DETAILED ACTION
This office action is in response to applicant’s filing dated June 29, 2026.
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 18, 20-28, and 117 are pending in the instant application. Acknowledgement is made of Applicant's remarks and amendments filed June 29, 2026. Acknowledgement is made of Applicant's amendment of claims 18, 20-24, and 29; cancelation of claims 1-17 and 19; and addition of new claim 117. Claims 30-116 were previously canceled.
Applicants elected without traverse (i) compound 18:
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as the elected compound species; (ii) graft versus host disease (GVHD) as the elected acute inflammatory condition species; and IL-6 as the elected pro-inflammatory cytokine species in the reply filed on November 10, 2025. The requirement is still deemed proper. Claims 23, 26, 28, and 29 remain withdrawn.
New claim 117 is directed to the elected invention and thus is presently under examination.
Claims 18, 20-22, 24, 25, 27, and 117 are presently under examination as they relate to the elected species: (i) compound 18:
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(ii) graft versus host disease (GVHD); and (iii) IL-6.
Priority
The present application claims benefit of priority to US Provisional Application 63/346,193 filed on May 26, 2022.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on June 29, 2026 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner, except where marked with a strikethrough.
Objections and/or Rejections and Response to Arguments
Rejections and/or objections not reiterated from previous office actions are hereby withdrawn. The following rejections and/or objections are either reiterated (Maintained Objections and/or Rejections) or newly applied (New Objections and/or Rejections, Necessitated by Amendment or New Objections and/or Rejections, NOT Necessitated by Amendment). They constitute the complete set presently being applied to the instant application.
Modified Objections and/or Rejections
Modifications Necessitated by Claim Amendment
Claim Rejections - 35 USC § 112(a)
Scope of Enablement
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 18, 20-22, 24, 25, and 27 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 graft versus host disease comprising administering Compound 18, does not reasonably provide enablement for a method of treating any acute inflammatory condition in a subject. 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 of treating an acute inflammatory condition in a subject comprising administering to the subject a therapeutically effective amount of Compound 18. Claims 20-22 narrow the scope of the acute inflammatory condition. Claims 24, 25, and 27 narrow the scope of the method to the intended result of reducing a pro-inflammatory cytokine.
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 Brannon et al (Nat Rev Mater, 2022; 7:796-813); Varela et al (Inflammation, 2018; 41(4):1115-1127); and Zhang et al (Inflammation Research, 2025; 74:74 pp. 1-21).
Brannon teaches acute inflammation is essential for initiating and coordinating the body’s response to injuries and infections; however, in acute inflammatory diseases, inflammation is not resolved but propagates further, which can ultimately lead to tissue damage such as in sepsis, acute respiratory distress syndrome and deep vein thrombosis; currently, clinical protocols are limited to systemic steroidal treatments, fluids and antibiotics that focus on eradicating inflammation rather than modulating it; strategies based on stem cell therapeutics and selective blocking of inflammatory molecules, despite showing great promise, still lack the scalability and specificity required to treat acute inflammation (abstract). Brannon teaches inflammation plays an essential part in the immune response against harmful stimuli and injury through recognition and containment of invading pathogens and toxins; overly responsive or uncontrolled inflammation can lead to tissue damage and organ dysfunction, and is associated with numerous human disorders, such as acute lung and liver injury, sepsis, asthma, inflammatory bowel disease, rheumatoid arthritis and neurodegenerative diseases; acute inflammation, regulated by the innate immune system, is responsible for the initial recognition of an inflammatory stimulus and focuses on the rapid containment of the offending pathogen or injury; such a response aims at accelerating inflammatory resolution and typically lasts on a scale of hours to days; if the acute inflammation response is excessive or fails to contain the inflammatory stimulus, the response is shifted to a chronic (pathological) phase characterized by prolonged inflammatory episodes and can last on a scale of weeks to years (page 796, left, 1st paragraph). Brannon teaches acute inflammation is initiated by either pathogenic infections or exogenously by mechanical trauma, ischaemia-reperfusion or chemicals (page 796, right, 1st paragraph). Brannon teaches cytokine- and antibody-based therapy; proteins can be designed to target cytokines, such as TNF, IL-1 and IL-6, or to dampen systemic inflammation in patients with immune disorders, by blocking antibodies or by inhibiting cytokines through receptor binding; cytokine inhibitors have shown excellent efficacy in treating inflammation in clinical trials (page 799, left, 2nd paragraph); however, cytokine-targeting therapeutics lack specificity, with reduced haematopoiesis as one of the most common side effects, ultimately leading to increased infections owing to reduced WBC populations (page 799, left, 3rd paragraph).
