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
In the response to the restriction requirement dated August 15, 2025, Applicant canceled claims 1-21 and added new claims 29-48. Applicant asserts that claims 29-48 recite a method similar to Group 1, original claims 1-10, which were drawn to a “method to minimize damage to a cell/group of cells/tissue in a subject as the result of disease or injury including pulmonary arterial hypertension (PAH), stroke, ischemia and reperfusion, by administering a therapeutically effective amount of an Anc80 viral vector that codes for the expression of a sphingolipid-metabolizing protein selected from a group of (1) a ceramidase; (2) sphingosine kinase (SPHK); (3) sphingosine-i-phosphate receptor (SIPR); (4) ceramidase kinase (CERK); or a combination of any of 1, 2, 3 and 4” and thereby, Applicant elects Group 1, corresponding to newly added claims 29-48. Applicant elected species 1, SEQ ID NO: 1, which corresponds to newly added claims 34 and 44.
Claims 35-36 and 45-46 are withdrawn as being drawn towards non-elected species. Applicant’s specification identified SEQ ID NO: 1 as an acid ceramidase in Para. [0016], therefore claims 31-32 and 41-42 are also withdrawn as being drawn towards non-elected species.
Claims 29-30, 33-34, 37-40, 43-44, and 47-48 are examined on the merits.
Priority
The present application is a 35 U.S.C. 371 national stage filing of the International Application No. PCT/US19/50634, filed on September 11, 2019.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on March 11, 2022; July 11, 2022; August 2, 2022; February 16, 2023; June 29, 2023; August 15, 2025; and November 3, 2025 are in compliance with the provisions of 37 CFR 1.97 and are being considered by the examiner.
However, Applicant is reminded that the listing of references in the specification is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered.
Claim Rejections - 35 USC § 112
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 47 is 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.
Claim 47, which depends from claim 39, recites the limitation "the viral vector", There is insufficient antecedent basis for this limitation in the claim as there is no prior recitation of a viral vector. The prior recitation of claim 39 is to an adeno-associated viral vector. Appropriate correction is required.
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.
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 29-30, 33, and 38 are rejected under 35 U.S.C. 103 as being unpatentable over Schuchman (US 2016/0038574 A1, found in IDS dated 03/11/2022) and Brittain et al. (2016, Fatty acid metabolic defects and right ventricular lipotoxicity in human pulmonary arterial hypertension. Circulation, 133(20), 1936-1944, hereafter “Brittain”).
With regard to claims 29 and 30, Schuchman teaches a method of treatment using an acid ceramidase (Para. [0008], line 2) wherein the ceramidase can be administered (Para. [0046], lines 1-2) to mammalian subjects, including humans (Para. [0045], lines 1-2) in vivo (Para. [0044], lines 5-6) and wherein the ceramidase treatment can be used to promote cell survival (Para. [0059], line 3)) in lung epithelium (Para. [0059], line 22), which is considered to reasonably read on treating damage to pulmonary tissue in a subject. Additionally, Schuchman teaches wherein the administration of an effective amount of the therapeutic (Para. [0058], line 1) ceramidase can be delivered using recombinant vector expression systems comprising a nucleic acid molecule encoding the ceramidase (Para. [0076], lines 1-3) including adenovirus vector expression systems (Para. [0082], line 8).
While Schuchman teaches use of a vector comprising a polynucleotide encoding a ceramidase for promoting cell survival in cardiomyocytes (Para. [0059], line 28) in addition to lung epithelium, as well as use of a vector comprising a polynucleotide encoding a ceramidase to treat a wide variety of diseases and disorders (Paras. [0033]-[0040]), Schuchman does not teach use of a vector comprising a polynucleotide encoding a ceramidase in treatment of pulmonary arterial hypertension.
Brittain teaches that right ventricular failure is the primary cause of death in pulmonary arterial hypertension (Pg 1936, left column, lines 1-2) and that accumulation of ceramide, a proapoptotic signal, is associated with right ventricular failure (Pg. 1936, right column, lines 2-4) which provides support for cellular damage due to ceramides. Further, Brittain teaches that ceramides are increased in the right ventricle in human subjects with pulmonary arterial hypertension (Fig 4).
