Notice of Pre-AIA or AIA Status
The present application, filed on or after December 14, 2023 is being examined under the first inventor to file provisions of the AIA .
Priority
This application filed on 12/14/2023 claims priority to PCT application no. PCT/KR2022/008555, filed on 06/16/2022, and claims foreign priority to application no. KR10-2021-0077914, filed on 06/16/2021. Acknowledgment is made of Applicant's claim for foreign priority under 35 U.S.C. 119 (a)-(d).
Status of Claims
The amendment of Claims on 12/14/2023 has been entered. Claims 1-2 and 4-6 of the claim set filed 12/14/2023 are under examination and are presently considered. Claims 3 and 7 are Canceled.
Information Disclosure Statement
The ISD filed on 12/14/2023 (6 pages) has been acknowledged and considered.
Drawings
The Drawings filed on 12/14/2023 (Figures 1-5) are acceptable subject to correction of the informalities indicated below:
Figure 3 is objected to as failing to comply with 37 CFR 1.84(p)(5) because it does not include the following reference sign(s) mentioned in the description: the specification recites Figure 3 “shows the blood glucose control effect confirmed through glucose tolerance test” (Specification, pg. 10, line 7); however, Figure 3 is a graph showing a change in body weight.
Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Claim Interpretation
Claims 1-2 and 4-6 are directed to a method comprising administering a Lactobacillus fermentum GB-102 strain deposited with accession number KCTC 14105BP and a Lactobacillus fermentum GB-103 strain deposited with the accession number of KCTC 14106BP in combination with regulatory T cells (Treg), for the suppression of weight gain, and the prevention or treatment of selected metabolic disease species.
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 Langi, 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/applyingonline/
eterminal-disclaimer.
Claims 1-2 and 4-6 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1-2 and 4-6 in copending U.S. Application No. 18/569,947 in further view of US 2011/0044939 A1 (2011; hereafter “Feuerer”, cited on Form 892).
Although the claims at issue are not identical, they are not patentably distinct
from each other. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
U.S. Application No. 18/569,947 discloses “a method for suppressing weight gain comprising administering a Lactobacillus fermentum stain in combination with natural killer cells” (Claim 1); “a method for suppressing weigh gain comprising a Lactobacillus fermentum GB-102 strain deposited with the accession number of KCTC 14105BP in combination with natural killer cells” (Claim 2); “a method for preventing or treating a metabolic disease comprising administering a Lactobacillus fermentum strain in combination with natural killer cells” (Claim 4); “a method for preventing or treating a metabolic disease comprising administering a Lactobacillus fermentum GB-102 strain deposited with accession number KCTC 14105BP in combination with natural killer cells” (Claim 5); “a method for preventing or treating a metabolic disease administering a Lactobacillus fermentum strain in combination with natural kill cells, wherein the metabolic disease is selected from the group consisting of obesity, diabetes, hypertension, arteriosclerosis, hyperlipidemia, hyperinsulinemia, insulin resistance, metabolic inflammation, fasting blood glucose disorder, impaired glucose tolerance and glucose tolerance syndrome” (Claim 6).
U.S. Application No. 18/569,947 does not disclose the use of regulatory T cells (Treg) in combination with GB-102 (KCTC 14106BP) for the suppression of weight gain, and the prevention or treatment of metabolic disease.
Feuerer teaches “regulatory T (Treg) cells are readily detectable in the abdominal adipose tissue of normal adult mice, accumulating with age to the unusually high fraction of around 50% of CD4 T lymphocytes” (Paragraph 0005). Feuerer teaches “abdominal fat Treg cells express high levels of the anti-inflammatory cytokine IL-10, which directly reduces adipocyte secretion of inflammatory mediators; thus, these cells and their anti-inflammatory properties can be used to inhibit elements of the metabolic syndrome” (Paragraph 0005). Feuerer teaches “methods for inhibiting, preventing, delaying, or reducing the development or severity of obesity-associated disorders in a subject”(Paragraph 0006). Feuerer teaches “methods include obtaining an initial population of Foxp3+CD25+CD4+ regulatory T cells; engineering said initial population of T cells to express IL-10 and optionally culturing said cells in the presence of adiponectin (Paragraph 0008). Feuerer teaches “methods for treating obesity and/or obesity-associated conditions, e.g., insulin resistance, metabolic syndrome, or type 2 diabetes, in a subject; the methods include administering a therapeutically effective amount of IL-10 and optionally adiponectin to the subject. In some embodiments, the IL-10 and adiponectin are administered systemically” (Paragraph 0015). Feuerer teaches “findings indicate that Tregs guard against excessive inflammation of the adipose tissue and local and downstream systemic consequences, and strongly suggest that Tregs residing in the fat are responsible” (Paragraph 0115). Feuerer teaches “administration can be systemic, or local, e.g., injection into an area of unwanted fat tissue, e.g., subcutaneous or omental fat. When both IL-10 and adiponectin are used, administration can be of a single composition, e.g., a pill or injectable solution, that includes both IL-10 and adiponectin, or can be administration of two separate compositions (paragraph 0071).
Therefore, U.S. Application No. 18/569,947 teaches a method of using a Lactobacillus fermentum strain (GB-102 strain deposited KCTC 14105BP) for suppressing weight gain, and preventing or treating metabolic disease species (e.g., obesity, diabetes, hypertension, arteriosclerosis, hyperlipidemia, hyperinsulinemia, insulin resistance, metabolic inflammation, fasting blood glucose disorder, impaired glucose tolerance and glucose tolerance syndrome). Feuerer further teaches the use of regulatory T cells in a method for inhibiting, preventing, delaying, or reducing metabolic disease species (e.g., obesity and/or obesity-associated conditions, insulin resistance, metabolic syndrome, or type 2 diabetes), in subjects.