Varela teaches inflammation is an adaptive process to the noxious stimuli that the human body is constantly exposed to; from the local inflammatory response to a full-blown systemic inflammation, a wide complex sequence of events occurs; persistent immunosuppression and catabolism may ensue, until multiple organ failure finally sets in; and since clinically useful and specific biomarkers are lacking, diagnosis may come late; a thorough understanding of these events (how they begin, how they evolve, and how to modulate them) is imperative, but as yet poorly studied (abstract). Varela teaches the inflammatory process has been best studied in response to infectious stimuli, particularly bacterial infections; it is not clear whether most of the principles studied in infection-induced inflammation apply to other causes (page 1115, right, last paragraph); released pro-inflammatory cytokines create a proinflammatory loop that can break away from the injured tissue and enter the bloodstream, leading to what has been called the “cytokine storm”; organ-specific receptors are activated by these cytokines and a systemic reaction ensues; this systemic reaction is called the acute-phase response; the purpose of each of these changes in protein quantity has not yet been fully clarified, but scavenging pathogens and modulation of the inflammatory response and its consequences may be an important goal (page 1117, left, 1st paragraph). Varela teaches much remains to be known about inflammation and how its progresses through the different phases presented; an understanding of this progress in a continuum would allow for future therapies to modulate the transition between these phases; also, current treatments simply rely on catching up with the damages the inflammatory process is dealing (page 112, left, 2nd paragraph).
Moreover, Zhang teaches sepsis is characterized by a dysregulated host response to infection, leading to organ dysfunction and associated with significant morbidity and mortality, posing a critical challenge to global public health; among its complications, sepsis frequently causes acute respiratory distress syndrome (ARDS), which has a high incidence and mortality rate, particularly in intensive care units (ICUs); currently, the management of sepsis-induced ARDS is largely limited to supportive care, as no specific pharmacological treatments are available (abstract). Zhang establishes that even in the development of drugs for a single acute inflammatory condition is extremely unpredictable.
Thus, Brannon, Varela, and Zhang establish that the art of developing therapeutics for treating acute inflammatory conditions is extremely unpredictable.
2. The breadth of the claims
Claims 18, 20-22, 24, 25, and 27, while narrow in terms of the compounds claimed to be useful for the claimed methods, are extremely broad in terms of the conditions claimed to be treated. Moreover, the instant claims do not require that an individual is in need of treating an acute inflammatory condition.
3. The amount of direction or guidance provided and the presence or absence of working examples
The specification provides examples wherein Compound I-18 increase QPRT expression; compounds I-17 and I-18 restore NAD+ biosynthesis; Compound I-18 increases expression of SIRT-1 in Kupffer cells and SIRT-3 in HK2 primary tubule cells; compounds I-17 and I18 activate SIRT1 in primary hepatocytes; Compound I-18 increases STAT3 and IL-10 expression; compounds I-17 and I18 decrease IL-6 expression. The Examiner notes that the specification discloses CLP-induced sepsis model; LPS-induced sepsis model; acute pancreatitis model; acute hepatic injury model; acute graft versus host disease model. However, in a review of the disclosure of these experimental models, disclosure of the compounds administered was not identified. The specification does not provide any data that shows that any of the claimed compounds treat any acute inflammatory condition.
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 compound of formula (I) could predictably be used to treat any acute inflammatory condition.
Determining if a particular compound of formula (I) will treat any acute inflammatory condition 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 18, 20-22, 24, 25, and 27 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.
Response to Arguments
Applicant argues:
The specification provides enabling support. The specification provides enabling support. The specification at paragraph [00233] states that "Inflammatory cytokines can be divided into two groups: those involved in acute inflammation and those responsible for chronic inflammation. Those involved in acute inflammation include, for example, IL-1, TNF-a, IL-6, IL-11, IL-8, and other chemokines, G- CSF, and GM-CSF." Then examples in the specification provide results to this regard. For example, the examples describe results for compound 18 with reduction of pro- inflammatory cytokines, TNFα, IL-1β, and IL-6 and the expression of the chemokine MCP-1. Compound 18 was administered to cells following LPS-induced inflammation. (LPS is a trigger of acute inflammation.) The pro-inflammatory cytokine, IL-6, is reduced with compound 18, and in a dose-dependent manner with compound 18 in Kupffer cells following LPS-induced inflammation. Figures 13 and 14 shows that the secretion of the inflammatory cytokine TNF-α is reduced with administration of compound 18. Figure 15 shows that the secretion of the inflammatory cytokine IL-1β following LPS-induced inflammation is reduced with administration of compound 18. These results show definitive effectiveness of the claimed compound to treat an acute inflammatory condition.
