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 .
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.
This office action is a response to applicant’s election submitted June 22, 2026, claims filed June 18, 2024 wherein claims 1, 4, 7, 11, 13-14, 16, 19, 22, 24, 26, 30, 43, 46, 49, 51, 53-54, 57, 59-60, and 64-67 were preliminarily amended and claims 5, 6, 8, 18, 20, 21, 23, 25, 27, 28, 35, 37, 38, 40, 42, 44, 45, 47, 48, 50, 52, 56, 58, and 60-63 were canceled are examined herein.
Claims 1-4, 7, 9-17, 19, 22, 24, 26, 29-34, 36, 39, 41, 43, 46, 49, 51, 53-55, 57, 59-60, and 64-67 are pending in this application.
Priority
This application is a 371 of PCT/US2022/031565 filed 05/31/2022 and claims benefit to US provisional application 63/194,357 filed 05/28/2021
Election/Restrictions
Applicant's election with traverse of Group I, claims 1-4, 7, 9-17, 19, 22, 24, 26, 29-34, 36, 39, 41, 43, 46, 49, 51, 53, 57, 59, 60, and 64-66 in the reply filed on June 22, 2026 is acknowledged. Applicant's election with traverse of the compound 158 as a species of formula I in the reply filed on June 22, 2026 is acknowledged. Claims 1-4, 7, 30, 46, 53, 57, 59, 60, and 64-66 read on the elected species compound 158
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.
The traversal is on the ground(s) that the Office has not established there would be a serious search burden to examine all of the Groups and compounds. This is not found persuasive because a search burden is not a requirement when making a restriction between multiple inventions in a 35 U.S.C. §371 application.
The requirement is still deemed proper and is therefore made FINAL.
Claims 9-17, 19, 22, 24, 26, 31,33-34, 36, 39, 41, 43, 49, 51, 54-55, 58, and 67 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected invention, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 21 June 2024.
In order to facilitate compact prosecution the scope was further expanded to include the following species:
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wherein R1 is
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(i.e. a substituted C5 alkyl) or H and R6 is H.
Thus claims 1-4, 7, 29-30, 32, 46, 53, 57, 59-60 and 64-66 read on the elected species compound 158 and are examined herein. In order to facilitate compact prosecution the full scope of the elected claims are examined herein.
Specification
The disclosure is objected to because it contains an embedded hyperlink and/or other form of browser-executable code (pg. 17, para. 0064). Applicant is required to delete the embedded hyperlink and/or other form of browser-executable code; references to websites should be limited to the top-level domain name without any prefix such as http:// or other browser-executable code. See MPEP § 608.01.
Claim Objections
Claims 9, 11, 13, 66 are objected to because of the following informalities:
In claims 9 and 11, the phrase “oxo” should be replaced with “C(=O)” similar to claim 1o to demonstrate a single alkylene group that is oxo substituted.
In claim 13 a comma should be added after “4-pyridyl”.
In claim 66, the phrase “ademonous” should read “adenomatous”.
Appropriate correction is required.
Claim Rejections - 35 USC § 112 (b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claim 46 and 60 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Regarding claim 46: Claim 46 recites inter alia, “Z is H2” in the following formula:
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. It is unclear whether Z is to be diatomic hydrogen or wherein Z is two singly bound hydrogen atoms, as shown in other formulas (see claim 49). The lack of clarity renders the claim indefinite.
Regarding claim 60: A broad range or limitation together with a narrow range or limitation that falls within the broad range or limitation (in the same claim) may be considered indefinite if the resulting claim does not clearly set forth the metes and bounds of the patent protection desired. See MPEP § 2173.05(c). In the present instance, claim 60 recites the broad recitation “muscular dystrophy”, and the claim also recites “(Duchenne (DMD), Becker (BMD), congenital)” which is the narrower statement of the range/limitation. The claim(s) are considered indefinite because there is a question or doubt as to whether the feature introduced by such narrower language is (a) merely exemplary of the remainder of the claim, and therefore not required, or (b) a required feature of the claims.
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 1-4, 7, 29-30, 32, 46, 53, 57, 59-60 are rejected under 35 U.S.C. 103 as being unpatentable over Clark (WO2020/106627 cited on PTO-892)
Regarding claims 1-4, 7, 29-30, 32, 46, 53, 57, 59-60: Clark teaches 13-membered macrolides for the treatment of infectious diseases which are azaketolides (abstract). Clark teaches compound 112
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(pg. 60). Clark teaches the macrolides can be used to treat an inflammatory condition (pg. 100, para. 00194). Clark teaches exemplary inflammatory conditions include cystic fibrosis (pg. 101, para. 0196). According to the instant specification genetic diseases that are associated with the presence of at least one premature termination codon mutation or other nonsense mutations include cystic fibrosis (pg. 138, para. 00177).
