DETAILED ACTION
This office action is in response to applicant’s filing dated September 16, 2025.
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 .
Status of Claims
Claims 1-19 are pending in the instant application.
Election/Restrictions
Applicant’s election without traverse of Group I, drawn to a method for treating neuroinflammation in an individual, comprising: administering to the individual a composition comprising a succinate/succinate receptor 1 inhibitor, wherein the neuroinflammation in the individual is ameliorated or reduced in the reply filed on September 16, 2025 is acknowledged.
Claims 11-19 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on September 1, 2025.
Applicant’s election without traverse of compound 7a:
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as the elected compound species and Alzheimer’s disease as the elected disorder species in the reply filed on September 16, 2025 is acknowledged.
Claim 5 is withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on September 1, 2025.
Claims 1-4 and 6-10 are presently under examination as they relate to the elected species:
Alzheimer’s disease and Compound 7a:
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Priority
The present application claims benefit of US Provisional Application No. 63/321,752 filed on March 20, 2022.
Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged. Applicant has not complied with one or more conditions for receiving the benefit of an earlier filing date under 35 U.S.C. 119(e) as follows:
The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original nonprovisional application or provisional application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of 35 U.S.C. 112(a) or the first paragraph of pre-AIA 35 U.S.C. 112, except for the best mode requirement. See Transco Products, Inc. v. Performance Contracting, Inc., 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994).
The disclosure of the prior-filed application, US Provisional Application No. 63/321,752, fails to provide adequate support or enablement in the manner provided by 35 U.S.C. 112(a) or pre-AIA 35 U.S.C. 112, first paragraph for one or more claims of this application. In a review of the provisional application disclosure of neuroinflammation associated with Alzheimer’s disease was not identified. Disclosure of “wherein the succinate/succinate receptor 1 inhibitor is administered to a location other than the brain of the individual,” “wherein the composition is administered systemically,” or “wherein the composition is a tablet, a plurality of nanoparticles, or liquid composition” was also not identified. Thus, the provisional application fails to provide written description support for instant claims 2-4 and 9.
The effective filing date of instant claims 1, 6-8, and 10 is March 20, 2022. The effective filing date of instant claims 2-4 and 9 is March 20, 2023.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on March 20, 2023 and January 26, 2024 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements are being considered by the examiner, except where marked with a strikethrough.
Drawings
Acknowledgement is made of the drawings received on March 20, 2023. These drawings are accepted.
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 1-4 and 6-10 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention. This is a written description rejection.
The Written Description Guidelines for examination of patent applications indicates, "the written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, or by disclosure of relevant, identifying characteristics, i.e., structure or other physical characteristics and/or other chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show applicant was in possession of the claimed genus." (Federal register, Vol. 66, No. 4, pages 1099-1111, Friday January 5, 2001, see especially page 1106 column 3) and (see MPEP 2164).
Claims 1-4 and 6-10 are directed to a method for treating neuroinflammation in an individual comprising administering to the individual a composition comprising a succinate/succinate receptor 1 inhibitor. Thus, the claims encompass a method of treating any neuroinflammation comprising administering a genus of compounds which function as a succinate/succinate receptor 1 inhibitor. Thus, the claims encompass a genus of compounds which function as a succinate/succinate receptor 1 inhibitor with no other defining structural components of the compound. Succinate/succinate receptor 1 inhibitors can be a small molecule, polypeptide, peptide, glycoprotein, peptide-mimetic, an antigen binding protein (ABP), a DNA, an RNA, RNAi, siRNA, shRNA, a peptide nuclei acid (PNA), a genetic construct for targeting gene editing, a CRSIPR/Cas9 construct, a guide nucleic acid and tracrRNA. Moreover, as evidenced by instant claim 4, neuroinflammation is associated with numerous desperate diseases with no overlap. The instant claims do not require that an individual in need of treating neuroinflammation. Neuroinflammation is associated with aging. Thus, any individual is susceptible to neuroinflammation associated aging. Thus, the claims encompass a genus of molecules which function as a succinate/succinate receptor 1 inhibitor with no other defined structural components for treating neuroinflammation in any subject.
