Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
DETAILED ACTION
Priority
Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 11 June 2026 has been considered by the examiner.
Status of applications, Amendments, and/or Claims
The Response filed 11 June 2026 has been entered in full. Claims 1-15 have been canceled and claims 16, 21, 34 have been amended currently. Claims 36-46 are new.
Therefore, claims 16-46 are the subject of this Office Action.
New Objections
Necessitated by Amendment
The numbering of claims is not in accordance with 37 CFR 1.126 which requires the original numbering of the claims to be preserved throughout the prosecution. When claims are canceled, the remaining claims must not be renumbered. When new claims are presented, they must be numbered consecutively beginning with the number next following the highest numbered claims previously presented (whether entered or not).
Misnumbered claim 40 been renumbered 42.
Misnumbered claim 41 been renumbered 43.
Misnumbered claim 42 been renumbered 44.
Misnumbered claim 43 been renumbered 45.
Misnumbered claim 44 been renumbered 46.
Modified Claim Rejections - 35 USC § 112
Necessitated by Amendment
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 16-46 rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claims 16-46 recites “reducing the likelihood of occurrence or re-occurrence”. The recitation is interchangeable with prevention”. However, the recitation is vague, because “reducing the likelihood of occurrence or re-occurrence” reads as “reducing the possibility of something to happen”, which is uncertain. Therefore, the scope of the claim is unclear in reference to “reducing the likelihood of occurrence or re-occurrence”.
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 16-46 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 “reducing the likelihood of occurrence or recurrence of reward dysregulation disorder”, which is interchangeable with “prevention” of the diseases recited in these claims.
The instant claims encompass a method of reducing the likelihood of occurrence or re-occurrence of 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, anorexia, bulimia, binge eating, overweight-related disorders, and obesity-related disorders, alcohol-related addiction, drug-related addiction, and game-related addiction, Parkinson's disease, Tourette Syndrome, however the specification does not teach the prevention of these diseases said to be preventable by the applicant’s method as in claims 16-46.
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 16-46.
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 of 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, anorexia, bulimia, binge eating, overweight-related disorders, and obesity-related disorders, alcohol-related addiction, drug-related addiction, and game-related addiction, Parkinson's disease, Tourette Syndrome, however the specification does not teach the method of preventing the occurrence or reoccurrence of the diseases 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 “reducing the likelihood of occurrence or recurrence” in claims 16-46 must be able to prevent the development of diseases recited in 16-46. 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 (in obese mice model).
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 16-46. 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.
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. Therefore, neither the art nor the specification teaches how to prevent the diseases in claims 16-46. 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.
Modified Claim rejections - 35 USC § 102
Necessitated by Amendment
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 16-29, 36-41, 46 are rejected under 35 U.S.C. 102 as being anticipated by Skolnick et al. (WO2020160183 A1; hereafter Skolnick; PTO-892).
As claims 16-29, 36-41, 46, Skolnick teaches “compositions and methods for treating Central Nervous System (CNS) disorders. See 183’, abstract.
Skolnick teaches Parabacteroides distasonis, Parabacteroides goldsteinii, Parabacteroides gordonii, Parabacteroides johnsonii, Parabacteroides merdae, Paraprevotella clara, Coprococcus catus, Coprococcus eutactus. See 183’, claim 8.
Skolnick teaches the administration of such microbes to subjects presenting with an observed CNS disorder, such as a mood disorder, anxiety, autism or a mental health disorder like schizophrenia, to treat or prevent one or more symptoms of the CNS disorder. See 183’, paragraph [0019].
Skolnick teaches bacteria from the genus Parabacteroides consisting of P. distasonis, P. goldsteinii, P. merdae, P. acidifaciens, P. bouchesdurhonensis, P. chartae, P. chinchilla, P. chongii, P. faecis, P. gordonii, P. johnsonii, P. massiliensis, P. pacaensis, P. provencensis, P. timonensis, Parabacteroides spp. and combinations thereof”.
Skolnick teaches compositions and methods of the technology may employ admixing of useful bacterial species, live or non-viable, or their isolated components, metabolic precursors, intermediates or products, with a pharmaceutically acceptable excipient, carrier, diluent or other agent that enhances delivery or activity of the administered composition. “In some embodiments, the composition further comprises an enteric coating or similar composition to promote survival of or avoid the acidity of the stomach and permit delivery into the small or large intestines”. See 183’ paragraph [0028].