Examiner's response:
The above argument has been carefully considered and has not been found persuasive.
As noted above, the state of the art of developing therapeutics for treating acute inflammatory conditions is highly unpredictable. As set forth above, in acute inflammatory diseases, inflammation is not resolved but propagates further, which can ultimately lead to tissue damage such as in sepsis, acute respiratory distress syndrome and deep vein thrombosis; currently, clinical protocols are limited to systemic steroidal treatments, fluids and antibiotics that focus on eradicating inflammation rather than modulating it; strategies based on stem cell therapeutics and selective blocking of inflammatory molecules, despite showing great promise, still lack the scalability and specificity required to treat acute inflammation. Thus, even for specific acute inflammatory conditions, such as the instantly claimed acute respiratory distress syndrome and sepsis, with known therapeutics (steroidal treatments and antibiotics), treatments lack scalability and specificity required to treat acute inflammation. Moreover, with regard to the argument that the specification provides evidence that compound 18 reduces pro- inflammatory cytokines, TNFα, IL-1β, and IL-6 and the expression of the chemokine MCP-1 following LPS-induced inflammation, as set forth above, the art teaches cytokine- and antibody-based therapy; proteins can be designed to target cytokines, such as TNF, IL-1 and IL-6, or to dampen systemic inflammation in patients with immune disorders, by blocking antibodies or by inhibiting cytokines through receptor binding; cytokine inhibitors have shown excellent efficacy in treating inflammation in clinical trials; however, cytokine-targeting therapeutics lack specificity, with reduced haematopoiesis as one of the most common side effects, ultimately leading to increased infections owing to reduced WBC populations . Thus, the effect of targeting specific cytokines such as TNF, IL-1 and IL-6 is insufficient to establish enablement for the full scope of conditions encompassed by acute inflammatory condition. LPS-induced inflammation is not an established model for every condition that would be encompassed by acute inflammatory condition. Thus, as set forth above, the instant claims 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 § 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 18, 20-22, 24, 25, 27 and 117 are rejected under 35 U.S.C. 103 as being unpatentable over Pellicciari et al (WO 2020/104456 A1).
Regarding claims 18, 20-22, and 117, Pellicciari teaches a method of treating a disease or disorder associated with reduced nicotinamide adenine dinucleotide (NAD+) levels comprising administering to the subject suffering from or susceptible to developing a disease or disorder associated with reduced NAD+ levels a therapeutically effective amount a compound of (I), or a pharmaceutically acceptable salt thereof (claims 2 and 44), wherein the disease is liver transplant associated graft versus host disease (claim 45). Pellicciari teaches a compound of Formula (I) (claim 2):
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Pellicciari does not explicitly teach a compound of formula (I) is the elected compound, Compound 18.
However, Pellicciari does teach Compound I-1 (claim 38):
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[AltContent: textbox (B)][AltContent: oval]and Compound I-4 (claim 38):
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Compound I-1 differs from the instantly elected compound in that Compound I-1 in the position labeled with a dashed circle denoted A contains a –CO2Et, while Compound 18 contains a –CO2H.
Compound I-4 differs from the instantly elected compound in that Compound I-4 contains a -OCH3 in the position labeled with a dashed circle denoted A, while Compound 18 contains a =O.
Moreover, Pellicciari teaches X of formula (I) is alternatively O, OH, or ORh, and Rh is C1-C4 alkyl (claim 2). Pellicciari teaches R7 of formula (I) is A, wherein A is –(C(R6)2)rCO2Rx, wherein Rx is alternatively H or C1-C6 alkyl (claim 2). Thus, Pellicciari teaches O and -OCH3 are alternatively useful in the position corresponding to instantly claimed X and –(CH2)CO2H and –(CH2)CO2Et are alternatively useful in the position corresponding to Ra and Rb for producing compounds useful in the claimed methods. It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date to arrive at the elected compound for use in a method of treating liver transplant associated graft versus host disease with a reasonable expectation of success from the teachings of Pellicciari.