In a review of the instant specification, the specification does not appear to provide guidance as to what structural components are critical to the desired function (see below). The specification discloses about 109 compounds as succinate/succinate receptor 1 inhibitors but only disclose the inhibitory activity of 3 compounds. Because there are an innumerably large number of bio-molecules/compounds within the scope of the generic claims, it would require extensive manpower to make and test each compound to determine which compound would possess the recited properties (i.e., function as a succinate/succinate receptor 1 inhibitor) and be useful in the instantly claimed methods.
The MPEP states that the purpose of the written description requirement is to ensure that the inventor had possession, as of the filing date of the application, of the specific subject matter later claimed by him. The courts have stated:
"To fulfill the written description requirement, a patent specification must describe an invention and do so in sufficient detail that one skilled in the art can clearly conclude that "the inventor invented the claimed invention." Lockwood v. American Airlines, Inc., 107 F.3d 1565, 1572, 41 USPQ2d 1961, 1966 (Fed. Cir. 1997); In re Gostelli, 872 F.2d 1008, 1012, 10 USPQ2d 1614, 1618 (Fed. Cir. 1989) ("[T]he description must clearly allow persons of ordinary skill in the art to recognize that [the inventor] invented what is claimed."). Thus, an applicant complies with the written description requirement "by describing the invention, with all its claimed limitations, not that which makes it obvious," and by using "such descriptive means as words, structures, figures, diagrams, formulas, etc., that set forth the claimed invention." Lockwood, 107 F.3d at 1572, 41 USPQ2d at 1966." Regents of the University of California v. Eli Lilly & Co., 43 USPQ2d 1398.
Further, for a broad generic claim, the specification must provide adequate written description to identify the genus of the claim. In Regents of the University of California v. Eli Lilly & Co. the court stated:
"A written description of an invention involving a chemical genus, like a description of a chemical species, 'requires a precise definition, such as by structure, formula, [or] chemical name,' of the claimed subject matter sufficient to distinguish it from other materials." Fiers, 984 F.2d at 1171, 25 USPQ2d 1601; In re Smythe, 480 F.2d 1376, 1383, 178 USPQ 279, 284985 (CCPA 1973) ("In other cases, particularly but not necessarily, chemical cases, where there is unpredictability in performance of certain species or subcombinations other than those specifically enumerated, one skilled in the art may be found not to have been placed in possession of a genus …") Regents of the University of California v. Eli Lilly & Co., 43 USPQ2d 1398.
The MPEP further states that if a biomolecule is described only by a functional characteristic, without any disclosed correlation between function and structure, it is "not sufficient characteristic for written description purposes, even when accompanied by a method of obtaining the claimed sequence." MPEP § 2163. The MPEP does state that for a generic claim the genus can be adequately described if the disclosure presents a sufficient number of representative species that encompass the genus. MPEP § 2163. If the genus has a substantial variance, the disclosure must describe a sufficient variety of species to reflect the variation within that genus. See MPEP § 2163. Although the MPEP does not define what constitute a sufficient number of representative species, the courts have indicated what do not constitute a representative number of species to adequately describe a broad generic. In Gostelli, the courts determined that the disclosure of two chemical compounds within a subgenus did not describe that subgenus. In re Gostelli, 872, F.2d at 1012, 10 USPQ2d at 1618.
In the instant case, the claims are drawn to a method for treating any neuroinflammation in an individual comprising administering to the individual a composition comprising a succinate/succinate receptor 1 inhibitor. As set forth above, neuroinflammation is associated with numerous desperate conditions with no overlap, including aging. The instant claims do not require that an individual in need of treating neuroinflammation. Neuroinflammation is associated with aging. Thus, the claims encompass a genus of molecules which function as a succinate/succinate receptor 1 inhibitor with no other defined structural components for treating neuroinflammation in any subject.
The claims are generic, broadly reciting a genus of “a succinate/succinate receptor 1 inhibitor.”
As stated supra, the MPEP states that written description for a genus can be achieved by a representative number of species within a broad generic. It is unquestionable that claims 1-4 and 6-10 are broad and generic, with respect to all possible compounds encompassed by the claims and all possible conditions.