Skolnick teaches the use of gut bacterial species (live or non-viable), or metabolic precursors, intermediates or products thereof, in the preparation of medicaments for treating dysbiosis and associated CNS disorders and other adverse symptoms in mammalian subjects. See 183’ paragraph [0030].
Skolnick teaches “The method wherein the Central Nervous disorder (CNS) is selected from a cognitive disorder, a mood disorder, an anxiety disorder, and a psychiatric disorder”. See 183’, claim 26.
Skolnick teaches the CNS disorder is autism, bipolar disorder, major depression, anxiety and schizophrenia. See 183’, 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. These neurotransmitters are essential for a variety of cognitive and emotional processes including alertness and attentive engagement, pleasure seeking, memory, and reward-prediction. See 183’, paragraph [00395].
Skolnick teaches 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). See 183’, paragraph [00264].
Skolnick teaches “wherein the subject is a human subject”. See 183’, paragraph [00263; 00292].
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”. See 183’, paragraph [0074]”.
Skolnick teaches “The dose of the therapeutic bacteria can comprise 1X104 colony forming units (CFUs), 1 X 105 CFUs, 1 x lO6 CFUs, 1 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”. See 183’, paragraph [00235].
Skolnick teaches “the composition is a probiotic or a medical food. 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. 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”. See 183’, paragraph [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 because if “the reward dysregulation disorder is selected in a group consisting of mental disorders, neurological disorders, and combinations thereof”, then any selected mental disorders, any selected neurological disorders and any selected combinations thereof is a reward dysregulation disorder. See claim 18. 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)"
Therefore, the inventios of claims 16-29, 36-41, 46 are anticipated by Skolnick.
Applicant’s arguments directed to the previous 102 for claims 16-29, 36-41, 46, will be addressed below. See response to arguments.
Modified Claim rejections - 35 USC § 103
Necessitated by Amendment
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.
Claim 30 remain rejected under 35 U.S.C. 103 as being unpatentable over Skolnick et al. (WO2020160183 A1; hereafter Skolnick; PTO-892) as applied to claims 16-29, 36-41, 46, above, in view of Fenster et al. (Published March 19, 2019; hereafter Fenster; PTO-892). The basis for this rejection is set forth at pp. 14-15 of the previous Office action. The instant claim is drawn to method wherein the composition is comprised in a kit, which further comprises means to administer said composition.
Skolnick teaches the limitations of claims 16-29, 36-41, 46, as fully discussed above and incorporated herein. While, 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, the right choice of production process, product formulation, and strains, high-quality probiotics, delivery formats to suit consumer requirements, which is pertinent to claim 30. Fenster teaches the inclusion of probiotics in dietary supplements primarily utilizes probiotics in the freeze-dried powder format. 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, 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 claim 30. Since Skolnick teaches a 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.
See MPEP 2144(II): “The strongest rationale for combining references is a recognition, expressly or impliedly in the prior art … that some advantage or expected beneficial result would have been produced by their combination.
Therefore, claim 30 would have been prima facie obvious, absent evidence to the contrary.
Applicant’s arguments directed to the previous 103 for claim 30 will be addressed below. See response to arguments.
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 16-29, 36-41, 46 above, and further in view of Bello et al. (Published April 24, 2010; hereafter Bello; PTO-892).
Bello teaches “eating disorders represent a set of psychiatric conditions characterized by disturbances in eating behaviors. These disturbances not only include alterations in eating patterns and diet choices, but involve distinct aberrant psychological perceptions towards food, eating, body weight, and body self-image”, which is pertinent to claims 31-33.
Bello teaches “Binge eating is a common behavioral feature of clinically diagnosed eating disorders including bulimia nervosa (BN), binge eating disorder (BED), and binge/purge subtype of anorexia nervosa (AN-BP). Although the definition of binge eating in AN-BP is not well-defined clinically and relies on subjective assessments relative to restrictive behaviors in AN-restrictive subtype (AN-R), binge eating is clearly defined in BN and BED by the 4th edition of Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), which is pertinent to claims 31-33.
