DETAILED ACTION
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 .
Election/Restrictions
Applicant’s election without traverse of Group (I) in the reply filed on 05/04/2026 is acknowledged.
Applicant’s election without traverse of compound
PNG
media_image1.png
130
248
media_image1.png
Greyscale
as the elected therapeutic agent and α-ketoglutarate as the elected TCA metabolite species in the reply filed on 05/04/2026 is acknowledged. A search for the elected compound identifies another related compound and as such, examination has been expanded to the expanded compound
PNG
media_image2.png
130
192
media_image2.png
Greyscale
.
Claims 12, 20, 22-32, 35, 37-38, 41-41, and 43-44 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim.
Priority
This application claims priority to U.S. Provisional Application No. 63/126,462 filed December 16, 2020 and U.S. Provisional Application No. 63/164,484 filed March 22, 2021.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 02/02/2024 and 04/30/2025 has been considered by the examiner.
Claims Status
Claims 3-4, 7-9, 14-15, 20, 22-27, 32, 35, 37-38, 40-41, 43-44, 55-56, and 75 are pending. Claims 1-2, 5-6, 10-13, 16-19, 21, 28-31, 33-34, 36, 39, 42, 45-54, and 57-74 are canceled. Claims 12, 20, 22-32, 35, 37-38, 41-41, and 43-44 are withdrawn. Claims 3-4, 7-9, 14-15, 55-56, and 75 are examined in accordance to the elected species.
Claim Objections
Claims 7, 9, and 55 are objected to because of the following informalities:
Claim 7 recites “wherein the level of at least one of the one or more TCA cycle metabolites is elevated.” The phrase appears to omit the preposition “of” following the word “level.” Accordingly, the claim lacks proper grammatical form and should be amended.
Claim 9 is objected to as being independent upon claim 3 rather than claim 4. While claim 9 is understood to further limit the “one of more TCA cycle metabolites” recited in claim 3, claim 4 specifically identifies the metabolites from which the α-ketoglutarate limitation recited in claim 9 is selected. Accordingly, for purpose of claim clarity and contingency of claim presentation, Applicant may wish to amend claim 9 to depend from claim 4.
Claim 55 is objected to because of informalities. The claim recites “wherein R4 is selected form hydrogen ….” The term “form” appears to be a typographical error and should be corrected to “from.”
Appropriate correction is required.
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 3-4, 7-9, 14-15, 55-56, and 75 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.
Claim 3 recites a method comprising identifying a subject having abnormal levels of one or more tricarboxylic acid (TCA) cycle metabolites and, based at least in part on such abnormal levels, administering a therapeutically effective amount of a therapeutic agent useful in the treatment of a disorder associated with Coenzyme A (CoA) reduction, elevation, sequestration, toxicity, or redistribution (CASTOR), a neurological disorder, and/or a metabolic disorder.
Claims 4, 7, 9, 12, 14, and 15 further encompass specific α-ketoglutarate levels. Elevated or depressed-α-ketoglutarate levels, additional biomarker profiles, CASTOR disorders, pantothenate kinase-associated neurodegeneration (PKAN), propionic acidemia, fatty acid oxidation defects, methylmalonic acidemia, glutaric acidemia, and HMG-CoA lyase deficiency.
Claims 55, 56, and 75 further require treatment using a selected genus and species of compounds.
The specification does not demonstrate possession of the full scope of the claimed correlation α-ketoglutarate levels and treatment decisions across the breadth of the recited disorders.
The disclosure primarily describes particular experimental studies involving PKAN-related CoA deficiency models and treatment with selected compounds. However, claims encompass numerous unrelated neuropsychological disorders, metabolic disorders, and CASTOR disorder without identifying a presentative species or common structural or functional characteristics demonstrating α-ketoglutarate levels serve as a reliable therapeutic biomarker throughout the full scope of the claimed disorders.
The specification does not provide sufficient blaze marks directing one of ordinary skill in the art to presently claimed genus of methods wherein α-ketoglutarate abnormalities are used to identify subjects requiring treatment across the entire scope of the neurological disorders, metabolic disorders, and CASTOR disorders.