Applicant has failed to show that they were in possession of all the diverse compounds encompassed by a succinate/succinate receptor 1 inhibitor. Applicant discloses a very narrow set of compounds described as a succinate/succinate receptor 1 inhibitor [0088], despite claiming any compound functioning as a succinate/succinate receptor 1 inhibitor. The possible variation of any molecule that functions as a succinate/succinate receptor 1 inhibitor within the scope of claims 1-4, 9, and 10 are limitless and would encompass compounds that function as a succinate/succinate receptor 1 inhibitor not yet discovered. In a review of the specification, the specification discloses about 109 compounds as succinate/succinate receptor 1 inhibitors but only disclose the inhibitory activity of 3 compounds. None of the examples show efficacy with treatment of any neuroinflammation. Because there are an innumerably large number of bio-molecules/compounds within the scope of the generic claims, it would require extensive manpower to make and test each compound to determine which compound would possess the recited properties (i.e., function as a succinate/succinate receptor 1 inhibitor) and be useful in the instantly claimed methods. The small set of compounds cannot be viewed as being reasonably representative of the genus in its claimed scope because no readily apparent combination of identifying characteristics is provided.
Given the broad scope of the claimed subject matter, Applicant has not provided sufficient written description that would allow the skilled in the art to recognize all the compounds claimed to be useful in the method of treating any neuroinflammation of claims 1-4 and 6-10.
Claim Rejections - 35 USC § 112
Scope of Enablement
Claims 1-4 and 6-10 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 a method of treating neuroinflammation associated with Alzheimer’s disease comprising administering Compound 7a, does not reasonably provide enablement for a method of treating any neuroinflammation comprising administering any succinate/succinate receptor 1 inhibitor. 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. This is a scope of enablement rejection.
To be enabling, the specification of the patent application must teach those skilled in the art how to make and use the full scope of the claimed invention without undue experimentation. In re Wright, 999 F.2d 1557, 1561 (Fd. Cir. 1993). Explaining what is meant by "undue experimentation," the Federal Circuit has stated that:
The test is not merely quantitative, since a considerable amount of experimentation is permissible, if it is merely routine, or if the specification in question provides a reasonable amount of guidance with respect to the direction in which experimentation should proceed to enable the determination of how to practice a desired embodiment of the claimed invention. PPG v. Guardian, 75 F.3d 1558, 1564 (Fed. Cir. 1996). As pointed out by the court in In re Angstadt, 537 F.2d 498 at 504 (CCPA 1976), the key word is "undue", not "experimentation".
The factors that may be considered in determining whether a disclosure would require undue experimentation are set forth In re Wands, 8 USPQ2d 1400 (CAFC 1988) at 1404 wherein, citing Ex parte Forman, 230 USPQ 546 (Bd. Apls. 1986) at 547 the court recited eight factors:
1- the quantity of experimentation necessary,
2- the amount of direction or guidance provided,
3- the presence or absence of working examples,
4- the nature of the invention,
5- the state of the prior art,
6- the relative skill of those in the art,
7- the predictability of the art, and
8- the breadth of the claims
These factors are always applied against the background understanding that scope of enablement varies inversely with the degree of unpredictability involved. In re Fisher, 57 CCPA 1099, 1108, 427 F.2d 833, 839, 166 USPQ 18, 24 (1970). Keeping that in mind, the Wands factors are relevant to the instant fact situation for the following reasons:
1. The nature of the invention, state and predictability of the art, and relative skill of those in the art
The invention relates to a method for treating neuroinflammation in an individual comprising administering to the individual a composition comprising a succinate/succinate receptor 1 inhibitor. Claims 2, 3, and 10 further narrows the limitations of the method to administer the inhibitor to a location other than the brain of the individual, systemically, and topically in the oral cavity, respectively. Claim 4 narrows the neuroinflammation to those mediated by the listed disorders. Claims 6-8 narrow the succinate/succinate receptor 1 inhibitor to the claimed compounds. Claim 9 narrows the composition to a film, a gel, a capsule, a tablet, a plurality of nanoparticles, or liquid composition.
The relative skill of those in the art is high, generally that of a D.V.M. or Ph.D. The artisan using Applicant’s invention would generally be a veterinarian with a V.M.D. degree and several years of experience.