A person of ordinary skill in the art would have been motivated to combine the method of U.S. Application No. 18/569,947 with the teachings of Feuerer because both the Lactobacillus fermentum strain GB 102 and regulatory T cells were used for the same purpose. Therefore, one would have been motivated to combine the teachings in order to result in a method for suppressing weight gain, and preventing or treating metabolic disease species using a Lactobacillus fermentum strain (GB-102 deposited KCTC 14105BP); in combination with regulatory T cells.
It would have been prima facie obvious to one of ordinary skill in the art to combine the teachings recited by Feuerer with the method of 18/569,947 to suppress weight gain, and for preventing or treating dysbiosis, and metabolic disease using a Lactobacillus fermentum strain(selected from GB-102) because all elements are known in the art to suppress weight gain by preventing or treating obesity; and prevent or treating other metabolic disease or conditions. Therefore, combining them would make the methods for suppressing weight gain, and the prevention or treatment of metabolic disease species more optimized and there would be a reasonable expectation that combining all elements together would yield an optimized method formulation. The combination would represent the use of multiple known therapeutic methods that treat the same metabolic diseases for improving treatment efficacy. A person of ordinary skill in the art would therefore have a reasonable expectation that administering Lactobacillus fermentum strain(selected from GB-102), with regulatory T cells would further support metabolic improvement; and yielded predictable results (the optimized suppression of weight gain, and the prevention or treatment of metabolic disease species) to one of ordinary skill in the art at the time of the invention; therefore, the instant claims are directed to a combination of known elements performing established functions that are obvious over U.S. Application No. 18/569,947, in view of Feuerer.
Claims 1-2 and 4-6 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-10of US12502412B2, in further view of US2011/0044939 A1 (2011; hereafter “Feuerer”, cited on Form 892).
US12502412B2 discloses “a method of preventing or treating a metabolic disease comprising administering Lactobacillus fermentum strain (Accession No. KCTC 14106BP) to the subject” (Claim 1); wherein the metabolic disease is any one selected from a group consisting of obesity, hypertension, arteriosclerosis, hyperlipidemia, fatty liver, non-alcoholic fatty liver disease, hyperinsulinemia, diabetes, and insulin resistance syndrome” (Claim 2); “wherein the strain inhibits fat accumulation in white adipose tissue (Claim 3); “wherein the strain reduces metabolic inflammation in white adipose tissue: (Claim 4); “wherein the strain inhibits fat accumulation in brown adipose tissue” (Claim 5); “wherein the strain inhibits fat accumulation in liver tissue” (Claim 6); “wherein the strain reduces a blood glucose level” (Claim 7); “wherein the strain reduces insulin resistance” (Claim 8); “wherein the Lactobacillus fermentum strain (Accession No. KCTC 14106BP) is comprised in a food composition” (Claim 9); “ wherein the Lactobacillus fermentum strain (Accession No. KCTC 14106BP) is comprised in a feed composition” (Claim 10).
US12502412B2 does not disclose the use of regulatory T cells (Treg) in combination with the Lactobacillus fermentum strain GB-103 (KCTC 14106BP) for the suppression of weight gain, and the prevention or treatment of selected from a group of metabolic disease species.
Feuerer teaches “regulatory T (Treg) cells are readily detectable in the abdominal adipose tissue of normal adult mice, accumulating with age to the unusually high fraction of around 50% of CD4 T lymphocytes” (Paragraph 0005). Feuerer teaches “abdominal fat Treg cells express high levels of the anti-inflammatory cytokine IL-10, which directly reduces adipocyte secretion of inflammatory mediators; thus, these cells and their anti-inflammatory properties can be used to inhibit elements of the metabolic syndrome” (Paragraph 0005). Feuerer teaches “methods for inhibiting, preventing, delaying, or reducing the development or severity of obesity-associated disorders in a subject”(Paragraph 0006). Feuerer teaches “methods include obtaining an initial population of Foxp3+CD25+CD4+ regulatory T cells; engineering said initial population of T cells to express IL-10 and optionally culturing said cells in the presence of adiponectin (Paragraph 0008). Feuerer teaches “methods for treating obesity and/or obesity-associated conditions, e.g., insulin resistance, metabolic syndrome, or type 2 diabetes, in a subject; the methods include administering a therapeutically effective amount of IL-10 and optionally adiponectin to the subject. In some embodiments, the IL-10 and adiponectin are administered systemically” (Paragraph 0015). Feuerer teaches “findings indicate that Tregs guard against excessive inflammation of the adipose tissue and local and downstream systemic consequences, and strongly suggest that Tregs residing in the fat are responsible” (Paragraph 0115). Feuerer teaches “administration can be systemic, or local, e.g., injection into an area of unwanted fat tissue, e.g., subcutaneous or omental fat. When both IL-10 and adiponectin are used, administration can be of a single composition, e.g., a pill or injectable solution, that includes both IL-10 and adiponectin, or can be administration of two separate compositions (paragraph 0071).
Therefore, US12502412B2 teaches a method of inhibiting fat accumulation (suppressing weight gain), and preventing or treating selected metabolic disease species comprising administering a Lactobacillus fermentum strain (Accession No. KCTC 14106BP) to a subject. Feuerer further teaches the use of regulatory T cells in a method for inhibiting, preventing, delaying, or reducing metabolic disease species.
A person of ordinary skill in the art would have been motivated to combine the method of US12502412B2 with the methods of Feuerer because combined, the teachings result in a method for suppressing weight gain through inhibiting fat accumulation; and preventing or treating metabolic disease species using the Lactobacillus fermentum strain (Accession No. KCTC 14106BP), in combination with regulatory T cells. The combination would result in the intended results of suppressing weight gain; and preventing or treating metabolic diseases using Lactobacillus fermentum strain(s), in combination with regulatory T cells.