Accordingly, the disclosure fails to reasonably convey possession of the full claimed genus at the time of filing.
Claims 3-4, 7-9, 14-15, 55-56, and 75 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 treating disease associated with CASTOR, including propionate acidemia using compound 1 and PZ3022, does not reasonably provide enablement for the full scope of the claimed invention. 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.
Claim 3 recites a method encompasses identifying subjects based upon abnormal levels of one or more tricarboxylic acid (TCA) cycle metabolites including α-ketoglutarate and administering therapeutic agents useful in the treatment of disorders associated with Coenzyme A (CoA) reduction, elevation, sequestration, toxicity, or redistribution (CASTOR), a neurological disorder, and/or a metabolic disorder. The dependent claims further encompass specific α-ketoglutarate concentration ranges, biomarker profiles, disease states, and treatment with the recited compound species.
The breadth of the claims is substantial. The claims encompass numerous distinct disease etiologies, and patient populations, including PKAN, propionic acidemia, methylmalonic acidemia, glutaric acidemia, and HMG-CoA lyase deficiency, neurological disorder, metabolic disorder, and disorders associated with CoA dysregulation.
The specification provides limited working examples directed to PKAN-related disease models and treatment with selected compounds such as PZ3022 and the elected compound. The disclosure does not provide guidance demonstrating the α-ketoglutarate serves as a predictive therapeutic biomarker throughout the entire scope of the claimed disorders.
The state of the art further demonstrates that α-ketoglutarate exhibits context-depending biological effects. Specifically, Duan et al. (Cancer Biology & Therapy 2019, Vol. 20, No. 3, pages 252-260) reports that α-ketoglutarate has been observed to exert both positive and negative effects on autophagy depending upon the articular cellular system studies. (See left column of page 253.) Likewise, Xia et al. (J Transl Genet Genom. 2026; 10:164-83) characterizes α-ketoglutarate as a pleiotropic metabolic regulator whose biological effects vary substantially across disease states and metabolic conditions. (See second paragraph of page 165.) Aragones et al. (PLoS ONE 11(4): e0154601, 2016, pages 1-11) further demonstrate that α-ketoglutarate may function as a biomarker in certain disease settings but lacks predictive value in other closely related disease states. (See pages 6 and 7.) Sharma et al. ((Adv. Nano Biomed Res.2021,1, pages 1-21) teaches numerous therapeutics have shown efficacy in animal AD models but failed in human patients. (Abstract.) Sharma further teaches the biggest clinical challenge that has not been achieved so far is the development of effective therapeutics to treat AD. Most of the clinical trials for AD have failed in the past few decades owing to a poor understanding of the disease. (See page 3, left column, Section 2.)
Application of Wands Factors supports a conclusion of non-enablement:
(1) Quantity of experimentation required
Substantial experimentation would be required to determine whether α-ketoglutarate levels correlate with treatment response for each claimed disease. Given the breadth of the claimed genus and the unpredictability of neurological disease biology, a skilled artisan would be required to scree numerous neurological disorders and numerous compounds/agents to determine whether abnormal lα-ketoglutarate levels are present and if each of the compounds/agents can modulate said levels, whether such abnormalities are clinically meaningful, and whether treatment of the claimed PKAN activators would provide therapeutic benefit.
(2) Amount of guidance provided
The specification provides limited guidance outside the disclosed PKAN-related embodiments.
(3) Presence or absence of working examples
The disclosure contains only limited number of working examples directed to particular disease models such as propionate acidemia disease model and compounds such as PZ3022 and compound 1 (elected compound).
(4) Nature of the invention
The invention concerns diagnostic and therapeutic correlations involving metabolic biomarkers, an area recognized as biologically complex and highly variable.
(5) State of the prior art
The prior art does not establish a universal relationship between α-ketoglutarate levels and therapeutic efficacy across the broad range of claimed disorders. Further, the prior art demonstrates that neurological disorders comprising diverse disease states having different underlying biological mechanisms and treatment paradigms. (See Sharma et al., Abstract; page 3, left column.)