Therefore, it would have been obvious to one having ordinary skill in the art, before the effective filing date of the claimed invention to apply the method of treatment using a vector comprising a polynucleotide encoding a ceramidase which can be used to treat cell damage in lung epithelium and cardiomyocytes as taught by Schuchman to subjects with pulmonary arterial hypertension wherein levels of ceramides are increased as taught by Brittain with a reasonable expectation of success. Brittain teaches that proapoptotic ceramides are increased in the cardiomyocytes of patients having pulmonary arterial hypertension. Brittain further teaches mortality due to right ventricle failure in pulmonary arterial hypertension and pulmonary arterial hypertension associated damage to the right ventricle is supported by the instant specification in Para. [0003]. Since Schuchman teaches that a vector comprising a polynucleotide encoding a ceramidase can be used to promote cell survival in cardiomyocytes as well as lung tissues, a skilled artisan would have been motivated to combine the teachings of Schuchman and Brittain in order to treat cellular damage of both heart and lung tissue in subjects having pulmonary arterial hypertension using a vector comprising a polynucleotide encoding a ceramidase.
With regard to claims 33, Schuchman teaches a ceramidase protein which is the product of the Ashah1 gene (Para. [0023], lines 1-2 and 21), which is considered to reasonably read on a polynucleotide encoding ASAH1.
With regard to claim 38, Schuchman teaches wherein the ceramidase composition can be administered vis intratracheal inoculation (Para. [0047], line 5).
Claim 34 is rejected under 35 U.S.C. 103 as being unpatentable over Schuchman and Brittain as applied to claim 29 above, and further in view of Medin et al. (US 11597917 B2, hereafter “Medin”).
With regard to claim 34, as detailed above, the combined teachings of Schuchman and Brittain teach use of a vector comprising a polynucleotide encoding a ceramidase which is the product of the Asah1 gene (Para. Para. [0023], lines 1-2 and 21), i.e., an ASAH1 ceramidase, for the treatment of damage to lung tissue in subjects having pulmonary arterial hypertension. Schuchman also teaches that the ceramidase may be used to treat Farber disease (Para. [0043]).
The combined teachings of Schuchman and Brittain do not teach wherein the ASAH1 comprises an amino acid sequence which is encoded by SEQ ID NO: 1.
Medin teaches a viral vector which expresses an ASAH1 ceramidase wherein the transgene encoding the ASAH1 comprises SEQ ID NO:8 (Claims 1, 10, and 11) and which can be used to treat Farber disease (Col10, lines 24-28 and 38-40) . SEQ ID NO: 8 as taught by Medin shares 100% homology to instantly claimed SEQ ID NO: 1 (see search 11/03/2025, SEQ ID NO: 1, rni file, result 1, duplicate 1).
Therefore, it would have been obvious to one having ordinary skill in the art, before the effective filing date of the claimed invention, to use the nucleotide sequence encoding ASAH1 having SEQ ID NO: 8, which shares 100% homology with instantly claimed SEQ ID NO:1, as taught by Medin as the sequence encoding ceramidase which is the product of the Asah1 gene as taught by Schuchman with a reasonable expectation of success. While Schuchman teaches use of an ASAH1 polypeptide, Schuchman is silent to the specific nucleic acid sequence which encodes the ASAH1 polypeptide. Since Schuchman teaches their ceramidase could be used to treat Farber disease (Para. 0043]) and Medin teaches a ceramidase having SEQ ID NO: 8 which can be used to treat Farber disease (Col. 10, lines 24-28 and 38-40), a skilled artisan would have been motivated to use SEQ ID NO: 8 as taught by Medin to encode the ASAH1 polypeptide as taught by Schuchman. Furthermore, the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Claim 37 is rejected under 35 U.S.C. 103 as being unpatentable over Schuchman and Brittain as applied to claim 29 above, and further in view of Jooss and Chirmule (2003, Immunity to adenovirus and adeno-associated viral vectors: implications for gene therapy. Gene therapy, 10(11), 955-963).