The factor is outweighed, however, by the unpredictable nature of the art. It is well established that “the scope of enablement varies with the degree of unpredictability of the factors involved” and physiological activity is considered to be an unpredictable factor. See In re Fisher, 166 USPQ 18, at 24 (In cases involving unpredictable factors, such as most chemical reactions and physiological activity, the scope of enablement obviously varies inversely with the degree of unpredictability of the factors involved); Nationwide Chemical Corporation, et. al. v. Wright, et. al., 192 USPQ 95 (one skilled in chemical and biological arts cannot always reasonably predict how different chemical compounds and elements might behave under varying circumstances); Ex parte Sudilovsky 21 USPQ2d 1702 (Applicant’s invention concerns pharmaceutical activity. Because there is no evidence of record of analogous activity for similar compounds, the art is relatively unpredictable); In re Wright 27 USPQ2d 1510 (the physiological activity of RNA viruses was sufficiently unpredictable that success in developing specific avian vaccine was uncertain). As illustrative of the state of the art, the examiner cites DiSabato et al (J Neurochem, 2016; 139(Suppl 2):136-153), Kim et al (Curr. Issues Mol. Biol., 2025; 47:8, pp 1-17), Gilissen et al (Pharmacology & Therapeutics, 2016; 159:56–65), and Liebing et al (The FEBS Journal, 2025; 292(8):2017-2050).
DiSabato, cited for evidentiary purposes, teaches neuroinflammation is defined as an inflammatory response within the brain or spinal cord; this inflammation is mediated by the production of cytokines, chemokines, reactive oxygen species, and secondary messengers; these mediators are produced by resident CNS glia (microglia and astrocytes), endothelial cells, and peripherally derived immune cells; there are immune, physiological, biochemical, and psychological consequences of these neuroinflammatory responses; moreover, the degree of neuroinflammation depends on the context, duration, and course of the primary stimulus or insult (page 136, left). DiSabato teaches the term neuroinflammation, however, is not universally equivalent (page 136, left). DiSabato teaches the concept of neuroinflammation is broad and encompasses two large areas of biological science in the nervous and immune systems; we are just now beginning to parse out the positive and negative aspects of immune system–nervous system interaction; it is difficult to make generalized conclusions about the positivity or negativity of neuroinflammation when considering systems as nuanced as those discussed; additionally, as a result of the complexity of the subject, we are unable to probe each topic discussed here as deeply as is necessary; perhaps the best way to sum up the state of the field is that its study requires careful consideration of context; complete removal of inflammatory cells has been shown to be an unreliable treatment for degenerative diseases or mood disorders, while modification of the M1/M2 polarization has shown more promise; rather than ask whether neuroinflammation is a friend or a foe, the science of neuroimmunology should instead study the individual situations and specific contexts in which the neuroinflammation is occurring (page 147, left, last paragraph).
Kim, cited for evidentiary purposes, teaches neuroinflammation is a complex and multifaceted response of the central nervous system (CNS) to injury, infection, or disease; acute neuroinflammation plays a critical role in preserving CNS homeostasis by facilitating pathogen clearance and promoting tissue repair; however, chronic and dysregulated neuroinflammation is progressively recognized as a central driver of neurodegenerative disorders (page 1, 1st paragraph); recent advances in the understanding of neuroinflammation have unveiled a dynamic interplay between various cellular components, including microglia, astrocytes, and peripheral immune cells; these cells mediate the delicate balance between neuroprotective and neurotoxic responses, influenced by molecular regulators such as transcription factors, cytokines, and signaling pathways; however, the traditional view of neuroinflammation as a static process has shifted, with emerging evidence highlighting novel regulators such as non-coding RNAs, epigenetic modifications, and metabolic states that shape the inflammatory landscape of the CNS (page 1, last bridge paragraph). Kim teaches the complexity of neuroinflammation extends beyond classic immune and cellular mechanisms, with emerging evidence highlighting the role of non-coding RNAs, epigenetic modifications, the gut–brain axis, and metabolic states as critical regulators (page 7, 1st paragraph); the treatment of neuroinflammation presents a significant challenge due to its dual role in the CNS—both protective and deleterious (page 9, 5th paragraph); although NSAIDs have shown some promise in reducing neuroinflammation, particularly in early-stage Alzheimer’s disease, their efficacy in chronic neurodegenerative conditions has been inconsistent (page 10, 1st paragraph). Kim teaches findings presented highlight the multifaceted nature of neuroinflammation and its critical role in the progression of neurological disorders; chronic neuroinflammation emerges as a key driver of neurodegeneration, fueled by the sustained activation of microglia, astrocytes, and peripheral immune cells (page 12, 1st paragraph); despite the progress in our understanding of the mechanisms of neuroinflammation, therapeutic interventions remain a significant challenge; traditional anti-inflammatory drugs, including NSAIDs and corticosteroids, have demonstrated limited efficacy in chronic neurodegenerative conditions due to their inability to target CNS-specific inflammation and their systemic side effects; while these drugs are effective in managing acute inflammation, their role in long-term disease modification is minimal (page 12, 2nd paragraph). Kim teaches developing immunomodulatory strategies represents a promising advancement in the field; drugs targeting TNF-α and IL-6, as well as JAK-STAT inhibitors, have shown potential in preclinical models, though their clinical utility in CNS disorders remains to be fully validated (page 12, 3rd paragraph). Kim teaches while significant strides have been made in understanding and targeting neuroinflammation, its complexity necessitates innovative, multidisciplinary approaches.