(6) Relative skill of those in the art
Although skilled artisan possesses expertise in metabolic biology, such expertise would not eliminate the need for extensive empirical testing.
(7) Predictability and unpredictability of the art
The art is highly unpredictable. Xia et al. demonstrate that α-ketoglutarate exhibits disease-specific and context-dependent biological behavior and may produce differing biological outcomes indifferent settings. (See Abstract.) Sharma demonstrates that neurological disorders, including Alzheimer’s disease, are highly complex and multifactorial disease for which effective therapeutic intervention remains challenging. The art therefore would not have provided a reasonable expectation that observation made in CASTOR disorders would be extrapolated to the broad genus of neurological diseases encompassed by the claims.
Because one of ordinary skill in the art would be required to conduct extensive research to determine each claimed disorder whether α-ketoglutarate levels are predictive of treatment response, therapeutic efficacy, or disease status, under experimentation would be required to practice the full scope of the claimed invention.
Accordingly, the claims are not enabled commensurate in scope with the breadth of the claimed invention.
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.
Claims 3-4, 7-9, 14-15, 55-56, and 75 are rejected under 35 U.S.C. 103 as being unpatentable over Jackowski et al. (WO2019/133632 A1) in view of AL Acqeel et al. (Brain & Development 1994; 16 (suppl): 33-37) cited in the IDS filed 04/30/2025 and Collado et al. (Mol Genet Metab. 2020 May 11;130(3):183–196).
Jackowski teaches a method of treating a coenzyme A reduction, elevation, sequestration, toxicity, or redistribution (CASTOR) disease in a subject, the method comprising the step of administering to the subject a therapeutically effective amount of a compound having a structure represented by a formula:
PNG
media_image3.png
83
239
media_image3.png
Greyscale
, wherein Ar1 is selected from aryl and heteroaryl and substituted with 0, 1, 2, or 3 groups independently selected from halogen, –NO2, –CN, –OH, –SH, –NH2 among others. (See claim 1) The compound includes
PNG
media_image2.png
130
192
media_image2.png
Greyscale
. (See claim 9.). Jackowski also teaches methods of treating a coenzyme A reduction, elevation, sequestration, toxicity, or redistribution (CASTOR) disease such as, for example, defects in fatty acid oxidation enzymes, methylmalonic acidemia, glutaric acidemia, propionic academia, and HMG-CoA lyase, via small molecule modulators of CoA levels. (See Abstract.) Moreover, Jackowski teaches the CASTOR disease also includes α-ketoglutarate dehydrogenase deficiency. (See paragraph [0111].) Particular preference was given on the fact compound PZ-3022 treatment of the Pcca mice (propionic academia mousse model) elevated free CoA and acetyl-CoA, and propionyl-CoA was reduced and that PZ-3022 treatment normalizes the levels of acyl-carnitines in the PCCA mousse model. (See paragraph [00512] and [00513].)
Jackowski does not expressly teach first providing a subject having abnormal levels of one or more TCA-cycle metabolites.
AL Acqeel teaches α-ketoglutarate dehydrogenase deficiency and reports markedly abnormal urinary excretion of α-ketoglutarate in affected subject. Al Aqeel also teaches that subject suffering from α-ketoglutarate dehydrogenase exhibit abnormal level of α-ketoglutarate, which is a recognized TCA-cycle metabolite. (See Abstract and page 35.)
Collado teaches that disorders such as propionic acid are characterized by disruption of TCA-cycle metabolism and altered anaplerotic and cataplerotic flux, resulting in abnormalities of TCA-cycle intermediates, including α-ketoglutarate metabolism. (See Abstract, Section 3.5.) Collado further teaches that TCA-cycle metabolites may serve as biomarkers of disease state and therapeutic response. (See section 3.1.1.)
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to identify or select subject exhibiting abnormal α-ketoglutarate levels prior to administration of the therapeutic compound (expanded compound) taught by Jackowski because Al Aqee teaches that abnormal α-ketoglutarate levels are characteristics of α-ketoglutarate dehydrogenase deficiency and Collado teaches that TCA-cycle metabolite abnormalities are recognized indicators of metabolic dysfunction associated with disorders such as those treated by Jackowski.
