Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claim status
The amendment on January 19, 2024 is acknowledged. Claims 1-15 are canceled. Claims 16-35 are new. Claims 16-35 are subjected to examination.
Priority
Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55. For the purpose of applying prior art, the effective filing date is July 20, 2021, the date that PCT/EP2022/070430 was filed.
Information Disclosure Statement
Accordingly, the information disclosure statement (IDS) submitted on January 19, 2024 are being considered by the examiner.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(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.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
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 of carrying out his invention.
Claims 18-33 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for preventing reward dysregulation disorders, does not reasonably provide enablement for preventing the diseases recited in these claims. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
The instant claims encompass a method of preventing addiction-related disorder, eating-related disorder, affective disorders, obsessive compulsive disorders, schizophrenia, attention deficit hyperactivity disorders (ADHD), autism spectrum disorder, major depressive disorder (MDD), and anxiety disorder, however the specification does not teach the prevention of these diseases said to be preventable by the applicant’s method as in claims 18-33.
The applicability of the method for preventing all the disorders asserted in the claims mentioned above is unknown and/or not readably reproducible by the artesian. In the specification, the applicant disclaims that the term “prevention” includes “preventing or avoiding the occurrence of symptom of a reward dysregulation disorder” (page 7, [0032]) and that “preventing” includes “may refer to a secondary prevention, i.e., to the prevention of the re-occurrence of a symptom or a relapse of a reward dysregulation disorder.” (see page 7; [0032]). However, there are no teachings in the specification regarding the claimed method for preventing the diseases recited in the claims by administering the bacteria in health patients with predisposition to develop the diseases as in claims 18-33.
Although, the use of Parabacteroides is recited in the specification for preventing the recurrence of reward dysregulation disorder, the term “prevent” is interchangeable with “treat”, because the patient had already developed the disease, and ultimately the continuous use of medication is intended to avoid recurrence of disease, which is well-known in the art. Also, it is well-known in the art that the diseases recited in the claims are related to reward deficiency syndrome (RSD), which is a heritable trait which makes impossible to completely prevent the disease before onset symptoms in health patients. There are no teachings regarding any interventions in the subject matter’s genetic components in order to prevent the development of onset symptoms. The enablement of scope requirement is not fulfilled by the applicant, since a person of ordinary skill in the art cannot make or use the full scope of the claimed invention without undue experimentation.
In order to comply with the enablement of scope requirement, the applicant must fully disclosure the method of preventing addiction-related disorder, eating-related disorder, affective disorders, obsessive compulsive disorders, schizophrenia, attention deficit hyperactivity disorders (ADHD), autism spectrum disorder, major depressive disorder (MDD), and anxiety disorder prior its development in the subject matter in the specifications.
Enablement is considered in view of the Wands factors (MPEP 2164.01 (A)). The factors considered when determining if the disclosure satisfies the enablement requirement and whether any necessary experimentation is undue include, but are not limited to (In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988)):
1) nature of the invention;
2) the breadth of the claims;
3) the state of the prior art;
4) the level of one of ordinary skill;
5) the level of predictability in the art;
6) the amount of direction or guidance provided by the inventor;
7) the existence of working examples; and
8) the quantity of experimentation needed to make or use the invention based on the content of the disclosure.
When the above factors are weighed, it is the examiner’s position that one skilled in the art could not practice the invention without undue experimentation. Some experimentation is not fatal; the issue is whether the amount of experimentation is “undue”; see In re Vaeck, 20 USPQ2d 1438, 1444.
Thus, the method of preventing in claims 16-35 must be able to completely eliminate the development of diseases recited in 16-35. It is apparent that there is no full scope of requirement, because two methods are claimed, however the specification only enables a fraction of them, which is the method of treating.
