Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Detailed Action
Claims 1-9 are currently pending.
Election/Restriction
Applicant’s election without traverse of Compound 43
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in the reply filed on 4/22/2026 is acknowledged.
Claims 1-9 are being examined on the merits herein.
The requirement is deemed proper and is therefore made final.
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.
Claim Rejections - 35 USC § 102
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 1-6 and 9 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Lee (WO2017023133, 5/30/2024 IDS).
Lee teaches the elected Compound 43
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, every compound listed in Claim 5, and the five specific compounds of examined Claim 6 in Table 1 beginning on Page 12. Compound 43, for example, is encompassed by the formulae of Claims 1-4 as indicated in applicant’s response dated 4/22/2026. The compounds are used to treat HDAC6 associated diseases including Charcot-Marie-Tooth disease (CMT) (Abstract; Para 273). Administration can be oral (Para 276). Applicant teaches CMT is associated with the peripheral nervous system (PNS) as required by Claim 1: “Charcot-Marie-Tooth…disease is the most common type of hereditary peripheral nerve disorder” and “Upon the development of Charcot- Marie-Tooth disease, progressive degeneration of peripheral nerves leads to atrophy of muscles” (Page 1). Thus, CMT is necessarily associated with the PNS as claimed and Lee anticipates the method of treating the claimed disease, CMT associated with PNS.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claims 1-9 are rejected under 35 U.S.C. 103 as being unpatentable over Lee (WO2017023133, 5/30/2024 IDS) in view of Ha (Br J Pharmacol. 2020 Aug 15;177(22):5096-5113.) or Benoy (Neurotherapeutics (2017) 14:417–428).
Lee teaches the elected Compound 43, every compound listed in Claim 5, and the five specific compounds of examined Claim 6 in Table 1 beginning on Page 12. The compounds are used to treat HDAC6 associated diseases including Charcot-Marie-Tooth disease (CMT) (Abstract; Para 273). Administration can be oral (Para 276). Applicant teaches CMT is associated with the peripheral nervous system (PNS): “Charcot-Marie-Tooth…disease is the most common type of hereditary peripheral nerve disorder” and “Upon the development of Charcot- Marie-Tooth disease, progressive degeneration of peripheral nerves leads to atrophy of muscles” (Page 1). Thus, CMT is necessarily associated with the PNS as claimed and Lee anticipates the method of treating the claimed disease, CMT associated with PNS.
Lee does not teach treating the particular subtypes of CMT described in Claims 7 or 8.
Ha teaches “A novel HDAC6 inhibitor, CKD-504, has potent therapeutic efficacy for CMT1A” (Abstract). The inhibition of HDAC6 is thought to be effective in the CMT subtype because “HDAC6 is involved in several processes including the induction of aggresome formation, autophagy, and protein refolding” reducing PMP22 which associated with CMT1A pathogenesis (Page 5109, Para 1 and 4.5 The possible…).
Benoy “established a screening method consisting of 3 different phases identifying selective and potent HDAC6 inhibitors that can functionally restore motor and sensory deficits in a CMT2F mouse model” (Page 426, Right Col.). “pharmacologic inhibition of the deacetylating function of HDAC6 not only normalized the defects seen in cultured DRG neurons, but also reversed the motor and sensory abnormalities and the electrophysiological defects observed in vivo” (Page 418, Intro).
One of ordinary skill in the art seeking to treat the particular CMT subtypes described in Ha or Benoy would find it obvious to select the HDAC6 inhibitors taught by Lee, including the elected species Compound 43, because Lee teaches that the compounds are effective for the treatment of CMT broadly. The same artisan would expect success in treating the particular subtypes taught in Ha or Benoy before the effective filing date of the examined invention because both teach HDAC6 modulators, like the Lee compounds, are effective to treat said subtypes listed in Claim 8 including CMT1A and CMT2F.
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.