Thus, DiSabato and Kim establish that the art of treating neuroinflammation is extremely unpredictable.
Gilissen teaches the understanding of SUCNR1 (succinate receptor 1) activation, signaling pathways and functions remains largely elusive, which calls for deeper investigations; SUCNR1 shows a high potential as an innovative drug target and is probably an important regulator of basic physiology; in order to achieve the full characterization of this receptor, more specific pharmacological tools such as small-molecules modulators will represent an important asset (Abstract); on the basis of the existing observations mostly acquired from in vitro and in vivo rodent models, SUCNR1 represents a promising drug target in various common human diseases, like hypertension, diabetes and IRI; however, the current paucity of specific pharmacological tools delays its validation as a drug target; up to now, no synthetic agonists and very few ligands have been described; more widely available tools should rapidly prompt further investigations on the putative binding pocket to facilitate the design of new modulators; such ligands might be used to address more deeply the role of the receptor, particularly in systems more relevant to human physiology (page 63, left, last bridge paragraph).
Liebing teaches SUCNR1 (succinate receptor 1) is abundantly expressed in immune cells and different organs and tissues, including the kidney, liver, and heart; the known roles of SUCNR1 include its involvement in regulating blood pressure via the renin-angiotensin system and its importance for macrophage function (page 2018, left, 3rd paragraph). Liebing teaches elevated SUC (succinate) levels occur in certain physiological conditions, such as endurance exercise and pathologies, including hypertension, type 2 diabetes mellitus, or obesity; thus, intra- and extracellular SUC concentrations may be high enough to activate SUCNR1, depending on the cellular context and metabolic state; SUCNR1 is associated with pro- and anti-inflammatory effects, and only a few reports have confirmed its Gq- besides Gi-coupling (page 2037, left, last bridge paragraph); SUCNR1 exhibits high basal Gq protein activation depending on cellular metabolism, which may hamper the detection of a response upon agonist addition; due to its observed contradictory role in inflammation, SUCNR1 has gained attention as a potential drug target (page 2037, right, last bridge paragraph). Liebing teaches the exploitation of SUCNR1 as a drug target needs to carefully consider the metabolic context and the fact that the actual agonist SUC is constantly produced by cells and microbiota under both physiological and pathophysiological conditions; SUCNR1 activation by these metabolites and the activation of Gi and Gq from different cellular compartments further increase this complexity; this localization- and metabolism-dependent signaling of SUCNR1 must be considered for further drug development targeting SUCNR1 (page 2041, left, last paragraph).
Thus, DiSabato and Kim establish that the art of treating targeting SUCNR1 as a therapeutic is extremely unpredictable.
2. The breadth of the claims
Claims 1-4, 9 and 10 are very broad in terms of the compounds claimed to be useful for treating any neuroinflammation. Claims 6-8 are narrow in terms of the compounds claimed, but are extremely broad in terms of neuroinflammation being treated. As evidenced by instant claim 4, neuroinflammation is associated with numerous desperate diseases with no overlap. Moreover, the instant claims do not require that an individual is in need of treating neuroinflammation. Neuroinflammation is associated with aging. Thus, any individual is susceptible to neuroinflammation associated aging. Thus, the claims encompass a genus of molecules which function as a succinate/succinate receptor 1 inhibitor with no other defined structural components for treating neuroinflammation in any subject.