Bello teaches “The loss of control over eating, food choice, and self-sustaining aspects of binge eating have generated considerable interest in examining the neural correlates involved in these behaviors. Dopamine is a neurotransmitter critically involved in the reward and motivational aspects of feeding (Baptista 1999; Erlanson-Albertsson 2005; Noble 2003a; Szczypka et al., 2000)”, 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 can be used to treat reward dysregulation disorders, such as compulsive feeding patterns of bulimia Nervosa (BN) and binge eating disorder (BED) as taught by Bello, it would have been obvious to substitute these known equivalents; see MPEP 2144.06.
See MPEP 2144(II): “The strongest rationale for combining references is a recognition, expressly or impliedly in the prior art … that some advantage or expected beneficial result would have been produced by their combination.
Reasonable expectation of success would be expected because Skolnick specifically teaches the method wherein the Central Nervous disorder (CNS) is selected from a cognitive disorder, a mood disorder, an anxiety disorder and does not specify any Central Nervous disorders, which includes psychiatric disorders that should not be treated by using this method.
Therefore, claims 31-33 would have been prima facie obvious, absent evidence to the contrary.
Applicant’s arguments directed to the previous 103 for claims 31-33 will be addressed below. See response to arguments.
New Claim rejections - 35 USC § 103
Necessitated by Amendment
Claims 34-35, 42-45 are under 35 U.S.C. 103 as being unpatentable over Skolnick et al. (WO2020160183 A1; hereafter Skolnick; PTO-892) as applied to claims 16-29, 36-41, 46 above, in view of Fenster et al. (Published March 19, 2019; hereafter Fenster; PTO-892) and further in view of Wang et al. (Published January 2, 2019; hereafter Wang; PTO-892) and evidenced by Fernandez-Veledo et al. (Published 2019; Fernandez-Veledo PTO-892). Fernandez-Veledo has been added to the rejection under 35 U.S.C. 103 to improve the clarity regarding “production of succinate by Parabacteroides”. The basis for this rejection is set forth at pp. 16-18 of the previous Office action. The instant claims are drawn to a composition comprising succinate as claim 34, and wherein the succinate is produced by bacteria from the genus Parabacteroides as claim 35, an overweight-related disorder, obesity-related disorder, binge eating as claims 42-44. Skolnick 16-29, 36-41, 46, as fully disclosed and incorporated herein.
While, Skolnick does not explicitly teach a composition comprising succinate or succinate is produced by Parabacteroides, Wang teaches that “In vitro cultivation of Parabacteroides distasonis demonstrated its capacity to transform bile acids and production of succinate, which is pertinent to claim 34. 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, which is pertinent to claims 34-35. Wang explicitly teaches that succinate supplementation in the diet decreased hyperglycemia in obese/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, 42-45.
Regarding the limitation, “the succinate is produced by the bacteria from genus Parabacteroides”, Fernandez-Veledo teaches that microbiota-derived metabolites act both as nutrients and as messenger molecules and can signal to distant organs in the body to shape host pathophysiology, and succinate has the distinction of being produced by both microbiota and the host. See for example, Figure 1. Fernadez-Veledo teaches that Parabacterioides distasonis is a succinate-producer, which is pertinent to claims 34-35, 42-45. See table 1; Figure 2.
PNG
media_image1.png
678
960
media_image1.png
Greyscale
PNG
media_image2.png
628
946
media_image2.png
Greyscale
PNG
media_image3.png
685
881
media_image3.png
Greyscale
Fernandez-Veledo teaches that “unlike other intermediary metabolites, succinate holds the unique distinction of being at the interface of host-gut microbiota metabolic interactions. Accordingly, succinate has emerged as a gut microbial-derived metabolite associated with dysbiosis-related diseases such as obesity and IBD. Moreover, its contribution to cross-feeding interactions might classify it as a primary metabolite essential for the stability and resilience of gut microbiota”. “The use of probiotics to shape the gut microbiota has the potential to herald a new era in the management of metabolic diseases linked to microbiota dysbiosis, such as obesity, and succinate may serve as a promising metabolite target for this approach”, which is pertinent to claims 34-35, 42-45.