Bowirrat et al. (Bowirrat A, Oscar-Berman M. Relationship between dopaminergic neurotransmission, alcoholism, and Reward Deficiency syndrome. Am J Med Genet B Neuropsychiatr Genet. 2005 Jan 5;132B(1):29-37. doi: 10.1002/ajmg.b.30080.) teaches that “Alcoholism is a complex, multifactorial disorder that results from the interplay between genetic and environmental factors. The D2 dopamine receptor (DRD2) has been associated with pleasure, and the DRD2 A1 allele has been referred to as a reward gene. Evidence suggests that there is a tripartite interaction involving dopamine receptor deficiency, a propensity to abuse alcohol, and reduced sensitivity to rewards. This interaction relies heavily on genetic characteristics of the individual, with certain ethnic groups having a greater tendency toward alcoholism than others. The DRD2 has been one of the most widely studied in neuropsychiatric disorders in general, and in alcoholism and other addictions in particular. The dopamine D2 (DRD2) gene, and especially its allele TaqI A1 allele and its receptor, also may be involved in comorbid antisocial personality disorder symptoms, high novelty seeking, and related traits. The mesocorticolimbic dopaminergic pathway system plays an especially important role in mediating reinforcement by abused drugs, and it may be a common denominator for addictions such as alcoholism. When the mesocorticolimbic dopamine reward system dysfunctions (perhaps caused by certain genetic variants), the end result is Reward Deficiency syndrome and subsequent drug-seeking behaviors. Reward Deficiency syndrome refers to the breakdown of the reward cascade, and resultant aberrant conduct, due to genetic and environmental influences. Alcohol and other drugs of abuse, as well as most positive reinforcers, cause activation and neuronal release of brain dopamine, which can decrease negative feelings and satisfy abnormal cravings. A deficiency or absence of DRD2 receptors then predisposes individuals to a high risk for multiple addictive, impulsive, and compulsive behaviors. Although other neurotransmitters (e.g., glutamate, gamma-aminobutyric acid (GABA), and serotonin) may be important in determining the rewarding and stimulating effects of ethanol, dopamine may be critical for initiating drug use and for reinstating drug use during protracted abstinence”.
Yet, Huckins et al. (Huckins LM, Brennand K, Bulik CM. Dissecting the biology of feeding and eating disorders. Trends Mol Med. 2024 Apr;30(4):380-391. doi: 10.1016/j.molmed.2024.01.009.) teaches that feeding and eating disorders (FEDs) are common and have been shown to be influenced by both genetic and environmental factors. Also, avoidant/restrictive food intake disorder, anorexia nervosa (AN), bulimia nervosa (BN), and binge-eating disorder (BED) are all heritable and genome-wide association studies (GWASs) reveal both psychiatric and metabolic/anthropometric genetic risk factors for AN. GWASs for other FEDs are underway. AN, BN, and BED might diverge etiologically in their genetic relation with metabolic and anthropometric traits. Davis also teaches that “understanding and characterizing the bidirectional relationship between FEDs and gut microbiota may be key to developing novel therapeutic opportunities; importantly, therapeutic interventions in the gut microbiota have already yielded positive outcomes for other psychiatric disorders [89, 90, 91]. However, identifying direction of effect is complicated by relatively small sample sizes, high heterogeneity across studies rendering meta-analysis challenging; a lack of detailed longitudinal studies of microbiota; and the difficulty inherent in obtaining microbiota samples pre- and post-FED development. Moreover, we propose that studies should not expect a simple, monolithic relationship between FEDs and gut microbiota. In the same way that we do not expect uniform directions of effect of gene expression changes in the brain, we should not expect that all microbiota will be equally dysregulated in FEDs. Rather, it is likely that some microbes may predispose to FEDs, some are dysregulated by FEDs, and others remain unaffected”.
Genovese et al. (Genovese A, Butler MG. The Autism Spectrum: Behavioral, Psychiatric and Genetic Associations. Genes (Basel). 2023 Mar 9;14(3):677. doi: 10.3390/genes14030677) teaches that “Autism-spectrum disorder (ASD) consists of a group of heterogeneous genetic neurobehavioral disorders associated with developmental impairments in social communication skills and stereotypic, rigid or repetitive behaviors. We review common behavioral, psychiatric and genetic associations related to ASD. Autism affects about 2% of children with 4:1 male-to-female ratio and a heritability estimate between 70 and 90%. The etiology of ASD involves a complex interplay between inheritance and environmental factors influenced by epigenetics. Over 800 genes and dozens of genetic syndromes are associated with ASD. Novel gene–protein interactions with pathway and molecular function analyses have identified at least three functional pathways including chromatin modeling, Wnt, Notch and other signaling pathways and metabolic disturbances involving neuronal growth and dendritic spine profiles. An estimated 50% of individuals with ASD are diagnosed with chromosome deletions or duplications (e.g., 15q11.2, BP1-BP2, 16p11.2 and 15q13.3), identified syndromes (e.g., Williams, Phelan-McDermid and Shprintzen velocardiofacial) or single gene disorders. Behavioral and psychiatric conditions in autism impacted by genetics influence clinical evaluations, counseling, diagnoses, therapeutic interventions and treatment approaches. Pharmacogenetics testing is now possible to help guide the selection of psychotropic medications to treat challenging behaviors or co-occurring psychiatric conditions commonly seen in ASD”.