3. The amount of direction or guidance provided and the presence or absence of working examples
The specification provides examples wherein Compound 7a was administered to treat periodontitis and compound 7a reduced periodontal related inflammation (See Examples 2-5). However, the specification does not provide any data that shows that any succinate/succinate receptor 1 inhibitor is useful for treating any neuroinflammation other than neuroinflammation associated with periodontitis.
4. The quantity of experimentation necessary
Because of the known unpredictability of the art (as discussed supra) and in the absence of experimental evidence commensurate in scope with the claims, the skilled artisan would not accept that any succinate/succinate receptor 1 inhibitor could be predictably used as treatment for any neuroinflammation.
Determining if a particular succinate/succinate receptor 1 inhibitor compound will treat any neuroinflammation would require formulation into a dosage form, and subjecting into clinical trials or to testing in an assay known to correlate to clinical efficacy of such treatment. This is undue experimentation given the limited guidance and direction provided by Applicants.
Accordingly, the inventions of claims 1-4 and 6-10 do not comply with the scope of enablement requirement of 35 U.S.C 112, first paragraph, since to practice the claimed invention a person of ordinary skill in the art would have to engage in undue experimentation with no assurance of success.
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 1-4 and 9 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Siegel et al (WO 2015/021226 A1).
While the examination has not been expanded beyond the elected species: Alzheimer’s disease (as the elected disorder species) or Compound 7a (as the elected compound species), the following rejection is made to further prosecution with regards to the claims which read on the elected species, and that are being anticipated by the prior art (Siegel) with regard to the broader genus of “disorders” and “succinate/succinate receptor 1 inhibitors.”
Regarding claim 1, Siegel teaches a composition for use in treating a disease or disorder associate with inflammation comprising a compound (claim 220); wherein the disease is a neurological disease or disorder (claim 221); wherein the disease or disorder is associated with dysregulation of a G-coupled protein receptor (claim 223); wherein the G-coupled protein receptor is G-coupled protein receptor succinate receptor 1 (claim 225); wherein the compound acts as an antagonist of G-coupled protein receptor succinate receptor 1 (claim 227). Moreover, Siegel teaches a method of treating a disease or disorder associate with inflammation comprising administering to a patient in need thereof a therapeutically effective amount of a compound (page 18, lines 20-22); in some embodiments the disease or disorder is a neurological disease (page 19, lines 12-16); in some embodiments the disease or disorder is associated with dysregulation of a G-coupled protein receptor (page 19, lines 19-20); in some embodiments, the G-coupled protein receptor is a succinate receptor (page 19, lines 20-21); in some embodiments, the G-coupled protein receptor is G-coupled protein receptor succinate receptor 1 (page 19, lines 21-22); and in some embodiments, the compound acts as an antagonist of G-coupled protein receptor succinate receptor 1 (page 19, lines 23-24). Thus, Siegel teaches a method for treating neuroinflammation in an individual comprising administering a composition comprising a succinate/succinate receptor 1 inhibitor.
With regard to claim 1, the wherein limitations of these claims, are considered to simply express the intended result of a process step positively recited, which is not given patentable weight (See MPEP 2111.04: [T]he court noted (quoting Minton v. Nat'lAss'n of Securities Dealers, Inc., 336 F.3d 1373, 1381, 67 USPQgd 1614, 1690 (Fed. Cir. 2003)) that a "'whereby clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited.'" Hoffer v. Microsoft Corp., 405 F.3d 1396, 1399, 74 USPQgd 1481, 1483 (Fed. Cir. 2005).). In the instant case, the wherein clause is directed to the intended result (i.e. neuroinflammation in the individual is ameliorated or reduced) of the process step positively recited (i.e. administering a succinate/succinate receptor 1 inhibitor to a subject suffering from neuroinflammation).
Regarding claims 2 and 3, Siegel teaches in some embodiments the compound is administered orally. This reads on administered to a location other than the brain of the individual and wherein the composition is administered systemically.