PROVISIONAL:
Claims 1-9 are provisionally rejected on the grounds of nonstatutory double patenting as being unpatentable over Claims 1-4, 8, and 11-12 of copending Application No. 18286037 (hereinafter referred to as Chong) in view of Silverman (Organic Chemistry of Drug Design and Drug Action, Elservier Academic Press, 2004, pg. 24-34), Lee (WO2017023133, 5/30/2024 IDS), Ha (Br J Pharmacol. 2020 Aug 15;177(22):5096-5113.), and Benoy (Neurotherapeutics (2017) 14:417–428).
Although the claims at issue are not identical, they are not patentably distinct from each other because both applications are directed to a genus of HDAC6 inhibitors for the treatment of neurological diseases like CMT.
Regarding the claims directed to compositions of matter, In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014), the court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Sun Pharm. Indus., Ltd. v. Eli Lilly & Co., 611 F.3d 1381, 95 USPQ2d 1797 (Fed. Cir. 2010). See MPEP 804 (II) (B) (1). See Chong specification Page 22 teaching the treatment of CMT with compounds of the invention. Applicant teaches CMT is associated with the peripheral nervous system (PNS): “Charcot-Marie-Tooth…disease is the most common type of hereditary peripheral nerve disorder” and “Upon the development of Charcot- Marie-Tooth disease, progressive degeneration of peripheral nerves leads to atrophy of muscles” (Instant Specification: Page 1). Thus, CMT is necessarily associated with the PNS as claimed.
Similar embodiments are taught between applications: elected Compound 43
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and Chong Compound 6
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differ only by the substitution of a thioamide with an amide.
Chong does not teach the single-atom substitution or the treatment of particular CMT subtypes via oral administration.
Silverman teaches that the exchange of a thioamide and amide is a well-known bioisosteric replacement and the groups are classified as a nonclassical bioisosteres, or isosteres which “do not have the same number of atoms and do not fit the steric and electronic rules of classical isosteres, but do produce similar biological activity” (Page 29, E.4 Bioisosterism, Lines 10-12; Page, Table 2.3). One of skill in the art seeking to form an HDAC6 inhibitor to treat the diseases identified in Chong would find it obvious to perform the substitution and expect success in doing so because Silverman teaches the exchange is known and generally results in “similar biological activity”.
Lee teaches the same compound as claimed and a close analog of the Chong compound as Compound 43 in Table 1 beginning on Page 12. The compound is taught to be administered orally for the treatment of CMT (Para 273 and 276).
Ha teaches “A novel HDAC6 inhibitor, CKD-504, has potent therapeutic efficacy for CMT1A” (Abstract). The inhibition of HDAC6 is thought to be effective in the CMT subtype because “HDAC6 is involved in several processes including the induction of aggresome formation, autophagy, and protein refolding” reducing PMP22 which associated with CMT1A pathogenesis (Page 5109, Para 1 and 4.5 The possible…).
Benoy “established a screening method consisting of 3 different phases identifying selective and potent HDAC6 inhibitors that can functionally restore motor and sensory deficits in a CMT2F mouse model” (Page 426, Right Col.). “pharmacologic inhibition of the deacetylating function of HDAC6 not only normalized the defects seen in cultured DRG neurons, but also reversed the motor and sensory abnormalities and the electrophysiological defects observed in vivo” (Page 418, Intro).
One of ordinary skill in the art seeking to treat the particular CMT subtypes described in Ha or Benoy would find it obvious to select the HDAC6 inhibitors taught by Chong and modified in view of Silverman because Chong teaches that the homologs are effective for the treatment of CMT and Lee teaches the compounds as claimed are effective for the same purpose. The same artisan would expect success in treating the particular subtypes taught in Ha or Benoy because both teach HDAC6 modulators, like the Chong and Lee compounds, are effective to treat said subtypes listed in Claim 8.
Since both applications teach similar inhibitors for the same use, the examiner maintains that the aforementioned claims of the instant application are substantially overlapping in scope as discussed hereinabove and are prima facie obvious over the cited claims of Chong.