It would have been prima facie obvious to one of ordinary skill in the art to combine the teachings recited by Feuerer with the method of US12502412B2 to inhibit fat accumulation (suppress weight gain), and for preventing or treating metabolic disease species using the Lactobacillus fermentum strain (Accession No. KCTC 14106BP) because all elements are known in the art to prevent or treat the metabolic diseases or conditions; therefore combining them would make the methods for the prevention or treatment of metabolic disease species more effective and there would be a reasonable expectation that combining all elements together would yield an optimized method formulation. The combination would represent the use of multiple known therapeutic methods that treat the same metabolic diseases for improving treatment efficacy. The combination would have yielded predictable results (i.e., the optimized suppression of weight gain, and the prevention or treatment of metabolic disease species) to one of ordinary skill in the art at the time of the invention; therefore, the instant claims are directed to a combination of known elements performing established functions that are obvious over US12502412B2, in view of Feuerer.
Claims 1-2 and 5-6 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 15-27 in copending U.S. Application No.17/758,210 in further view of US 2011/0044939 A1 (2011; hereafter “Feuerer”, cited on Form 892).
Although the claims at issue are not identical, they are not patentably distinct
from each other. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
U.S. Application No. 17/758,210 discloses “a method of preventing and treating a metabolic disease comprising administering a Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof to an individual” (Claim 15); “a method of preventing or treating a metabolic disease comprising administering Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof to an individual, wherein the metabolic disease is any one selected from a group consisting of obesity, hypertension, arteriosclerosis, hyperlipidemia, fatty liver, non-alcoholic fatty liver disease. hyperinsulinemia, diabetes, and insulin resistance syndrome” (Claim 16); “a method of preventing and treating a metabolic disease comprising administering a Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof to an individual wherein the strain inhibits fat accumulation in white adipose tissue” (Claim 17); “a method of preventing and treating a metabolic disease comprising administering a Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof to an individual, wherein the strain reduces metabolic inflammation in white adipose tissue” (Claim 18); “a method of preventing and treating a metabolic disease comprising administering a Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof to an individual, wherein the strain reduces fat accumulation in brown adipose tissue” (Claim 19); “a method of preventing and treating a metabolic disease comprising administering a Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof to an individual, wherein the strain inhibits fat accumulation in liver tissue” (Claim 20); “a method of preventing and treating a metabolic disease comprising administering a Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof to an individual, wherein the strain reduces a blood glucose level” (Claim 21); “a method of preventing and treating a metabolic disease comprising administering a Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof to an individual, wherein the strain reduces insulin resistance” (Claim 22); “a method of preventing and treating a metabolic disease comprising administering a Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof to an individual, wherein the strain regulates the concentration of metabolic hormones and adipokines in blood” (Claim 23); “a method of preventing and treating a metabolic disease comprising administering a Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof to an individual , wherein the metabolic hormone is GLP-1“ (Claim 24); “a method of preventing and treating a metabolic disease comprising administering a Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof to an individual , wherein the adipokine is PAI-1 or resistin“ (Claim 25); “a method of preventing and treating a metabolic disease comprising administering a Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof to an individual, wherein the Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof is comprised in a food composition” (Claim 26); “a method of preventing and treating a metabolic disease comprising administering a Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof to an individual, wherein the Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof is comprised in a feed composition” (Claim 27).
U.S. Application No. 17/758,210 does not disclose the use of regulatory T cells (Treg) in combination with GB-102 (KCTC 14105BP) for the suppression of weight gain, and the prevention or treatment of selected from a group of metabolic disease species.
Feuerer teaches “regulatory T (Treg) cells are readily detectable in the abdominal adipose tissue of normal adult mice, accumulating with age to the unusually high fraction of around 50% of CD4 T lymphocytes” (Paragraph 0005). Feuerer teaches “abdominal fat Treg cells express high levels of the anti-inflammatory cytokine IL-10, which directly reduces adipocyte secretion of inflammatory mediators; thus, these cells and their anti-inflammatory properties can be used to inhibit elements of the metabolic syndrome” (Paragraph 0005). Feuerer teaches “methods for inhibiting, preventing, delaying, or reducing the development or severity of obesity-associated disorders in a subject”(Paragraph 0006). Feuerer teaches “methods include obtaining an initial population of Foxp3+CD25+CD4+ regulatory T cells; engineering said initial population of T cells to express IL-10 and optionally culturing said cells in the presence of adiponectin (Paragraph 0008). Feuerer teaches “methods for treating obesity and/or obesity-associated conditions, e.g., insulin resistance, metabolic syndrome, or type 2 diabetes, in a subject; the methods include administering a therapeutically effective amount of IL-10 and optionally adiponectin to the subject. In some embodiments, the IL-10 and adiponectin are administered systemically” (Paragraph 0015). Feuerer teaches “findings indicate that Tregs guard against excessive inflammation of the adipose tissue and local and downstream systemic consequences, and strongly suggest that Tregs residing in the fat are responsible” (Paragraph 0115). Feuerer teaches “administration can be systemic, or local, e.g., injection into an area of unwanted fat tissue, e.g., subcutaneous or omental fat. When both IL-10 and adiponectin are used, administration can be of a single composition, e.g., a pill or injectable solution, that includes both IL-10 and adiponectin, or can be administration of two separate compositions (paragraph 0071).
Therefore, U.S. Application No. 17/758,210 teaches a method of inhibiting fat accumulation (suppressing weight gain); and preventing or treating selected metabolic disease species comprising administering a Lactobacillus fermentum strain (Accession No. KCTC 14105BP) or a culture thereof to an individual. Feuerer further teaches the use of regulatory T cells in a method for inhibiting, preventing, delaying, or reducing metabolic disease species (e.g., obesity and/or obesity-associated conditions, insulin resistance, metabolic syndrome, or type 2 diabetes), in subject.
A person of ordinary skill in the art would have been motivated to combine the method of U.S. Application No. 17/758,210 with the teachings of Feuerer because combined, the teachings result in a method for suppressing weight gain through inhibiting fat accumulation, and preventing or treating metabolic disease species using a Lactobacillus fermentum strain (Accession No. KCTC 14105BP) in combination with regulatory T cells. The combination would result in the intended results of suppressing weight gain, and preventing or treating metabolic diseases using Lactobacillus fermentum strain(s), in combination with regulatory T cells.