Although Clark does not explicitly demonstrate treatment of cystic fibrosis, wherein Clark suggests cystic fibrosis as a condition to be treatment it would have been prima facie obvious to do so with a reasonable expectation of success given it is explicitly suggested by Clark.
Claims 64-65 are rejected under 35 U.S.C. 103 as being unpatentable over Clark (WO2020/106627, cited on PTO-892) and as applied to claims 1-4, 7, 29-30, 32, 46, 53, 57, 59-60 above in view of Rosin-Arbesfeld (US 2015/0328247, cited on PTO-892, hereinafter referred to as Rosin) and Baradaran-Heravi (Nucleic Acids Research, 2021, cited on PTO-892, hereinafter referred to as Baradaran).
Regarding claim 64-65: As discussed above the prior art render obvious a method of using macrolide antibiotics for the treatment of premature stop codon associated diseases as recited by instant claim 57.
They do not teach wherein the disease to be treated is junctional or recessive dystrophic epidermolysis bullosa.
However, Rosin teaches treatment of genetic neurodegenerative diseases caused by or associated with nonsense mutations or premature termination codons using macrolides (abstract). Rosin teaches treatment strategies of genetic diseases resulting from nonsense mutations within the coding sequence of a gene have emerged based on the use of aminoglycoside antibiotics (pg. 1, para. 0026). Rosin teaches macrolides to be used include erythromycin, azithromycin, and clarithromycin (pg. 2, para. 0044).
Baradaran teaches premature termination codon (PTC) readthrough is considered a potential treatment for genetic diseases caused by nonsense mutations (abstract). Aminoglycosides and their derivatives are among the most potent PTC readthrough compounds found to date (pg. 3692. Col. 2, para. 2). Baradaran suggests PTC readthrough as a therapeutic for junctional or recessive dystrophic epidermolysis bullosa.
Taken together, it would have been prima facie obvious to apply the method for the treatment of junctional or recessive dystrophic epidermolysis bullosa as suggested by Rosin and Baradaran. A person of ordinary skill in the art would have had the motivation to do so with a reasonable expectation of success as macrolide antibiotics are recognized as PTC readthrough agents and the art suggests PTC readthrough agents as a known technique for the treatment of these diseases.
Claim 66 is rejected under 35 U.S.C. 103 as being unpatentable over Clark (WO2020/106627, cited on PTO-892) as applied to claims 1-4, 7, 29-30, 32, 46, 53, 57, 59-60 above in view of and Rosin-Arbesfeld (US 2015/0328247, cited on PTO-892, hereinafter referred to as Rosin) and Roll (Clinical trial NCT04454151, 2020, cited on PTO-892).
Regarding claim 66: As discussed above the prior art render obvious a method of using macrolide antibiotics for the treatment of premature stop codon associated diseases as recited by instant claim 57.
They do not teach wherein the disease to be treated is familial adenomatous polyposis.
However, Rosin teaches treatment of genetic neurodegenerative diseases caused by or associated with nonsense mutations or premature termination codons using macrolides (abstract). Rosin teaches treatment strategies of genetic diseases resulting from nonsense mutations within the coding sequence of a gene have emerged based on the use of aminoglycoside antibiotics (pg. 1, para. 0026). Rosin teaches macrolides to be used include erythromycin, azithromycin, and clarithromycin (pg. 2, para. 0044).
Roll teaches azithromycin treatment for readthrough of APC gene stop codon mutations in familial adenomatous polyposis (i.e. FAP, pg. 2, brief title). Roll teaches members of the aminoglycoside family of antibiotics have been found to induce ribosomal read-through of nonsense mutations, leading to expression of a full length, functional protein. Investigators have recently shown that members of the aminoglycoside and macrolide antibiotic families can induce read-through of the nonsense mutations in the APC gene and lead to reduced oncogenic phenotypes in CRC cells and indifferent mice models (pg. 5, para. 2). Roll teaches the macrolide antibiotic-Azithromycin to induce read-through of thenonsense mutations in the APC gene and to induce expression of a full length, functional APC protein in patients suffering from FAP (pg. 5, para. 3).
Taken together, it would have been prima facie obvious to apply the method for the treatment of FAP as suggested by Rosin and Roll. A person of ordinary skill in the art would have had the motivation to do so with a reasonable expectation of success as macrolide antibiotics are recognized as PTC readthrough agents and the art suggests PTC readthrough agents as a known technique for the treatment of these diseases.