One of ordinary skill in the art would have been motivated to utilize known disease-associated metabolic biomarkers when selecting and treating patients because doing so would permit identification, diagnosis, and monitoring of affected individuals. A reasonable expectation of success would have existed because all references concern the same metabolic disease pathways and recognize α-ketoglutarate abnormalities as manifestations of the underlying disease process.
With respect to the elected compound, the difference between the elected compound species and the expanded compound species lies in the position of the fluorine atom on the phenyl ring. (See below)
Elected compound species Expanded compound species
PNG
media_image4.png
130
248
media_image4.png
Greyscale
PNG
media_image5.png
130
192
media_image5.png
Greyscale
.
Jackowski teaches a compound having a structure represented by a formula:
PNG
media_image3.png
83
239
media_image3.png
Greyscale
, wherein Ar1 may be substituted with one or more halogen substituents. (See claim 1). Jackowski also teaches on pages 202-203 Ar1-aryl; substituted with 0, 1, 2, or 3 substituents, and substituents independently selected from halogen on the genus compound.
One of ordinary skill in the medicinal chemistry arts would have found it obvious to prepare and use closely related positional isomers of a lead compound, including relocating a fluorine substituent to another available position on the same aromatic/phenyl ring because such compounds represent predictable variant within the scope of the genus taught by Jackowski.
A person of ordinary skill in the art would have had a reasonable expectation of success because the claimed compound preserves the identical pharmacophore, ring system, linker, amide, functionality, Q2 substituent, and chloropyridazine moiety disclosed by Jackowski. The relocation of a single fluorine atom on the same aromatic/phenyl ring constitutes a routine structural variation that would reasonably be expected to retain biological activity taught by Jackowski.
Furthermore, the claimed positional isomer represents one of a finite number of predictable fluorinated species falling within the halogen-substituted Ar1 genus expressly taught by Jackowski. Selection of a known member from a finite set of identified, predictable solutions would have been obvious to one of ordinary skill in the art. See KSR Int’l Co. v. Teleflex Inc., 550 U.S. 398 (2007).
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 3-4, 7-9, 14-15, 55-56, and 75 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-19 of U.S. Patent No. US11,547,709 B2; over claims 1-14 of U.S. Patent No. 12/545,663 B2 in view of Jackowski et al. (WO2019/133632 A1) in view of AL Acqeel et al. (Brain & Development 1994; 16 (suppl): 33-37) cited in the IDS filed 04/30/2025 and Collado et al. (Mol Genet Metab. 2020 May 11;130(3):183–196).
The reference patent teaches a method of treating propionic acidemia (PA) in a subject in need thereof, the method comprising administering to the subject a therapeutically effective amount of a compound having a structure represented by a formula:
PNG
media_image6.png
232
632
media_image6.png
Greyscale
or a pharmaceutically acceptable salt thereof. (See claim 1)> The compound is selected from:
PNG
media_image7.png
946
334
media_image7.png
Greyscale
. (See claim 3.)
The reference patent does not expressly teach first providing a subject having abnormal levels of one or more TCA-cycle metabolites.
Jackowski teaches a method of treating a coenzyme A reduction, elevation, sequestration, toxicity, or redistribution (CASTOR) disease in a subject, the method comprising the step of administering to the subject a therapeutically effective amount of a compound having a structure represented by a formula:
PNG
media_image3.png
83
239
media_image3.png
Greyscale
, wherein Ar1 is selected from aryl and heteroaryl and substituted with 0, 1, 2, or 3 groups independently selected from halogen, –NO2, –CN, –OH, –SH, –NH2 among others. (See claim 1) The compound includes
PNG
media_image2.png
130
192
media_image2.png
Greyscale
. (See claim 9.). Jackowski also teaches methods of treating a coenzyme A reduction, elevation, sequestration, toxicity, or redistribution (CASTOR) disease such as, for example, defects in fatty acid oxidation enzymes, methylmalonic acidemia, glutaric acidemia, propionic academia, and HMG-CoA lyase, via small molecule modulators of CoA levels. (See Abstract.) Moreover, Jackowski teaches the CASTOR disease also includes α-ketoglutarate dehydrogenase deficiency. (See paragraph [0111].) Particular preference was given on the fact compound PZ-3022 treatment of the Pcca mice (propionic academia mousse model) elevated free CoA and acetyl-CoA, and propionyl-CoA was reduced and that PZ-3022 treatment normalizes the levels of acyl-carnitines in the PCCA mousse model. (See paragraph [00512] and [00513].)