It would have been obvious to one of ordinary skill in the art to modify the teachings of Skolnick, thereby arriving at the invention of claims 34-35, 42-45. Since the method of preventing and/or treating obesity by administering succinate produced by Parabacteroides was taught by Wang, it would be beneficial to administering one or more line or non-live bacteria from the genus Parabacteroides to a subject in need as taught Skolnick by because as explicitly taught by Wang and evidenced by Fernandez-Veledo, Succinate is produced by the gut microbiota, and Parabacteriodes is a succinate-producer. Since it is well-known that compositional and metabolic changes to the microbiota (termed dysbiosis) are associated with diverse pathological process, it would be beneficial and very desirable to administer a probiotic-bacteria such as Parabacteriodes to improve gut heath in a subject with eating disorders, since it is expected that a subject with eating disorder will probably have an unbalanced/perturbed compositional and metabolic microbiota due to the unhealthy eating habits. Therefore, it would be obvious to substitute these known equivalents; MPEP 2144.06.
See MPEP 2144(II): “The strongest rationale for combining references is a recognition, expressly or impliedly in the prior art … that some advantage or expected beneficial result would have been produced by their combination.
Furthermore, In re Kerkhoven (205 USPQ 1069, CCPA 1980) summarizes:
"It is prima facie obvious to combine two compositions each of which is taught by prior art to be useful for the same purpose in order to form a combination that is to be used for the very same purpose: the idea of combining them flows logically from their having been individually taught in the prior art."
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 such as succinate, probiotics, mental disorders, 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.
Therefore, claims 34-35, 42-45 would have been prima facie obvious, absent evidence to the contrary.
Applicant’s arguments directed to the previous 103 for claims 34-35, 42-45 will be addressed below. See response to arguments.
Response to Amendments
Applicant’s arguments as they pertain to the rejections have been fully considered but are not persuasive for the following reasons.
Applicant argues at pg. 8 of the Response (filed 11 June 2026) that the claims were amended by substituting the term "preventing" with "reducing the likelihood of occurrence or re-occurrence of reward dysregulation disorders" and that “the amendment is supported by paragraph [0033] of the instant specification as published US 2024/0415895 A1. Applicant also argues that the new dependent claims 36 to 46 are introduced, reciting “either treatment or "reducing the likelihood of occurrence or re-occurrence" as alternatives”. Applicant’s arguments have been fully considered, but not persuasive. The currently amendment to the claims wherein the term “prevent” has been replaced by "reducing the likelihood of occurrence or re-occurrence” has not modified the intend of the method claimed in invention, because reducing the likelihood of occurrence or re-occurrence is a form of preventing the probability/possibility of occurrence or reoccurrence. There are no teachings in the specification regarding the claimed method of “reducing the likelihood of occurrence or reoccurrence of the diseases” recited in the claims by administering the bacteria and/ or succinate in health patients with predisposition to develop the diseases as in claims 18-35 and new claims 36-46. For example, the specification does not teach that the claimed method of reducing the likelihood of occurrence or reoccurrence of the disorders developed by genetic factors. Further, 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”. 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”. “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”. 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. See previous office action, page 5-8. 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.