Claims 1-4, 57, 59-60 are rejected under 35 U.S.C. 103 as being unpatentable over Rosin-Arbesfeld (US 2015/0328247, cited on PTO-892, hereinafter referred to as Rosin), in view of Rafka et al. (WO 00/31097, cited in previous action) and Sugimoto et al. (EP 1985620, cited in previous action).
Regarding claims 1-4, 57, 59-60: Rosin teaches treatment of genetic neurodegenerative diseases caused by or associated with nonsense mutations or premature termination codons using macrolides (abstract). Rosin teaches treatment strategies of genetic diseases resulting from nonsense mutations within the coding sequence of a gene have emerged based on the use of aminoglycoside antibiotics (pg. 1, para. 0026). Rosin teaches diseases to be treated include Duchenne muscular dystrophy (pg. 1, para. 0025). Rosin teaches macrolides to be used include erythromycin, azithromycin, and clarithromycin (pg. 2, para. 0044). Rosin establishes the use of antibiotic macrolides for the treatment of genetic diseases associated with nonsense mutations or premature termination codons.
Rosin does not teach wherein the macrolide antibiotic is
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wherein R1 is
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(i.e. a substituted C5 alkyl) or H and R6 is H.
However, Rafka teach 13-membered azalides for the treatment of bacterial infections comprising a compound having the formula 3:
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(claim 11). Bacterial infections include Hemophilus influenza and pneumococci (p.8-9). Rafka teaches the specific compound 1A, which is a compound of formula 3 wherein R1 is
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(i.e. a substituted C5 alkyl) and R6 is H (pg. 32, line 21).
Sugimoto teach 10a-azalide compound for the treatment of Hemophilus influenza and erythromycin resistant pneumococci (abstract). Sugiomoto teaches 10-azalides which are derivatives from macrolide antibiotics (pg. 1, paras. 0004-0006, 0007) The 10-azalide compound is represented by the formula (I):
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, wherein R2 and R3 combine together to represent oxo group or a group represented by formula 37
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(claim 1). Sugimoto also teaches wherein R8, R9, R10 and R11 can be H (pg., para. 0429, example 8).
While a 13-membered macrolide having an oxo at position 3 is novel, the compound of formula (I) wherein position 3 is an oxo is not considered an inventive step, because substitution of an oxo group or cladinose ring at position 3 were known alternative substitutions per the teachings of Sugimoto et al. Accordingly, it would have been obvious to combine the teachings of Rafka et al. and Sugimoto et al. to arrive at the presently claimed compound. Specifically, modifying the compound 1B of Rafka, by substituting the lower cladinose ring with oxo, as taught by Sugimoto, would lead to the following compound:
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wherein R1 is
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(i.e. a substituted C5 alkyl) or H, and R6 is H. This compound meets the structural limitations of a compound of formula I as recited by instant claim 1 wherein R2a, R2b, R4a, R4b are selected from H and C1 alkyl; R5 is
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R6a is C1 alkyl; R6b is H; R8a and R8b are selected from H and C1 alkyl; R9a is H; R10a and R10b are selected from H and C1 alkyl; R11a and R11b are selected from substituted C5 alkyl and H. According to the instant specification alkyl includes branched alkyls and can be substituted with hydroxy groups (pgs. 8-9, paras. 0022-0023). Additionally, as taught by Sugimoto R8-R11 can be H. A prima facie case of obviousness may be made when chemical compounds have very close structural similarities and similar utilities. "An obviousness rejection based on similarity in chemical structure and function entails the motivation of one skilled in the art to make a claimed compound, in the expectation that compounds similar in structure will have similar properties.
Taken together, it would have been prima facie obvious to utilize the compound rendered obvious over Rafka and Sugimoto for the treatment of genetic neurodegenerative diseases caused by or associated with nonsense mutations or premature termination codons as taught by Rosin. A person of ordinary skill in the art would have had the motivation to do so with a reasonable expectation of success the art recognizes the general ability of macrolide antibiotics to treat such diseases, and a person of ordinary skill in the art would recognize the compounds of Rafka and Sugimoto as macrolide antibiotics to serve this purpose. Wherein macrolide antibiotics are known in the art to treat genetic diseases associated with nonsense mutations or premature termination codons, it is prima facie obvious to substitute equivalents for the same purpose (See MPEP 2144.09 (I)).
Claims 64-65 are rejected under 35 U.S.C. 103 as being unpatentable over Rosin-Arbesfeld (US 2015/0328247, cited on PTO-892, hereinafter referred to as Rosin), Rafka et al. (WO 00/31097, cited in previous action) and Sugimoto et al. (EP 1985620, cited in previous action) as applied to claims 1-4, 57, 59-60 above in view of Baradaran-Heravi (Nucleic Acids Research, 2021, cited on PTO-892, hereinafter referred to as Baradaran).