This is a provisional nonstatutory double patenting rejection.
NONPROVISIONAL:
1. Claims 1-9 are rejected on the grounds of nonstatutory double patenting as being unpatentable over Claims 1-8 of U.S. Patent No. 10464911 (hereinafter referred to as Chong) in view of Silverman (Organic Chemistry of Drug Design and Drug Action, Elservier Academic Press, 2004, pg. 24-34), Lee (WO2017023133, 5/30/2024 IDS), Ha (Br J Pharmacol. 2020 Aug 15;177(22):5096-5113.), and Benoy (Neurotherapeutics (2017) 14:417–428).
Although the claims at issue are not identical, they are not patentably distinct from each other because both applications are directed to a genus of HDAC6 inhibitors for the treatment of neurological diseases like CMT.
Regarding the claims directed to compositions of matter, In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014), the court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Sun Pharm. Indus., Ltd. v. Eli Lilly & Co., 611 F.3d 1381, 95 USPQ2d 1797 (Fed. Cir. 2010). See MPEP 804 (II) (B) (1). See Chong specification Column 28 teaching the treatment of CMT with compounds of the invention. Applicant teaches CMT is associated with the peripheral nervous system (PNS): “Charcot-Marie-Tooth…disease is the most common type of hereditary peripheral nerve disorder” and “Upon the development of Charcot- Marie-Tooth disease, progressive degeneration of peripheral nerves leads to atrophy of muscles” (Instant Specification: Page 1). Thus, CMT is necessarily associated with the PNS as claimed.
Similar embodiments are taught between applications: elected Compound 43
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and Chong Example 35
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differ only by the substitution of a sulfoxide with a carbonyl.
Chong does not teach the functional group substitution or the treatment of particular CMT subtypes via oral administration.
Silverman teaches that the exchange of a sulfoxide for an ester is a well-known bioisosteric replacement and the groups are classified as a nonclassical bioisosteres, or isosteres which “do not have the same number of atoms and do not fit the steric and electronic rules of classical isosteres, but do produce similar biological activity” (Page 29, E.4 Bioisosterism, Lines 10-12; Page 30, Table 2.3). One of skill in the art seeking to form an HDAC6 inhibitor to treat the diseases identified in Chong would find it obvious to perform the substitution and expect success in doing so because Silverman teaches the exchange is known and results in “similar biological activity”.
Lee teaches the same compound as claimed and a close analog of the Chong compound as Compound 43 in Table 1 beginning on Page 12. The compound is taught to be administered orally for the treatment of CMT (Para 273 and 276).
Ha teaches “A novel HDAC6 inhibitor, CKD-504, has potent therapeutic efficacy for CMT1A” (Abstract). The inhibition of HDAC6 is thought to be effective in the CMT subtype because “HDAC6 is involved in several processes including the induction of aggresome formation, autophagy, and protein refolding” reducing PMP22 which associated with CMT1A pathogenesis (Page 5109, Para 1 and 4.5 The possible…).
Benoy “established a screening method consisting of 3 different phases identifying selective and potent HDAC6 inhibitors that can functionally restore motor and sensory deficits in a CMT2F mouse model” (Page 426, Right Col.). “pharmacologic inhibition of the deacetylating function of HDAC6 not only normalized the defects seen in cultured DRG neurons, but also reversed the motor and sensory abnormalities and the electrophysiological defects observed in vivo” (Page 418, Intro).
One of ordinary skill in the art seeking to treat the particular CMT subtypes described in Ha or Benoy would find it obvious to select the HDAC6 inhibitors taught by Chong and modified in view of Silverman because Chong teaches that the homologs are effective for the treatment of CMT and Lee teaches the compounds as claimed are effective for the same purpose. The same artisan would expect success in treating the particular subtypes taught in Ha or Benoy because both teach HDAC6 modulators, like the Chong and Lee compounds, are effective to treat said subtypes listed in Claim 8.