It would have been prima facie obvious to one of ordinary skill in the art to combine the teachings recited by Feuerer in the method of 17/758,210 to inhibit fat accumulation (suppress weight gain), and for preventing or treating metabolic disease species using the Lactobacillus fermentum strain GB-102 because all elements are known in the art to prevent or treat metabolic disease or conditions; therefore combining them would make the methods for the prevention or treatment of metabolic disease species more effective and there would be a reasonable expectation that combining all elements together would yield an optimized method formulation. The combination would represent the use of multiple known therapeutic methods that treat the same metabolic diseases for improving treatment efficacy. The combination would have yielded predictable results (i.e., the optimized suppression of weight gain, and the prevention or treatment of metabolic disease species) to one of ordinary skill in the art at the time of the invention; therefore, the instant claims are directed to a combination of known elements performing established functions that are obvious over U.S. Application No. 17/758,210, in view of Feuerer.
Claims 1-2 and 4-6 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 17 in copending U.S. Application No. 19/227,022 (in further view of US 2011/0044939 A1; cited on Form 892; hereafter “Feuerer”).
Although the claims at issue are not identical, they are not patentably distinct
from each other. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
U.S. Application No. 19/227,022 discloses “a method of preventing obesity, comprising administering to a subject in need thereof an effective amount of a composition comprising; a least one selected from the group consisting of a Lactobacillus fermentum strain (Accession No. KCTC 14105BP), a lysate thereof, and a culture solution thereof; at least one selected from the group consisting of a Lactobacillus fermentum GB103 strain (Accession No. KCTC 14106BP), a lysate thereof, and a culture solution thereof; and at least one selected from the group of a Lactobacillus plantarum GB104 strain (Accession No. KCTC 14107BP), a lysate thereof, and a culture solution thereof” (Claim 17).
U.S. Application No. 19/227,022 does not disclose the use of regulatory T cells (Treg), in combination with GB-102 (KCTC 14106BP) or GB103 strain (Accession No. KCTC 14106BP) for the suppression of weight gain, and the prevention or treatment of selected from a group of metabolic disease species.
Feuerer teaches “regulatory T (Treg) cells are readily detectable in the abdominal adipose tissue of normal adult mice, accumulating with age to the unusually high fraction of around 50% of CD4 T lymphocytes” (Paragraph 0005). Feuerer teaches “abdominal fat Treg cells express high levels of the anti-inflammatory cytokine IL-10, which directly reduces adipocyte secretion of inflammatory mediators; thus, these cells and their anti-inflammatory properties can be used to inhibit elements of the metabolic syndrome” (Paragraph 0005). Feuerer teaches “methods for inhibiting, preventing, delaying, or reducing the development or severity of obesity-associated disorders in a subject”(Paragraph 0006). Feuerer teaches “methods include obtaining an initial population of Foxp3+CD25+CD4+ regulatory T cells; engineering said initial population of T cells to express IL-10 and optionally culturing said cells in the presence of adiponectin (Paragraph 0008). Feuerer teaches “methods for treating obesity and/or obesity-associated conditions, e.g., insulin resistance, metabolic syndrome, or type 2 diabetes, in a subject; the methods include administering a therapeutically effective amount of IL-10 and optionally adiponectin to the subject. In some embodiments, the IL-10 and adiponectin are administered systemically” (Paragraph 0015). Feuerer teaches “findings indicate that Tregs guard against excessive inflammation of the adipose tissue and local and downstream systemic consequences, and strongly suggest that Tregs residing in the fat are responsible” (Paragraph 0115). Feuerer teaches “administration can be systemic, or local, e.g., injection into an area of unwanted fat tissue, e.g., subcutaneous or omental fat. When both IL-10 and adiponectin are used, administration can be of a single composition, e.g., a pill or injectable solution, that includes both IL-10 and adiponectin, or can be administration of two separate compositions (paragraph 0071).
Therefore, U.S. Application No. 19/227,022 discloses a method of preventing or treating obesity; comprising administering to a subject in need at least one selected from the groups of Lactobacillus fermentum strains (e.g. Accession No. KCTC 14105BP, Accession No. KCTC 14106BP, Accession No. KCTC 14107BP), a lysate, and a culture solution. Feuerer further teaches the use of regulatory T cells in a method for inhibiting, preventing, delaying, or reducing metabolic disease species (e.g., obesity and/or obesity-associated conditions, insulin resistance, metabolic syndrome, or type 2 diabetes), in subjects.
A person of ordinary skill in the art would have been motivated to combine the method of U.S. Application No. 19/227,022 with the teachings of Feuerer because combined, the teachings yield the intended result of a method of preventing or treating obesity (weight gain) using a Lactobacillus fermentum strains with deposited accession No. KCTC 14105BP and accession No. KCTC 14106BP; and the use of regulatory T cells for inhibiting, preventing, delaying, or reducing metabolic disease species (e.g., obesity and/or obesity-associated conditions, insulin resistance, metabolic syndrome, or type 2 diabetes), in subjects.
It would have been prima facie obvious to one of ordinary skill in the art to combine the teachings recited by Feuerer with the method of 19/227,022 to prevent or treat obesity (weight gain) using a Lactobacillus fermentum strains with deposited accession No. KCTC 14105BP and accession No. KCTC 14106BP; and the use of regulatory T cells for inhibiting, preventing, delaying, or reducing metabolic disease species (e.g., obesity and/or obesity-associated conditions, insulin resistance, metabolic syndrome, or type 2 diabetes). The combination would represent the use of multiple known therapeutic methods that treat the same metabolic diseases. Therefore, combining them would make the methods for the prevention or treatment of obesity (weight gain), and ., obesity-associated conditions, insulin resistance, metabolic syndrome, or type 2 diabetes more effective and there would be a reasonable expectation that combining all elements together would yield an optimized method formulation. The combination would have yielded predictable results (i.e., the optimized prevention or treatment of obesity through preventing/suppressing or treating weight gain, and the prevention or treatment of other metabolic disease species such as other obesity-associated conditions) to one of ordinary skill in the art at the time of the invention; therefore, the instant claims are directed to a combination of known elements performing established functions that are obvious over U.S. Application No. 19/227,022, in view of Feuerer.