Furthermore Demontis et al. (Demontis, D., Duan, J., Hsu, YH.H. et al. Rare genetic variants confer a high risk of ADHD and implicate neuronal biology. Nature 649, 909–917 (2026) https://doi.org/10.1038/s41586-025-09702-8) teaches that “attention-deficit hyperactivity disorder (ADHD) is a childhood-onset neurodevelopmental disorder with a large genetic component. It affects around 5% of children and 2.5% of adults, and is associated with several severe outcomes. Common genetic variants associated with the disorder have been identified, but the role of rare variants in ADHD is mostly unknown. Here, by analyzing rare coding variants in exome-sequencing data from 8,895 individuals with ADHD and 53,780 control individuals, we identify three genes (MAP1A, ANO8 and ANK2; P < 3.07 × 10−6; odds ratios 5.55–15.13) that are implicated in ADHD. The protein–protein interaction networks of these three genes were enriched for rare-variant risk genes of other neurodevelopmental disorders, and for genes involved in cytoskeleton organization, synapse function and RNA processing. Top associated rare-variant risk genes showed increased expression across pre- and postnatal brain developmental stages and in several neuronal cell types, including GABAergic (γ-aminobutyric-acid-producing) and dopaminergic neurons. Deleterious variants were associated with lower socioeconomic status and lower levels of education in individuals with ADHD, and a decrease of 2.25 intelligence quotient (IQ) points per rare deleterious variant in a sample of adults with ADHD (n = 962). Individuals with ADHD and intellectual disability showed an increased load of rare variants overall, whereas other psychiatric comorbidities had an increased load only for specific gene sets associated with those comorbidities. This suggests that psychiatric comorbidity in ADHD is driven mainly by rare variants in specific genes, rather than by a general increased load across constrained genes”.
Therefore, neither the art nor the specification teaches how to prevent the diseases in claims 16-35. Thus, one of skill in the art cannot reasonably conclude that Applicant had possession of the claimed invention at the time the instant application was filed.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 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 –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 16-20, 22-29 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Skolnick et al. (WO2020160183 A1; hereafter Skolnick; PTO-892).
As to claim 16-17, 26-27, Skolnick teaches compositions and methods for treating central nervous system (CNS) diseases or disorders associated with microbiome dysbiosis. “The technology described herein focuses in principal aspects on mammalian enteric microbes that are “heirloom” species strongly conserved across generations, on which the host relies symbiotically for metabolic pathways and products essential to normal host development and function. In certain aspects, the products of heirloom gut microfloral taxa of interest support healthy psychiatric and cognitive development and function” [0021].
Skolnick also teaches “the composition of any one of claims 1-7, wherein the at least one isolated non-pathogenic queuine-producing bacteria belongs to a species selected from Parabacteroides distasonis, Parabacteroides goldsteinii, Parabacteroides gordonii, Parabacteroides johnsonii, Parabacteroides merdae, Paraprevotella clara, Coprococcus catus, Coprococcus eutactus “(claim 8).
As to claim 18, Skolnick teaches “The method wherein the CNS disorder is selected from a cognitive disorder, a mood disorder, an anxiety disorder, and a psychiatric disorder” (claim 26). The method of any one of claims 24-27, wherein the CNS disorder is selected from autism, bipolar disorder, major depression, anxiety and schizophrenia” (claim 27).