Regarding claim 64-65: As discussed above the prior art render obvious a method of using macrolide antibiotics for the treatment of premature stop codon associated diseases as recited by instant claim 57.
They do not teach wherein the disease to be treated is junctional or recessive dystrophic epidermolysis bullosa.
However, Baradaran teaches premature termination codon (PTC) readthrough is considered a potential treatment for genetic diseases caused by nonsense mutations (abstract). Aminoglycosides and their derivatives are among the most potent PTC readthrough compounds found to date (pg. 3692. Col. 2, para. 2). Baradaran suggests PTC readthrough as a therapeutic for junctional or recessive dystrophic epidermolysis bullosa.
Taken together, it would have been prima facie obvious to apply the method for the treatment of junctional or recessive dystrophic epidermolysis bullosa as suggested by Baradaran. A person of ordinary skill in the art would have had the motivation to do so with a reasonable expectation of success as macrolide antibiotics are recognized as PTC readthrough agents and the art suggests PTC readthrough agents as a known technique for the treatment of these diseases.
Claim 66 is rejected under 35 U.S.C. 103 as being unpatentable over Rosin-Arbesfeld (US 2015/0328247, cited on PTO-892, hereinafter referred to as Rosin), Rafka et al. (WO 00/31097, cited in previous action) and Sugimoto et al. (EP 1985620, cited in previous action) as applied to claims 1-4, 57, 59-60 above, in view of Roll (Clinical trial NCT04454151, 2020, cited on PTO-892).
Regarding claim 66: As discussed above the prior art render obvious a method of using macrolide antibiotics for the treatment of premature stop codon associated diseases as recited by instant claim 57.
They do not teach wherein the disease to be treated is familial adenomatous polyposis.
However, Roll teaches azithromycin treatment for readthrough of APC gene stop codon mutations in familial adenomatous polyposis (i.e. FAP, pg. 2, brief title). Roll teaches members of the aminoglycoside family of antibiotics have been found to induce ribosomal read-through of nonsense mutations, leading to expression of a full length, functional protein. Investigators have recently shown that members of the aminoglycoside and macrolide antibiotic families can induce read-through of the nonsense mutations in the APC gene and lead to reduced oncogenic phenotypes in CRC cells and indifferent mice models (pg. 5, para. 2). Roll teaches the macrolide antibiotic-Azithromycin to induce read-through of the nonsense mutations in the APC gene and to induce expression of a full length, functional APC protein in patients suffering from FAP (pg. 5, para. 3).
Taken together, it would have been prima facie obvious to apply the method for the treatment of FAP as suggested by Roll. A person of ordinary skill in the art would have had the motivation to do so with a reasonable expectation of success as macrolide antibiotics are recognized as PTC readthrough agents and the art suggests PTC readthrough agents as a known technique for the treatment of these diseases.
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 1-4, 7, 29-30, 32, 46, 53, 57, 59-60 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims of U.S. Patent No. 12,552,825 (cited on PTO-892) in view of Rosin-Arbesfeld (US 2015/0328247, cited on PTO-892, hereinafter referred to as Rosin), Rafka et al. (WO 00/31097, cited in previous action) and Sugimoto et al. (EP 1985620, cited in previous action).
The patented claims teach the following compound 143:
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(claim 12). The patented claims teach a method of treating infectious diseases in a subject comprising administering compounds of claim 1 (claim 15). The patented claims teach a genus of compounds of which the compound 143 belongs (claim 1).
The patented claims do not teach treatment of a genetic disease associated with a premature termination codon mutation.
However, Rosin teaches treatment of genetic neurodegenerative diseases caused by or associated with nonsense mutations or premature termination codons using macrolides (abstract). Rosin teaches treatment strategies of genetic diseases resulting from nonsense mutations within the coding sequence of a gene have emerged based on the use of aminoglycoside antibiotics (pg. 1, para. 0026). Rosin teaches diseases to be treated include Duchenne muscular dystrophy (pg. 1, para. 0025). Rosin teaches macrolides to be used include erythromycin, azithromycin, and clarithromycin (pg. 2, para. 0044). Rosin establishes the use of antibiotic macrolides for the treatment of genetic diseases associated with nonsense mutations or premature termination codons.
Rafka teach 13-membered azalides for the treatment of bacterial infections comprising a compound having the formula 3:
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(claim 11). Bacterial infections include Hemophilus influenza and pneumococci (p.8-9).