Claim Rejections - 35 USC § 112(a)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
IN GENERAL. —The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
Claims 2 and 5 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly
connected, to make and/or use the invention ....
The microorganism Lactobacillus fermentum (Accession No. KCTC 14105BP) and/or (Accession No. 14106BP) are recited in the claims and, thus, is essential to the claimed invention. Because the microorganism is essential to the claimed invention, it must be obtainable by a repeatable method set forth in the specification or otherwise readily available to the public. If the microorganism is not so obtainable or available, the requirements of 35 U.S.C. § 112 may be satisfied by a deposit of the biological materials.
In this instant case, Applicant deposited the organisms under and subject to the Budapest Treaty on the International Recognition of the Deposit of Microorganisms for the Purpose of Patent Procedure, and in conformity with the requirements of 37 CFR 1.801-1.809; a deposit of the biological material Lactobacillus fermentum GB102 was made by the Applicant hereof on January 14, 2020 at Korean Collection for Type Cultures (KCTC), Korea Research Institute of Bioscience and Biotechnology (KRIBB), 181, Ipsin-gil, Jeongeup-si,14, 2020 (Accession Number: KCTC 14105BP), and a deposit of the biological material Lactobacillus fermentum GB 103 was made by the Applicant hereof on January 14, 2020 at Korean Collection for Type Cultures (KCTC), Korea Research Institute of Bioscience and Biotechnology (see Amendments to the Specification, Section I).
The deposits are noted under the Budapest Treaty; however, an affidavit or declaration by Applicant, or a statement by an attorney of record over his or her signature and registration number, stating that the specific strain has been deposited under the Budapest Treaty and that the specific strain will be irrevocably and without restriction or condition released to the public upon the issuance of a patent, would satisfy the deposit requirement made herein.
Claims 4-6 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the enablement requirement because the present claims, while enabling for the treatment (i.e., any action that can ameliorate or beneficially alter the symptoms of obesity or obesity-related diseases by administration of the composition according to the present invention [Specification, pg. 37, line 23- pg. 38, line 1]) or prevention (i.e., any action that suppress o delays the onset of obesity or obesity-related diseases by administration of the composition according to the present invention [Specification, pg. 37, lines 19-22]) of the metabolic disease species obesity, diabetes, and metabolic inflammation using Lactobacillus fermentum strains and Regulatory T Cells (Tregs) as active ingredients; do not reasonably provide enablement for treatment or prevention of the other metabolic disease species recited in the claims (i.e. hypertension, arteriosclerosis, hyperlipidemia, hyperinsulinemia, insulin resistance, fasting blood glucose disorder, impaired glucose tolerance and glucose tolerance syndrome).
The Applicant discloses a decrease in body weight of mice with obesity-induced through free feeding of a high- fat diet for 8 weeks when administering the GB-102 strain and Treg cells alone or in combination thereto; resulting in a significant decrease in weight gain (see Specification, pgs. 9, lines 23-25; pg. 10, lines 1-6-10; Fig. 2, pg. 53, lines 1-6; Table 6).
The Applicant further discloses the blood glucose control effect of the present invention through glucose tolerance testing (IPGTT), when GB-102 and Treg cells were administered to the mice alone or in combination (see Specification pg. 10, lines 17-25, pg. 11, lines 1-16; Fig. 4 and 5; pg. 55, lines 10-18, Table 8). It is noted that the blood glucose effect disclosed in the instant invention is interpreted as a treatment.
The Applicant further discloses “administering Lactobacillus, which is expected to have an immune enhancing effect due to changes in the intestinal microflora of mice that were fed a 60% kcal high fat diet to induce high obesity, and Treg cells, which are related to obesity symptoms and blood sugar control, singly or in combination with GB-102 or GB 103” (see Specification pg. 50, line 21- pg. 51, line 1). It is noted that the immune enhancing effect disclosed in the instant invention is interpreted as a treatment.
The claims contain subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the invention commensurate in scope with the claims. The specification does not disclose the treatment or prevention of all metabolic disease species claimed (i.e. hypertension, arteriosclerosis, hyperlipidemia, hyperinsulinemia, insulin resistance, fasting blood glucose disorder, impaired glucose tolerance, and glucose tolerance syndrome); however, the specification describes biological interventions as treatments or preventions directed toward obesity, diabetes (glucose regulation), and metabolic inflammation by administering a Lactobacillus fermentum strain and regulatory T cells.
The Breadth of the Claims
According to the specification, metabolic disease refers to a disease caused by an abnormality in metabolism, metabolic disease may be used interchangeably with metabolic syndrome (Detailed Description of the Invention, pg. 31, lines 14-17). Additionally, the specification provides multiple descriptions of metabolic disease, including metabolic syndrome, metabolic abnormalities, generic clusters of risk factors, and cardiovascular disease associations (Description of the Related Art, pg. 1, lines 20-24). The claims encompass many species of metabolic diseases (i.e. obesity, diabetes, hypertension, arteriosclerosis, hyperlipidemia, hyperinsulinemia, insulin resistance, metabolic inflammation, fasting blood glucose disorder, impaired glucose tolerance, and glucose tolerance syndrome).
In view of the prior art of Grundy et al. 2005 (cited on Form 892; hereafter “Grundy”) teaches metabolic syndrome is a constellation of risk factors, and therapy is directed at the individual risk components, rather than a single unified syndrome treatment (pg. 1, para. 2, see Form 892). The cited prior art establishes that metabolic syndrome is not a single, unified disease entity, but rather a heterogeneous constellation of risk factors. In view of this heterogeneity, the specification does not enable the full scope of the claimed methods. The specification provides enabling disclose for the treatment or prevention of obesity, diabetes, and metabolic inflammation through administration of Lactobacillus fermentum strain and regulatory T cells. The specification does not disclose how the claimed method would prevent or treat the remaining claimed metabolic disease species, including hypertension, arteriosclerosis, hyperlipidemia, hyperinsulinemia, insulin resistance, fasting blood glucose disorder, impaired glucose tolerance, and glucose tolerance syndrome.