Skolnick teaches “compositions and methods are provided to prevent or treat gut dysbiosis mediated changes in metabolism and function of tyrosine hydroxylase (TH) and tyrosine in the synthesis of catecholamine neurotransmitters dopamine and norepinephrine. In the CNS, TH oxidizes BH* to B¾ as it performs its function of tyrosine conversion, and this BH4 recycling is a rate-limiting step in dopamine and norepinephrine synthesis These neurotransmitters are essential for a variety of cognitive and emotional processes including alertness and attentive engagement, pleasure seeking, memory, and reward-prediction [00395]. As such, impaired activity of TH due to gut dysbiosis and attendant queuine and BH4 deficit, can often correlate with impaired dopamine and norepinephrine synthesis, and with associated adverse CNS impacts, for example anhedonia, lethargy, flat affect, attention deficit, and learning difficulties. All of the latter symptoms are associated with schizophrenia and, to some extent, depression and bipolar disorders, as well as attention deficit disorder. Dysfunction and death of dopaminergic neurons is also strongly implicated in Parkinson’s disease, and a shortage of norepinephrine from the locus coeruleus has been proposed as a key mediator in the pathology of Alzheimer’s disease (wherein norepinephrine promotes microglial phagocytosis of amyloid beta, and plays an additional role in curtailing neuroinflammation); see e.g., Heneka et al. PNAS 107, 6058-6063, (2010). In view of this, each of the disorders noted above is specifically contemplated for benefit from the methods and/or compositions described herein that increase or restore the production of queuine and/or queuine-related metabolites” [00395]. “The use of claim 77, wherein the CNS disease or disorder is selected from a cognitive disorder, a mood disorder, an anxiety disorder, and a psychiatric disorder” (claim 78).
As to claim 19-22, Skolnick teaches “In one or more embodiments of any of the above-aspects, the queuine associated mental illness or disease (also referred to herein as a central nervous system (CNS) disorder associated with queuine deficiency) that can be treated by administration of a composition described herein is selected from the group consisting of: clinical depression, bipolar disorder, schizophrenia, anxiety, anxiety disorders, addiction, social phobia, major depressive disorder, treatment-resistant major depressive disorder (TR-MDD), major depressive disorder and its subtypes (melancholic depression, atypical depression, catatonic depression, postpartum depression, and seasonal affective disorder), Neurodegenerative amyloid disorders (Parkinson’s, Alzheimer’s, and Huntington’s diseases), restless leg syndrome, neuropathic pain, pain disorders, dementia, epilepsy, stiff-person syndrome, premenstrual dysphoric disorder, autism spectrum disorders, sleep disorders, obsessive-compulsive disorder, Tourette’s syndrome, intellectual disability, Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections (PANDAS), post-treatment Lyme disease syndrome, and attention deficit hyperactivity disorder (ADHD).
As to claim 23, Skolnick teaches “wherein the subject is a human subject”.
As to claim 24, Skolnick teaches “the composition is administered orally, intravenously, intramuscularly, intrathecally, subcutaneously, sublingually, buccally, rectally, vaginally, by the ocular route, by the otic route, nasally, via inhalation, by nebulization, cutaneously, transdermally, or combinations thereof, and formulated for delivery with a pharmaceutically acceptable excipient, carrier or diluent” [0074]”.
As to claim 25, Skolnick teaches “The dose of the therapeutic queuine producing bacteria can comprise 1X104 colony forming units (CFUs), 1 X 105 CFUs, 1 x lO6 CFUs, I x lO7 CFUs, 1 X 108 CFUs, 1 X 109 CFUs, 1 x 1010CFUs, 1X1011 CFUs or greater than 1X 1011CFUs of the desired bacteria “[00235].
As to claims 28-29, Skolnick teaches “the composition is a probiotic or a medical food comprising at least one queuine producing bacteria. The bacteria can be administered, for instance, as a probiotic, as a capsule, tablet, caplet, pill, troche, lozenge, powder, and/or granule. The strain can also be formulated as a nutraceutical, conventional food, medical food, or drug. The queuine producing bacteria can also be administered as part of a fecal transplant or via suppository. In some embodiments, the composition is formulated for delivery to the gut, as described further herein. In some embodiments, tire composition further comprises a prebiotic” [00237].