Sugimoto teach 10a-azalide compound for the treatment of Hemophilus influenza and erythromycin resistant pneumococci (abstract). Sugiomoto teaches 10-azalides which are derivatives from macrolide antibiotics (pg. 1, paras. 0004-0006, 0007) The 10-azalide compound is represented by the formula (I):
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, wherein R2 and R3 combine together to represent oxo group or a group represented by formula 37
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(claim 1).
Taken together, it would have been prima facie obvious to utilize the compound of the patented claims over for the treatment of genetic neurodegenerative diseases caused by or associated with nonsense mutations or premature termination codons as taught by Rosin, Rafka and Sugimoto. A person of ordinary skill in the art would have had the motivation to do so with a reasonable expectation of success the art recognizes the general ability of macrolide antibiotics to treat such diseases, and a person of ordinary skill in the art would recognize the compounds of the patented claims as macrolide antibiotics to serve this purpose. Wherein macrolide antibiotics are known in the art to treat genetic diseases associated with nonsense mutations or premature termination codons, it is prima facie obvious to substitute equivalents for the same purpose (See MPEP 2144.09 (I)).
Claims 64-65 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims of U.S. Patent No. 12,552,825 (cited on PTO-892), Rosin-Arbesfeld (US 2015/0328247, cited on PTO-892, hereinafter referred to as Rosin), Rafka et al. (WO 00/31097, cited in previous action) and Sugimoto et al. (EP 1985620, cited in previous action) as applied to claims 1-4, 7, 29-30, 32, 46, 53, 57, 59-60 above in view of Baradaran-Heravi (Nucleic Acids Research, 2021, cited on PTO-892, hereinafter referred to as Baradaran).
Regarding claim 64-65: As discussed above the patented claims in view of the prior art render obvious a method of using macrolide antibiotics for the treatment of premature stop codon associated diseases as recited by instant claim 57.
They do not teach wherein the disease to be treated is junctional or recessive dystrophic epidermolysis bullosa.
However, Baradaran teaches premature termination codon (PTC) readthrough is considered a potential treatment for genetic diseases caused by nonsense mutations (abstract). Aminoglycosides and their derivatives are among the most potent PTC readthrough compounds found to date (pg. 3692. Col. 2, para. 2). Baradaran suggests PTC readthrough as a therapeutic for junctional or recessive dystrophic epidermolysis bullosa.
Taken together, it would have been prima facie obvious to apply the method for the treatment of junctional or recessive dystrophic epidermolysis bullosa as suggested by Baradaran. A person of ordinary skill in the art would have had the motivation to do so with a reasonable expectation of success as macrolide antibiotics are recognized as PTC readthrough agents and the art suggests PTC readthrough agents as a known technique for the treatment of these diseases.
Claim 66 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims of U.S. Patent No. 12,552,825 (cited on PTO-892), Rosin-Arbesfeld (US 2015/0328247, cited on PTO-892, hereinafter referred to as Rosin), Rafka et al. (WO 00/31097, cited in previous action) and Sugimoto et al. (EP 1985620, cited in previous action) as applied to claims 1-4, 7, 29-30, 32, 46, 53, 57, 59-60 above in view of Roll (Clinical trial NCT04454151, 2020, cited on PTO-892).
Regarding claim 66: As discussed above the patented claims in view of the prior art render obvious a method of using macrolide antibiotics for the treatment of premature stop codon associated diseases as recited by instant claim 57.
They do not teach wherein the disease to be treated is familial adenomatous polyposis.
However, Roll teaches azithromycin treatment for readthrough of APC gene stop codon mutations in familial adenomatous polyposis (i.e. FAP, pg. 2, brief title). Roll teaches members of the aminoglycoside family of antibiotics have been found to induce ribosomal read-through of nonsense mutations, leading to expression of a full length, functional protein. Investigators have recently shown that members of the aminoglycoside and macrolide antibiotic families can induce read-through of the nonsense mutations in the APC gene and lead to reduced oncogenic phenotypes in CRC cells and indifferent mice models (pg. 5, para. 2). Roll teaches the macrolide antibiotic-Azithromycin to induce read-through of the nonsense mutations in the APC gene and to induce expression of a full length, functional APC protein in patients suffering from FAP (pg. 5, para. 3).
Taken together, it would have been prima facie obvious to apply the method for the treatment of FAP as suggested by Roll. A person of ordinary skill in the art would have had the motivation to do so with a reasonable expectation of success as macrolide antibiotics are recognized as PTC readthrough agents and the art suggests PTC readthrough agents as a known technique for the treatment of these diseases.
Conclusion
No claims are allowed in this action.
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/SAMUEL L GALSTER/Examiner, Art Unit 1693
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