The enormous breadth of the claims weighs heavily against enablement because the specification does not disclose the full scope of the method for the treatment or prevention of each metabolic disease species claimed (i.e. hypertension, arteriosclerosis, hyperlipidemia, hyperinsulinemia, insulin resistance, fasting blood glucose disorder, impaired glucose tolerance, and glucose tolerance syndrome). The specification is enabling for the treatment or prevention of the species obesity, diabetes, and metabolic inflammation by administering a Lactobacillus fermentum strain and regulatory T cells.
The Nature of the Invention
The claims are directed to methods for the treatment or prevention of a diverse group of metabolic diseases (i.e. obesity, diabetes, hypertension, arteriosclerosis, hyperlipidemia, hyperinsulinemia, insulin resistance, metabolic inflammation, fasting blood glucose disorder, impaired glucose tolerance, and glucose tolerance syndrome) using biological materials (Lactobacillus fermentum GB-102 strain deposited with the accession number of KCTC 14105BP, Lactobacillus fermentum GB-103 strain deposited with the accession number of KCTC 14106BP, and regulatory T cells) as active ingredients.
The instant specification discloses “administering Lactobacillus, which is expected to have an immune enhancing effect due to changes in the intestinal microflora of mice that were fed a 60% kcal high fat diet to induce high obesity, and Treg cells, which are related to obesity symptoms and blood sugar control, singly or in combination with GB-102 or GB 103” (see Specification pg. 50, line 21- pg. 51, line 1). Therefore, the disclosed effects are reducing obesity-related symptoms and improving blood glucose control (Specification, p.50, lines 21-25). The instant specification discloses “Fig. 2, a graph showing a change in body weight of mice with obesity induced through free feeding of a high-fat diet for 8 weeks when administering the GB-102 strain and Treg cells alone or in combination thereto” (see Specification, pg. 9, line 23 - pg. 10, line 1; Fig. 2). Therefore, the disclosed effects are a decrease in body weight of mice with obesity, when administering the GB-102 strain and Treg cells alone or in combination. The instant specification further discloses “Fig. 4, shows the blood glucose control effect confirmed through glucose tolerance test by measuring blood glucose at the tail end of mice, to which glucose is administered intraperitoneally, when GB-102 and Treg cells are administered to the mice alone or in combination (see Specification pg. 10, lines 17-25, Fig. 4). Therefore, the disclosed effects are a blood glucose control effect when GB-102 and Treg cells were administered to the mice alone or in combination.
This factor weighs strongly against full enablement because the claims, nor the specification disclose how to prevent or treat each metabolic disease species as claimed using a novel method. The specification does not disclose the treatment or prevention of all metabolic disease species claimed (i.e. hypertension, arteriosclerosis, hyperlipidemia, hyperinsulinemia, insulin resistance, fasting blood glucose disorder, impaired glucose tolerance, and glucose tolerance syndrome); however, the specification does provide a method of treatment or prevention for obesity, diabetes using a Lactobacillus fermentum strain and regulatory T cells. Accordingly, the prior art discloses the treatment or prevention of some metabolic diseases; including obesity, metabolic inflammation, and glucose regulation.
The State of the Prior Art
At the time of filing, bacterial strains (probiotics), including Lactobacillus strains and regulatory T cells are known in the art to have potential therapeutic benefits for specific metabolic disorders; mainly obesity, obesity-associated disorders, diabetes, and metabolic inflammation. However, the prior art did not establish a generalized or predictable framework for the prevention or treatment of the broader genus of metabolic diseases.
Paek at al., 2019 (see Form 892; hereafter “Paek”), discloses “a Lactobacillus fermentum MG4231 strain or Lactobacillus fermentum MG4244 strain exhibits anti-obesity activity for inhibiting lipase enzyme activity, inhibiting preadipocyte differentiation and inhibiting triglyceride accumulation” (Abstract); “thereby being variously used for a pharmaceutical composition, a food composition or a quasi-drug composition, and health functional food for treating and preventing obesity-related diseases” (Abstract).
Feuerer teaches “methods for treating obesity and/or obesity-associated conditions, e.g., insulin resistance, metabolic syndrome, or type 2 diabetes, in a subject; the methods include administering a therapeutically effective amount of IL-10 and optionally adiponectin to the subject. In some embodiments, the IL-10 and adiponectin are administered systemically” (Paragraph 0015). Therefore, Feuerer teaches obtaining a population of fat-tissue specific regulatory T Cells, and administering said population of fat-tissue specific regulatory T cells to the subject for treating obesity and/or obesity-associated conditions.
Yoon et al., 2020 (cited on Form 892; hereafter “Yoon”) discloses “the administration of Lactobacillus fermentum strains to ameliorate diet-induced obesity in some humans and mice”(Abstract).
Zeng at al., 2013 (cited on Form 892; hereafter “Zeng”), discloses “a key role for Tregs (regulatory T cells) in metabolic disorders, for instance as they accumulate in the adipose tissue to protect against obesity-related inflammation and insulin resistance” (Abstract).
Bhathena (previously referenced) discloses “lowering risk of diabetes, onset of insulin resistance, hyperhyeprinsulinemia, obesity, etc.) [Example, p. 3 right-hand column 3rd and 4th paragraphs, p. 7 left-hand column 2nd paragraph, and Abstract] and “keeping in view the gaps, the various mechanisms by which FA may improve the control of glucose tolerance, lipid metabolism, body mass and other markers presented, need to be further investigated” (Conclusion, p. 8, 1st col., 1st paragraph).