Regarding the limitation "reward dysregulation disorders”, the claim teaches all structural features from the claim, so it is presumed to be capable of the claimed intended use. See MPEP 2112.01: "Where the claimed and prior art products are identical or substantially identical in structure or composition, or are produced by identical or substantially identical processes, a prima facie case of either anticipation or obviousness has been established. In re Best, 562 F.2d 1252, 1255, 195 USPQ 430, 433 (CCPA 1977). "When the PTO shows a sound basis for believing that the products of the applicant and the prior art are the same, the applicant has the burden of showing that they are not." In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990). Therefore, the prima facie case can be rebutted by evidence showing that the prior art products do not necessarily possess the characteristics of the claimed product. In re Best, 562 F.2d at 1255, 195 USPQ at 433." See also MPEP 2111.02: "To satisfy an intended use limitation which is limiting, a prior art structure which is capable of performing the intended use as recited in the preamble meets the claim. See, e.g., In re Schreiber, 128 F.3d 1473, 1477, 44 USPQ2d 1429, 1431 (Fed. Cir. 1997)"
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 30 is rejected under 35 U.S.C. 103 as being unpatentable over Skolnick et al. (WO2020160183 A1; hereafter Skolnick; PTO-892) in view of Fenster et al. (Published March 19, 2019; hereafter Fenster; PTO-892) as applied to claims 16-20, 22-29 above.
Skolnick teaches a method of preventing and/or treating reward dysregulation disorders comprising administering, to an individual in need thereof, a composition comprising one or more bacteria from the genus Parabacteroides and/or extract thereof and/or metabolites thereof, which is pertinent to claims 16-20, 22-29.
However, Skolnick does not teach wherein the composition is comprised in a kit, which further comprises means to administer said composition.
Fenster teaches the production and delivery of probiotics and that with the right choice of production process, product formulation, and strains, high-quality probiotics can be successfully included in a wide variety of delivery formats to suit consumer requirements. Fenster teaches “the inclusion of probiotics in dietary supplements primarily utilizes probiotics in the freeze-dried powder format”. Fenster also teaches “Capsules, tablets, and powder in stick packaging or sachets are the most commonly found formats on store shelves and are usually stored at ambient conditions. Dietary supplement products should deliver the probiotic count declared on the label throughout the shelf life of the product”, which is pertinent to claim 30. Fenster also teaches “the probiotics included in such products can be different from the species that are used for oral administration, but they do not have to be, which is pertinent to claim 30. Fenster teaches “the production process of such probiotics is not different from other probiotics in the sense that it needs to be specially adapted to the medical device delivery format. As with all probiotic strains, production will be strain dependent”, which is pertinent to claim 30.
It would have been obvious to one of ordinary skill in the art to combine the teachings of Skolnick and Fenster, thereby arriving to the invention 30. Since Skolnick’s method of preventing and/or treating reward dysregulation disorders by administering the probiotic bacteria, Parabacteroides to an individual was shown to be effective and Fester teaches production and delivery of probiotics, and specially its inclusion in dietary supplements, it would have been obvious to substitute these known equivalents; see MPEP 2144.06.
Claims 31-33 are rejected under 35 U.S.C. 103 as being unpatentable over Skolnick et al. (WO2020160183 A1; hereafter Skolnick; PTO-892) in view of Fenster et al. (Published March 19, 2019; hereafter Fenster; PTO-892) as applied to claims 16-20, 22-29 above, and further in view of Bello et al. (Published April 24, 2010; hereafter Bello; PTO-892).
The reasons why claims 16-20, 22-29 would have been obvious over Skolnick in view of Fenster are set forth above. However, neither reference teaches wherein the reward dysregulation is a mental disorder selected in a group consisting of anorexia and bulimia (claim 31), binge-eating (claim 32) and wherein the mental disorder is an eating-related disorder that is not an overweight-related disorder or an obesity-related disorder (claim 33).
Bello teaches that central dopaminergic mechanisms are involved in the motivational aspects of eating and food choices and a role for dopamine in perpetuating the compulsive feeding patterns of bulimia Nervosa (BN) and binge eating disorder (BED), which is pertinent to claims 31-33.
Therefore, it would have been obvious to a PHOSITA to modify the teachings of Skolnick and Bello, thereby arriving to the inventions 31-33. Since the methods of Skolnick was used to treat reward dysregulations, which includes compulsive feeding patterns of bulimia Nervosa (BN) and binge eating disorder (BED) was shown to be effective to treat a said mental disorder and does not specify any reward dysregulation disorder that cannot be treatable by using the method mentioned above, it would have been obvious to substitute these known equivalents; see MPEP 2144.06.