Regarding claim 4, Siegel teaches in some embodiments the neurological disease or disorder is Alzheimer’s disease (page 21, lines 5-6).
Regarding claim 9, Siegel teaches the therapeutic compound and other ingredients may be compressed into tablets (page 53, lines 9-11).
Claim Rejections - 35 USC § 103
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 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 6-8 and 10 are rejected under 35 U.S.C. 103 as being unpatentable over Siegel et al (WO 2015/021226 A1) as applied to claims 1-4 and 9 above, and further in view of Li et al (WO 2019/136022 A1).
As set forth above, Siegel teaches a method for treating neuroinflammation in an individual comprising administering a composition comprising a succinate/succinate receptor 1 inhibitor.
Regarding claims 6 and 7, Siegel teaches all the limitations of claims 6 and 7, except wherein the succinate/succinate receptor inhibitor is the elected Compound 7a.
However, Li teaches cpd-7a has the structure [0033]:
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Li teaches the compounds (also referred to herein as antagonists), such as 7a can target succinate receptor [0048]; and the succinate/succinate receptor 1 inhibitor is compound 7a (claim 3). Thus, Li teaches cpd-7a, which is equivalent to the instantly elected Compound 7a, is a succinate/succinate receptor 1 inhibitor.
Since Siegel teaches a method for treating neuroinflammation in an individual comprising administering a composition comprising a succinate/succinate receptor 1 inhibitor, and since Li teaches that Compound 7a is a succinate/succinate receptor 1 inhibitor, it would have been prima facie obvious for a person of ordinary skill in the art before the effective filing date of the invention to substitute one functional equivalence (any succinate/succinate receptor 1 inhibitor) for another (Compound 7a) with an expectation of success, since the prior art establishes that both function in similar manner, thus resulting in the practice of the method of claims 6 and 7 with a reasonable expectation of success.
Regarding claim 8, Li teaches the dosage of a compound of the present disclosure can be from 1.0 mg/kg to 500 mg/kg; for example, compound 4C can be used from 10 mg/kg to 100 mg/kg; for example, the dosage can be 10, 20, 30, 40, 50, 60, 70, 80, 90 and 100 mg/kg; in an embodiment, the dose is 50 mg/kg per application; and other compounds described herein, including 7a and 7b, can be used at similar dosages [0050]. It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date to utilize the dosage amounts of compound 7a as a starting point for optimizing the concentration of Compound 7a formulated in the composition comprising Compound 7a to treat neuroinflammation including inflammation associated with Alzheimer’s disease, since Siegel teaches inhibiting succinate/succinate receptor 1 is useful for treating neuroinflammation including inflammation associated with Alzheimer’s disease and Li teaches these amounts as effective for inhibiting succinate/succinate receptor 1 and because dosage and treatment regimen are result-effective variables, i.e. a variable that achieves a recognized result. Therefore, the determination of the optimum or workable dosages would have been well within the practice of routine experimentation by the skilled artisan. Furthermore, absent any evidence demonstrating a patentable difference between the compositions and the criticality of the claimed dosage range, the determination of the optimum or workable dosing regimen given the guidance of the prior art would have been generally prima facie obvious to the skilled artisan. Please see MPEP 2144.05 [R-2](II)(A) and In re Aller, 220 F. 2d 454, 456, 105 USPQ 233, 235 (CCPA 1955). ("[W]here the general conditions of claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation.").
Taken together, all this would result in the practice of the method of claim 8 with a reasonable expectation of success.
Regarding claim 10, Li teaches the inhibitor of the succinate/Sucnr1 signaling is provided
as a topical formulation for use in the oral cavity; and treatment can be carried out for the any length of time as needed, such as over a period of days, weeks or months or longer and can be done as frequently as desired; for example, it can be done daily, or weekly or more or less frequently. It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date to administer Compound 7a in a topical formulation for use in the oral cavity since the prior art teaches this as composition suitable for administering Compound 7a.
Taken together, all this would result in the practice of the method of claim 10 with a reasonable expectation of success.
Conclusion
Claims 1-4 and 6-10 are rejected.
No claim is allowed.
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/Rayna Rodriguez/ Primary Examiner, Art Unit 1628