Applicant argues at pg. 9-11 of the Response (filed 11 June 2026) that 1) Skolnick is silent as to a method for treating or reducing the likelihood of occurrence of reward dysregulation disorders; 2) Skolnick merely teaches methods (i) for increasing queuine levels (claim 21 of Skolnick), or (ii) for treating or preventing a gut microbiome dysbiosis-mediated central nervous system (CNS) disorder associated with queuine deficiency (claim 24 or 77 of Skolnick); 3) the teaching of Skolnick is explicitly restricted to sub-selections of broader conditions (i.e. CNS disorders), the selection being linked to insufficient levels of queuine; with queuine being defined itself as "hypermodified nucleobase"; 5) There is no evidence in Skolnick, that the sub-selection of CNS disorders associated to queuine deficiency would necessarily and consistently (100%) impact the reward dysregulation system; There is simply no basis to assert that it is the case, in Skolnick (which is entirely silent on the reward system), and the Examiner did not provide any rational. Finally, applicant argues that Skolnick is silent on Succinate; 6) Skolnick is silent on the administration of nonviable bacterial or bacterial extracts as active agents. Applicant’s arguments have been fully considered, but not persuasive. Applicant should note that Skolnick et al. (WO2020160183) entered by the examiner explicitly teaches that non-pathogenic Parabacterioides strains are queuine-producing bacterial strains. See paragraph [0039]. Further, Skolnick teaches the administration of queuine-producing bacterial strains to subjects presenting with an observed Central Nervous System (CNS) disorders, such as a mood disorder, anxiety, autism or a mental health disorder to treat or prevent one or more symptoms of the CNS disorder is anticipated because all the disorders claimed in the invention are Central nervous system (CNS) diseases. It is noted that applicant’s arguments heavily rely upon the queiune component, which is a naturally produced by Parabacterioides strains as taught by Skolnick. However, there is no indication that the Parabacterioides strains claimed in the invention do not produce queiune, and that the disorders claimed in the invention are not Central Nervous System (CNS) disorders. Also, Skolnick does not disclaim that the queuine producer strains of Parabacterioides do not produce succinate. It is apparent that the Parabacterioides strains disclose in the prior art and in the claimed invention are naturally occurring bacteria strains, and no genetic modification was performed to remove the ability of the strains of producing any products such as queiune and succinate. For sake of clarity, Skolnick do teach the administration of queuine-producing bacterial strains to subjects presenting with an observed Central Nervous System (CNS) disorders, and also that queuine is a compound produced by the bacteria recited in the specifications, which include Parabacterioides strains. However, Parabacterioides strains also produce succinate. Thus, Skolnick teaches a succinate-producer strain, because Parabacterioides produces succinate. The same rationale also is applied to the claimed invention because the method discloses the bacteria, Parabacterioides, which is also a queiune-producer strain. The applicant should note that the examiner is aware that both queiune and succinate are naturally produced by Parabacterioides. However, queuine is not explicitly claimed in the invention, and for this reason any arguments regarding to queuine will not be fully addressed by the examiner in this office action.
Regarding to Skolnick being silent on succinate. Applicant’s arguments have been fully considered, but not persuasive. The invention claims the method wherein succinate is produced by bacteria from genus Parabacteroides, and claim 35 of the present invention teaches the inherency. However, for sake of clarity, and clear records, the examiner has provided support for the limitation, wherein succinate is produced by bacteria Parabacteroides. The claim limitation is taught by Wang and evidenced by Fernandez-Veledo. Skolnick does not mention succinate however the prior arts support the inherency for the claim limitation, succinate produced by Parabcterioides. See table 1; page 4. In addition, Wang teaches the benefits of succinate supplementation to a subject in need. Regarding the limitation succinate, MPEP 2112 states: "Products of identical chemical composition cannot have mutually exclusive properties." In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990). “The claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977)… There is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference. Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003)”. Thus, the rationale used by examiner is that non-pathogenic Parabacterioides strains, which are both queuine and succinate-producer strains can be used in a method to prevent and/or treat Central Nervous System (CNS) disorders, which include reward dysregulation disorders because these disorders are also recognized as CNS disorders as taught by Skolnick et al. (WO2020160183) and Bello.
Applicant also argues that there is no basis to assert the reward dysregulation mechanisms of Skolnick. However, it is apparent that the specification only teaches data regarding the administration of Parabacterioides and/or succinate to obese mouse model to assert/imply benefits of the claimed method to reduce the “likelihood” of occurrence or re-occurrence and/or treating addiction and binge-type eating disorders, and does not provide any solid mechanism regarding the method. See specification, paragraph [0216]; Example 1; paragraph [0171, 0202], paragraph [0171, 0202]. However, there is no taught and/or basis for this assertion, in the specification for all “reward dysregulation disorders” claimed in the invention. For example, the invention claims “a neurological disorder selected in a group consisting of Parkinson's disease, Tourette Syndrome” in claim 27. Further, the invention claims the method to administering the composition to a human individual (claim 23), however there is no basis to assert that an obese human patient would respond the same way as obese mice to the method claimed in the invention for any of the disorders in the invention.