Since both claim sets teach HDAC6 inhibitors which are isosteric homologs for the same use, the examiner maintains that the aforementioned claims of the instant application are substantially overlapping in scope as discussed hereinabove and are prima facie obvious over the cited claims of Chong.
2. Claims 1-9 are rejected on the grounds of nonstatutory double patenting as being unpatentable over Claims 1-16 of U.S. Patent No. 10717716 (hereinafter referred to as Chong) in view of Lee (WO2017023133, 5/30/2024 IDS), Ha (Br J Pharmacol. 2020 Aug 15;177(22):5096-5113.), and Benoy (Neurotherapeutics (2017) 14:417–428).
Although the claims at issue are not identical, they are not patentably distinct from each other because both applications are directed to a genus of HDAC6 inhibitors for the treatment of HDAC6-associated diseases.
Regarding the claims directed to compositions of matter, In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014), the court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Sun Pharm. Indus., Ltd. v. Eli Lilly & Co., 611 F.3d 1381, 95 USPQ2d 1797 (Fed. Cir. 2010). See MPEP 804 (II) (B) (1). See Chong Abstract teaching the treatment of HDAC6-associated diseases with compounds of the invention including CMT (Col. 205). Applicant teaches CMT is associated with the peripheral nervous system (PNS): “Charcot-Marie-Tooth…disease is the most common type of hereditary peripheral nerve disorder” and “Upon the development of Charcot- Marie-Tooth disease, progressive degeneration of peripheral nerves leads to atrophy of muscles” (Instant Specification: Page 1). Thus, CMT is necessarily associated with the PNS as claimed.
The same embodiments are taught between applications: elected Compound 43
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and Chong Compound 43
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Chong does not teach the treatment of particular CMT subtypes via oral administration.
Lee teaches the same compound as elected and the Chong compound as Compound 43 in Table 1 beginning on Page 12. The compound is taught to be administered orally for the treatment of CMT, an HDAC6-associated disorder (Para 273 and 276).
Ha teaches “A novel HDAC6 inhibitor, CKD-504, has potent therapeutic efficacy for CMT1A” (Abstract). The inhibition of HDAC6 is thought to be effective in the CMT subtype because “HDAC6 is involved in several processes including the induction of aggresome formation, autophagy, and protein refolding” reducing PMP22 which associated with CMT1A pathogenesis (Page 5109, Para 1 and 4.5 The possible…).
Benoy “established a screening method consisting of 3 different phases identifying selective and potent HDAC6 inhibitors that can functionally restore motor and sensory deficits in a CMT2F mouse model” (Page 426, Right Col.). “pharmacologic inhibition of the deacetylating function of HDAC6 not only normalized the defects seen in cultured DRG neurons, but also reversed the motor and sensory abnormalities and the electrophysiological defects observed in vivo” (Page 418, Intro).
One of ordinary skill in the art seeking to treat the particular CMT subtypes described in Ha or Benoy would find it obvious to select the HDAC6 inhibitors taught by Chong because Chong teaches that the compounds are effective for the treatment of HDAC6 inhibitors. The same artisan would expect success in treating the particular subtypes taught in Ha or Benoy because both teach HDAC6 modulators, like the Chong and Lee compounds, are effective to treat said CMT subtypes listed in Claim 8.
Since both claim sets teach the same HDAC6 inhibitors for the same use, the examiner maintains that the aforementioned claims of the instant application are substantially overlapping in scope as discussed hereinabove and are prima facie obvious over the cited claims of Chong.
Conclusion
No claim is allowable.
Inquiries
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Richard G. Peckham whose telephone number is (703)756-4621. The examiner can normally be reached 8:30am - 4:30pm EST.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Kortney Klinkel can be reached on (571) 270-5239. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/RICHARD GRANT PECKHAM/Examiner, Art Unit 1627
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