Taken together, all this would result in the practice of the method of claims 18, 20-22, and 117 with a reasonable expectation of success.
Regarding claims 24, 25, and 27, Pellicciari teaches a compound of Formula (I) are administered at different time points [00664] and secondary endpoints include markers of inflammation including IL-6 [00666].
With regard to the limitation wherein the method reduces a pro-inflammatory cytokine (instant claim 24), wherein the pro-inflammatory cytokine is IL-6, Pellicciari renders obvious a method of treating liver transplant associated graft versus host disease comprising the elected compound and suggests measuring IL-6.
In regard to "wherein” clauses, MPEP 2111.04 states:
The determination of whether each of these clauses is a limitation in a claim depends on the specific facts of the case. See, e.g., Griffin v. Bertina, 283 F.3d 1029, 1034, 62 USPQ2d 1431 (Fed. Cir. 2002) (finding that a “wherein” clause limited a process claim where the clause gave “meaning and purpose to the manipulative steps”). In Hoffer v. Microsoft Corp., 405 F.3d 1326, 1329, 74 USPQ2d 1481, 1483 (Fed. Cir. 2005), the court held that when a “‘whereby’ clause states a condition that is material to patentability, it cannot be ignored in order to change the substance of the invention.” Id. However, the court noted (quoting Minton v. Nat’l Ass’n of Securities Dealers, Inc., 336 F.3d 1373, 1381, 67 USPQ2d 1614, 1620 (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.’” Id. In the instant case, the wherein clause is directed to the intended result (i.e. reducing pro-inflammatory cytokine, IL-6) of the process step positively recited (i.e. administering a compound of formula (I), elected compound 18 to treat graft versus host disease).
Taken together, all this would result in the practice of the method of claims 24, 25, and 27 with a reasonable expectation of success.
Response to Arguments
Applicant argues:
The office has identified no teaching or suggestion in Pellicciari to arrive at the claimed method. In contrast, the pending claims are directed to the treatment of an acute inflammatory condition with compound 18. Unexpected results for the treatment of an acute inflammatory condition with compound 18 can be found in the specification, as described above. The examples provide for compound 18 that was administered to cells following LPS-induced inflammation. (LPS is a trigger of acute inflammation.) The example describes results for compound 18 with reduction of pro- inflammatory cytokines, TNFα, IL-β, and IL-6 and the expression of the chemokine MCP-1. These unexpected results show definitive effectiveness of the claimed compound to treat an acute inflammatory condition.
Examiner's response:
The above argument has been carefully considered and has not been found persuasive.
As set forth above, Pellicciari teaches a method of treating liver transplant associated graft versus host disease comprising administering a compound of Formula (I):
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including structurally similar compounds, Compounds I-1 and I-4. As set forth above, Compound I-1 differs from the instantly elected compound in that R7 of formula (I) is –(CH2)CO2Et, while Compound 18 contains a -(CH2)CO2H in the corresponding position. However, as set forth above, Pellicciari teaches R7 of formula (I) is A, wherein A is –(C(R6)2)rCO2Rx, wherein Rx is alternatively H or C1-C6 alkyl (claim 2) for producing compounds useful in the disclosed methods including a method of treating liver transplant associated graft versus host disease. As set forth above, Compound I-4 differs from the instantly elected compound in that X of formula (I) is -OCH3, while compound 18 contains a =O in the corresponding position. As set forth above, Pellicciari teaches O and -OCH3 are alternatively useful in the position corresponding to X of formula (I). As set forth above, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date to arrive at the elected compound for use in a method of treating liver transplant associated graft versus host disease with a reasonable expectation of success from the teachings of Pellicciari. Moreover, it is not unexpected that Compound 18 is useful for treating the acute inflammatory condition graft versus host disease since Pellicciari teaches structurally similar compounds are useful for treating liver transplant associated graft versus host disease and teaches the modifications that would result in the elected compound are also suitable for producing compounds useful for treating liver transplant associated graft versus host disease.
Conclusion
Claims 18, 20-22, 24, 25, 27, and 117 are rejected.
No claim is 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to RAYNA B RODRIGUEZ whose telephone number is (571)272-7088. The examiner can normally be reached 8am-5:00pm, Monday - Thursday.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Amy L Clark can be reached at 571-272-1310. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/Rayna Rodriguez/ Primary Examiner, Art Unit 1628
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