Applicant also argues that Skolnick is entirely silent on the reward system. However, claims 18-20 teach all the limitations regarding to reward dysregulation disorder in the claims, and all the reward dysregulation disorders taught in the claims are classified as Central Nervous System (CNS) disorders. Further, Skolnick teaches that CNS disorders, including psychiatric and mental health disorders can be prevented or treated by using the method of administering Parabacteroides to a subject. Bello specifically teaches that eating disorders represent a set of psychiatric conditions characterized by disturbances in eating behaviors, and that binge eating is a common behavioral feature of clinically diagnosed eating disorders including bulimia nervosa (BN), binge eating disorder (BED), and binge/purge subtype of anorexia nervosa (AN-BP). Bello also teaches that binge eating is clearly defined in BN and BED by the 4th edition of Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), which is the guide utilized by psychiatrists for diagnosis of mental disorders. Further, it is noted that the applicant has not specified any reward dysregulation mechanism that should not be used for the claimed invention.
It must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). Furthermore, in response to applicant's argument that the examiner's conclusion of obviousness is based upon “most fairly be described as teachings” reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon straightforward evidences. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
Therefore, it would have been obvious to one of ordinary skill in the art at the time the invention was filed to administer a Parabacterioides composition wherein the bacteria strain is alive or non-alive to a subject in need to prevent or treat any of the Central Nervous system diseases/disorders as taught by Skolnick and Bello because Wang taught the benefits of Parabacteriodes, which is a succinate-producer strain and additional supplementation of succinate to an obese mouse model and Fernadez-Veledo taught succinate synthesis by host and gut bacteria, and that Parabacteroides is indeed a succinate-producer strain.
Applicants’ arguments at pg. 11 of the Response (filed 11 June 2026) that Skolnick is entirely silent upon alcohol-related addiction, drug related addition, and game-related addiction. Applicant’s arguments have been fully considered, but not persuasive. The examiner agrees that Skolnick does not explicitly teach alcohol-related addiction, drug related addition, and game-related addiction, however the applicant should recognize that the results obtained from the obese mice model taught in the specifications used to assert the claims in the invention only suggests or indicate the potential relation of the method and alcohol-related addiction, drug related addition, and game-related addiction disorders. It is noted the invention does teach most of the mental disorders claimed in the invention and only speculates a potential use of the method even for the obese mouse model. One of skill in the art would explore all the method of preventing or treating any reward dysregulation disorders wherein the probiotic bacteria, such as Parabacterioides is administered to a subject in need. Since bacteria Paracterioides possess intrinsic characteristics such as production of products (e.g. succinate) that are very desirable and beneficial for promoting the improvement of gut health in a subject in need as a way to promote the overall health, e.g. mental health.
Finally, Applicants’ arguments at pg. 11 of the Response (filed 11 June 2026) that Skolnick is silent to administration of non-viable bacteria. Applicant’s arguments have been fully considered, but not persuasive. Skolnick does teach the administration of non-viable See the set forth 102 rejections of this Office Action, and Skolnick; paragraph [0028].
Motivation for combining the references is clear from the teachings as each reference teaches methods of use and/or bacterial composition. While there is not a single reference that includes all the limitations of the claims, the various aspects of the claims are contained in multiple references and it would have been prima facie obvious to combine the teachings as stated above to arrive at the claimed invention with an expectation of success for the reasons provided, it would have been obvious to substitute these known equivalents; see MPEP 2144.06.
It must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). Furthermore, in response to applicant's argument that the examiner's conclusion of obviousness is based upon “most fairly be described as teachings” reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon straightforward evidences. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
See MPEP 2144(II): “The strongest rationale for combining references is a recognition, expressly or impliedly in the prior art … that some advantage or expected beneficial result would have been produced by their combination.
Furthermore, In re Kerkhoven (205 USPQ 1069, CCPA 1980) summarizes:
"It is prima facie obvious to combine two compositions each of which is taught by prior art to be useful for the same purpose in order to form a combination that is to be used for the very same purpose: the idea of combining them flows logically from their having been individually taught in the prior art."
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".
Conclusion
No claims are allowed.
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Advisory Information
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-3:00PM.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Heather Calamita can be reached at (571) 272-2876. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/PRICILA NMN HAUK TEODORO/Examiner, Art Unit 1645
/HEATHER CALAMITA/Supervisory Patent Examiner, Art Unit 1684
Prosecution Insights