AL Acqeel teaches α-ketoglutarate dehydrogenase deficiency and reports markedly abnormal urinary excretion of α-ketoglutarate in affected subject. Al Aqeel also teaches that subject suffering from α-ketoglutarate dehydrogenase exhibit abnormal level of α-ketoglutarate, which is a recognized TCA-cycle metabolite. (See Abstract and page 35.)
Collado teaches that disorders such as propionic acid are characterized by disruption of TCA-cycle metabolism and altered anaplerotic and cataplerotic flux, resulting in abnormalities of TCA-cycle intermediates, including α-ketoglutarate metabolism. (See Abstract, Section 3.5.) Collado further teaches that TCA-cycle metabolites may serve as biomarkers of disease state and therapeutic response. (See section 3.1.1.)
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to identify or select subject exhibiting abnormal α-ketoglutarate levels prior to administration of the therapeutic compound (expanded compound) taught by the reference patent and Jackowski because Al Aqee teaches that abnormal α-ketoglutarate levels are characteristics of α-ketoglutarate dehydrogenase deficiency and Collado teaches that TCA-cycle metabolite abnormalities are recognized indicators of metabolic dysfunction associated with disorders such as those treated by the reference patent and Jackowski.
One of ordinary skill in the art would have been motivated to utilize known disease-associated metabolic biomarkers when selecting and treating patients because doing so would permit identification, diagnosis, and monitoring of affected individuals. A reasonable expectation of success would have existed because all references concern the same metabolic disease pathways and recognize α-ketoglutarate abnormalities as manifestations of the underlying disease process.
With respect to the elected compound, the difference between the elected compound species and the expanded compound species lies in the position of the fluorine atom on the phenyl ring. (See below)
Elected compound species Expanded compound species
PNG
media_image4.png
130
248
media_image4.png
Greyscale
PNG
media_image5.png
130
192
media_image5.png
Greyscale
.
Jackowski teaches a compound having a structure represented by a formula:
PNG
media_image3.png
83
239
media_image3.png
Greyscale
, wherein Ar1 may be substituted with one or more halogen substituents. (See claim 1). Jackowski also teaches on pages 202-203 Ar1-aryl; substituted with 0, 1, 2, or 3 substituents, and substituents independently selected from halogen on the genus compound.
One of ordinary skill in the medicinal chemistry arts would have found it obvious to prepare and use closely related positional isomers of a lead compound, including relocating a fluorine substituent to another available position on the same aromatic/phenyl ring because such compounds represent predictable variant within the scope of the genus taught by the reference patent and Jackowski.
A person of ordinary skill in the art would have had a reasonable expectation of success because the claimed compound preserves the identical pharmacophore, ring system, linker, amide, functionality, Q2 substituent, and chloropyridazine moiety disclosed by reference patent and Jackowski. The relocation of a single fluorine atom on the same aromatic/phenyl ring constitutes a routine structural variation that would reasonably be expected to retain biological activity taught by the reference patent and Jackowski.
Furthermore, the claimed positional isomer represents one of a finite number of predictable fluorinated species falling within the halogen-substituted Ar1 genus expressly taught by Jackowski. Selection of a known member from a finite set of identified, predictable solutions would have been obvious to one of ordinary skill in the art. See KSR Int’l Co. v. Teleflex Inc., 550 U.S. 398 (2007).
Conclusion
Claims 3-4, 7-9, 14-15, 55-56, and 75 are not allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JEAN P CORNET whose telephone number is (571)270-7669. The examiner can normally be reached Monday-Thursday from 7.00am-5.30pm.
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, 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.
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.
/JEAN P CORNET/ Primary Examiner, Art Unit 1628
Prosecution Insights