art and the fact that each of the three components of the composition used in the claimed method is conventionally employed in the art for treating cooling water systems, the board held that it would have been prima facie obvious, within the meaning of 35 U.S.C. 103, to employ these components in combination for their known functions and to optimize the amount of each additive....Appellant argues... hindsight reconstruction or at best,... obvious to try’.... We agree with appellant.”). One of ordinary skilled in the art would have been motivated to combine the two each known (GLP-1 agonists) to be useful for the same purpose (treating diabetes, obesity, improving glucose utilization, NASH), with a reasonable expectation that at least here will be an additive effect.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
No claims are allowed.
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/ERINNE R DABKOWSKI/Examiner, Art Unit 1654