Collectively, the cited prior art demonstrates that therapeutic use of probiotics and regulatory T cells was known only in narrow, indication-specific contexts, with each reference addressing distinct disease mechanisms, biological pathways, and therapeutic objectives. The prior art does not teach that success in preventing or treating obesity, metabolic inflammation, or diabetes would reasonably predict efficacy across the diverse metabolic disease species recited in the claims, including hypertension, arteriosclerosis, hyperlipidemia, hyperinsulinemia, insulin resistance, fasting blood glucose disorder, impaired glucose tolerance, and glucose tolerance syndrome. There appears to be predictability in the art relating to the use of Lactobacillus fermentum strains, and regulatory T cells for treating specified metabolic disease in human subjects and other mammals (i.e., mice); specifically cited, obesity and/or obesity-associated conditions diabetes, and metabolic inflammation.
Accordingly, the state of the prior art reflects therapeutic strategies that are tailored to specific metabolic conditions rather than broadly applicable across an entire of metabolic diseases. The prior art therefore does not provide full scope of the claimed invention. Consistent with the disclosure, the cited prior art demonstrates that Lactobacillus fermentum strains and regulatory T cells have been investigated for limited metabolic indications. As cited above, both Lactobacillus fermentum strains and regulatory T cells are known in the art for the treatment or prevention of some metabolic diseases; however overwhelmingly including obesity, diabetes (glucose regulation), and metabolic inflammation.
The Level of Predictability in the Art
The use of Lactobacillus fermentum strains and regulatory T cells to suppress weight gain, and prevent or treat limited metabolic disease species, such as obesity, diabetes, and metabolic inflammation was known in the art at the time of filing. However, treatment or prevention of metabolic disease using the claimed methods was not extended to all metabolic diseases; and not predictable across the full scope of metabolic diseases recited in the claims. While some studies show promising results in in animal models and limited human contexts, the effects are highly inconsistent for the vast genus of metabolic diseases.
A person of ordinary skill in the art would not have been able to reasonably predict whether the claimed methods would be effective for the full range of metabolic disease species recited in the claims based on the disclosures in the specification or the cited prior art. These factors weigh against enablement because the claims, nor the specification provides treatment, or prevention methods for each of the claimed metabolic disease species (i.e. hypertension, arteriosclerosis, hyperlipidemia, hyperinsulinemia, insulin resistance, fasting blood glucose disorder, impaired glucose tolerance, and glucose tolerance syndrome). Therefore, the level of skill in the art cannot compensate for the lack of disclosure for the method of prevention or treatment of hypertension, arteriosclerosis, hyperlipidemia, hyperinsulinemia, insulin resistance, fasting blood glucose disorder, impaired glucose tolerance, and glucose tolerance syndrome. However, the specification is enabling for the prevention or treatment of the species obesity, diabetes, and metabolic inflammation.
The Amount of Direction Provided by Inventor/ Existence of Working Examples
The specification discloses a decrease in body weight (see Specification, pgs. 9, lines 23-25; pg. 10, lines 1-6-10; Fig. 2, pg. 53, lines 1-6; Table 6), a blood glucose control effect (see Specification pg. 10, lines 17-25, pg. 11, lines 1-16; Fig. 4 and 5; pg. 55, lines 10-18, Table 8), and an immune enhancing effect (see Specification pg. 50, line 21- pg. 51, line 1). However, the specification lacks disclosure of a method (administering Lactobacillus fermentum strains combined with regulatory T cells), for the treatment or prevention of the metabolic disease species hypertension, arteriosclerosis, hyperlipidemia, hyperinsulinemia, insulin resistance, metabolic inflammation, fasting blood glucose disorder, impaired glucose tolerance, and glucose tolerance syndrome. However, the specification is enabling for the treatment or prevention of the species obesity, diabetes, and metabolic inflammation. Collectively, the specification and cited prior art describe biological interventions directed toward obesity, metabolic inflammation, and diabetes (glucose regulation).
Level of Ordinary Skill
A person of ordinary skill in the art at the time of filing would have general knowledge regarding the use of Lactobacillus fermentum strains (known probiotics), regulatory T cells, and metabolic disease research; however little is known in the art and the art is unpredictable in regards to the use of Lactobacillus fermentum strains and regulatory T cells as a prevention measure or treatment for other metabolic diseases, apart from the metabolic disease species most commonly named in studies; which are obesity, diabetes, and metabolic inflammation. Lactobacillus fermentum strains (known probiotics), nor regulatory T cells are known in the art as being a universal preventative measure or treatment for all or most metabolic disorders, hence the unpredictability in the art.
Quantity of Experimentation Needed
Practicing the full scope of the claimed invention would require extensive and undue experimentation because determining whether the claimed methods (administering Lactobacillus fermentum strains and regulatory T cells as active ingredients) would be effective for preventing or treating each disease species claimed (e.g., hypertension, arteriosclerosis, hyperlipidemia, hyperinsulinemia, insulin resistance, fasting blood glucose disorder, impaired glucose tolerance, and glucose tolerance syndrome) would require substantial experimental investigation; such as multiple experimentation models with data collection (e.g., hypertension model, arteriosclerosis model, etc.) and analyzing outcomes (e.g., blood pressure data, lipid panel data, and other data) for each metabolic disease species. Such experimentation exceeds routine optimization and constitutes undue experimentation.
Applicant's disclosure, combined with prior art is considered to be enabling for the treatment or prevention of the metabolic disease species obesity, diabetes, and metabolic inflammation administering the claimed Lactobacillus fermentum strains and regulatory T cells as active ingredients.
In conclusion, upon careful consideration of the factors used to determine whether undue experimentation is required, in accordance with the Federal Circuit decision of In re Wands, 858 F.2d at 737, 8 USPQ2d at 1404 (Fed. Cir. 1988), the amount of guidance, direction, and exemplification disclosed in the specification, as filed, is not deemed sufficient to have enabled the skilled artisan to make and/or use the full scope of the claimed invention at the time the application was filed without undue and/or unreasonable experimentation.
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.
Claim(s) 1, 4, and 6 are rejected under 35 U.S.C. 103 as being unpatentable over Yoon et al., 2020 (cited on Form 892; hereafter “Yoon”), in further view of US 2011/0044939 A1 (2011; hereafter “Feuerer, cited on Form 892).