Claims 34-35 are rejected under 35 U.S.C. 103 as being unpatentable over Skolnick et al. (WO2020160183 A1; hereafter Skolnick; PTO-892) in view of Fenster et al. (Published March 19, 2019; hereafter Fenster; PTO-892) as applied to claims 16-20, 22-29 above, and further in view of Wang et al. (Published January 2, 2019; hereafter Wang; PTO-892).
The reasons why claims 16-20, 22-29 would have been obvious over Skolnick in view of Fenster are set forth above.
However, neither reference teaches administering a composition comprising succinate or succinate is produced by Parabacteroides.
Wang teaches “metabolic benefits of Parabacteroides distasonis (PD) on decreasing weight gain, hyperglycemia, and hepatic steatosis in ob/ob and high-fat diet (HFD)-fed mice. Wang also teaches treatment with live P. distasonis (LPD) dramatically altered the bile acid profile with elevated lithocholic acid (LCA) and ursodeoxycholic acid (UDCA) and increased the level of succinate in the gut. Wang teaches “In vitro cultivation of PD demonstrated its capacity to transform bile acids and production of succinate, which is pertinent to claim 34, 35.
Wang teaches that succinate supplementation in the diet decreased hyperglycemia in ob/ob mice via the activation of intestinal gluconeogenesis (IGN). Gavage with a mixture of LCA and UDCA reduced hyperlipidemia by activating the FXR pathway and repairing gut barrier integrity”. Wang also teaches that “co-treatment with succinate and LCA/UDCA mirrored the benefits of LPD”. The binding target of succinate was identified as fructose-1,6-bisphosphatase, the rate-limiting enzyme in IGN. The succinate and secondary bile acids produced by P. distasonis played key roles in the modulation of host metabolism. Wang teach that succinate serves as an agonist of fructose-1,6-bisphosphatase (FBPase) in the IGN pathway. Wang teaches that the gut commensal Parabacteroides distasonis is a promising probiotic that can modulate host metabolism to alleviate obesity and metabolic dysfunctions, which is pertinent to claim 34. Wang also teaches that succinate produced by the gut microbiota improved glucose homeostasis and body weight gain by serving as an intestinal gluconeogenic substrate (de Vadder and Mithieux, 2018, De Vadder et al., 2016), which is pertinent to claims 34-35.
It would have been obvious to one of ordinary skill in the art to modify the teachings of Skolnick and Fenster, thereby arriving at the invention of claims 34-35. Since the method of preventing and/or treating obesity by administering succinate produced by Parabacteroides was taught by Wang, it would be beneficial to adapt the method of administering one or more bacteria from the genus Parabacteroides and/or extract thereof and/or metabolites thereof of Skolnick because it was shown to be effective to treat reward dysregulation disorders and does not specify any reward dysregulation disorder that cannot be treatable by using the method mentioned above. Also, Fenster’s taught high-quality probiotics and wide variety of delivery formats to suit consumer requirements, it would be obvious to substitute these known equivalents; MPEP 2144.06.
Additionally, KSR International Co. v. Teleflex Inc., 127 S. Ct. 1727, 1741 (2007), discloses that the simple substitution of one known element for another to obtain predictable results is obvious unless its application is beyond that person's skill. KSR International Co. v. Teleflex Inc., 127 S. Ct. 1727, 1741 (2007) also discloses that "the combination of familiar elements according to known methods is likely to be obvious when it does no more than yield predictable results". In the instant case, all elements (Parabacteroides, metabolites, probiotics, reward dysregulation disorders) are known in the art. In addition, combining these elements yields a method/composition wherein each element merely performs the same function as it does separately; thus, the results of the combination would be recognized as predictable to one of ordinary skill in the art. Therefore, the claimed invention is prima facie obvious in view of the teachings of the prior art, absent any convincing evidence to the contrary.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to PRICILA HAUK TEODORO whose telephone number is (571)272-2784. The examiner can normally be reached M-F 6:15AM-3:15PM.
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/PRICILA NMN HAUK TEODORO/Examiner, Art Unit 1645
/DANIEL E KOLKER/Supervisory Patent Examiner, Art Unit 1645