Yoon teaches administering Lactobacillus fermentum strains for oxidative phosphorylation in adipose tissue, resulting in increased energy expenditure to protect against diet-induced obesity (Abstract). Yoon teaches “notably, the administration of Lactobacillus spp. ameliorates diet-induced obesity in humans and mice (Abstract). Yoon teaches “oral administration of L. fermentum LM1016 markedly ameliorated glucose clearance and fatty liver in high-fat diet-fed mice”, and “decreased inflammation and increased oxidative phosphorylation in gonadal white adipose tissue, as demonstrated by transcriptome analysis” (Abstract). Yoon further teaches “metabolome analysis showed that metabolites derived from L. fermentum LM1016-attenuated adipocyte differentiation and inflammation in 3T3-L1 preadipocytes” and these pronounced metabolic improvements suggested that the application of L. fermentum LM1016 could have clinical applications for the treatment of metabolic syndromes, such as diet-induced obesity.
Yoon does not disclose the use of regulatory T cells (Treg) in combination with a Lactobacillus fermentum strain for the suppression of weight gain, and the prevention or treatment of selected from a group of metabolic disease species (i.e., obesity, diabetes, and metabolic inflammation).
Feuerer teaches “regulatory T (Treg) cells are readily detectable in the abdominal adipose tissue of normal adult mice, accumulating with age to the unusually high fraction of around 50% of CD4 T lymphocytes” (Paragraph 0005). Feuerer teaches “abdominal fat Treg cells express high levels of the anti-inflammatory cytokine IL-10, which directly reduces adipocyte secretion of inflammatory mediators; thus, these cells and their anti-inflammatory properties can be used to inhibit elements of the metabolic syndrome” (Paragraph 0005). Feuerer teaches “methods for inhibiting, preventing, delaying, or reducing the development or severity of obesity-associated disorders in a subject”(Paragraph 0006). Feuerer teaches “methods include obtaining an initial population of Foxp3+CD25+CD4+ regulatory T cells; engineering said initial population of T cells to express IL-10 and optionally culturing said cells in the presence of adiponectin (Paragraph 0008). Feuerer teaches “methods for treating obesity and/or obesity-associated conditions, e.g., insulin resistance, metabolic syndrome, or type 2 diabetes, in a subject; the methods include administering a therapeutically effective amount of IL-10 and optionally adiponectin to the subject. In some embodiments, the IL-10 and adiponectin are administered systemically” (Paragraph 0015). Feuerer teaches “findings indicate that Tregs guard against excessive inflammation of the adipose tissue and local and downstream systemic consequences, and strongly suggest that Tregs residing in the fat are responsible” (Paragraph 0115). Feuerer teaches “administration can be systemic, or local, e.g., injection into an area of unwanted fat tissue, e.g., subcutaneous or omental fat. When both IL-10 and adiponectin are used, administration can be of a single composition, e.g., a pill or injectable solution, that includes both IL-10 and adiponectin, or can be administration of two separate compositions (paragraph 0071).
Regarding Claims 1, 4, and 6, Yoon teaches administering Lactobacillus fermentum strains for ameliorating or improving obesity (suppression or reduction of weight gain) humans and mice; and Feuerer further teaches the use of regulatory T cells in a method for inhibiting, preventing, delaying, or reducing metabolic disease species (e.g., obesity and/or obesity-associated conditions, insulin resistance, metabolic syndrome, or type 2 diabetes), in subjects.
A person of ordinary skill in the art before the effective filling date of the instant invention would have been motivated to combine the methods of Yoon and Feuerer for the intended result of suppressing or reducing weight gain by the prevention or treatment for obesity; and preventing or treating metabolic disease species (e.g., diabetes, inflammatory disease, obesity) in subjects (human or mice) by administering a Lactobacillus fermentum stain (taught by Yoon), combined with regulatory T cells (taught by Feuerer) in order to further regulate and improve metabolic disease outcomes; with a reasonable expectation of success because the combination would represent the use of multiple known therapeutic methods that treat metabolic diseases for improving treatment efficacy of multiple metabolic disorders. The combined teachings of Yoon and Feuerer would yield an optimized intended result of suppressing weight gain via the prevention or treatment of obesity; and preventing or treating metabolic disease species (e.g., diabetes, inflammatory disease, obesity).
It would have been prima facie obvious to one of ordinary skill in the art to combine the teachings recited by Feuerer, with the teachings of Yoon for the intended result of the suppress weight gain by preventing or treating obesity; and for preventing or treating metabolic disease species using a Lactobacillus fermentum strain known in the art for preventing or treating metabolic diseases or conditions; therefore combining them would make the methods for the prevention or treatment of metabolic disease species more effective and there would be a reasonable expectation that combining all elements together would yield an optimized method formulation. The combination would represent the use of multiple known therapeutic methods that treat the same metabolic diseases for improving treatment efficacy. The combination would have yielded predictable results (the optimized suppression of weight gain, and the prevention or treatment of metabolic disease species) to one of ordinary skill in the art at the time of the invention; therefore, the instant claims are directed to a combination of known elements performing established functions that are obvious over Yoon, in further view of Feuerer.
Statement Regarding Prior Art
With respect to Claims 2 and 5, the prior art of record does not disclose or suggest the specific Lactobacillus fermentum strains GB-102 (Accession Number: KCTC 14105BP) and GB-103 (Accession No. KCTC 14106BP). In particular, no prior art has been identified that teaches the claimed Lactobacillus fermentum strains GB-102 (Accession Number: KCTC 14105BP) and GB-103 (Accession No. KCTC 14106BP) under 35 U.S.C. § 102 or 103 for use in the methods as instantly claimed.
Conclusion
No claims are allowed.
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/ENOSAKHARE ERHUNMWUNSEE/Examiner, Art Unit 1651
/MELENIE L GORDON/Supervisory Patent Examiner, Art Unit 1651