With regard to claim 37, as detailed above, the combined teachings of Schuchman and Brittain teach use of a vector comprising a polynucleotide encoding a ceramidase for the treatment of damage to lung tissue in subjects having pulmonary arterial hypertension and wherein the ceramide composition can be administered using a adenovirus vector based expression system.
The combined teachings of Schuchman and Brittain do not teach wherein the viral vector is an adeno-associated viral vector.
Jooss and Chirmule teach that use of adenovirus vectors for in vivo gene delivery can induce inflammatory responses whereas adeno-associated viral vectors are characterized by their lack of immune response to the transgene (Abstract). Additionally, Jooss and Chirmule teach that use of adenoviral vectors are complicated by the fact that many human subjects have neutralizing antibodies which can prohibit gene transfer (Pg. 956, right column, last full para.) and that use of recombinant adeno-associated vectors (AAV) can avoid an immune response leading to long-term transgene expression which is an advantage over adenoviral vectors (Pg. 957, right column, first full para.). Further, Jooss and Chirmule teach that use of adenovirus vectors is associated with induction of an inflammatory reaction (Pg. 958, left column, first full para.) whereas adeno-associated viral vectors does not induce inflammatory responses (Pg. 958, right column, second full para.)
Therefore, it would have been obvious to one having ordinary skill in the art, before the effective filing date of the claimed invention, to substitute the adenoviral vector as taught by Schuchman with an adeno-associated viral vector as taught by Jooss and Chirmule with a reasonable expectation of success. Jooss and Chirmule teach that use of adeno-associated vectors are able to deliver long-term transgene expression without inducing an immune response and without the inflammatory responses which are negative consequences of the use of adenoviral vectors. Thus, one having ordinary skill in the arts would have been motivated to use the adeno-associated viral vector as taught by Jooss and Chirmule to deliver the polypeptide encoding a ceramidase as taught by Schuchman as a skilled artisan would have recognized that use of an adeno-associated viral vector would lead to stable expression of the ceramidase while avoiding the negative immune and inflammatory responses associated with adenoviral vector use.
Claims 39-40, 43 and 47-48 are rejected under 35 U.S.C. 103 as being unpatentable over Schuchman, Brittain and Jooss and Chirmule.
With regard to claim 39 and 40, Schuchman teaches a method of treatment using a vector comprising a polynucleotide encoding an acid ceramidase (Para. [0008], line 2) wherein the ceramidase can be administered (Para. [0046], lines 1-2) to mammalian subjects, including humans (Para. [0045], lines 1-2) in vivo (Para. [0044], lines 5-6) and wherein the ceramidase treatment can be used to promote cell survival (Para. [0059], line 3)) in lung epithelium (Para. [0059], line 22), which is considered to reasonably read on treating damage to pulmonary tissue in a subject. Additionally, Schuchman teaches wherein the administration of an effective amount of the therapeutic (Para. [0058], line 1) ceramidase can be delivered using recombinant expression systems comprising a nucleic acid molecule encoding the ceramidase (Para. [0076], lines 1-3) including adenovirus vector expression systems (Para. [0082], line 8).
While Schuchman teaches use of a vector comprising a polynucleotide encoding a ceramidase for promoting cell survival in cardiomyocytes (Para. [0059], line 28) in addition to lung epithelium, as well as use of a vector comprising a polynucleotide encoding a ceramidase to treat a wide variety of diseases and disorders (Paras. [0033]-[0040]), Schuchman does not teach use of a vector comprising a polynucleotide encoding a ceramidase in treatment of pulmonary arterial hypertension.
Brittain teaches that right ventricular failure is the primary cause of death in pulmonary arterial hypertension (Pg 1936, left column, lines 1-2) and that accumulation of ceramide, a proapoptotic signal, is associated with right ventricular failure. (Pg. 1936, right column, lines 2-4). Further, Brittain teaches that ceramides are increased in the right ventricle in human subjects with pulmonary arterial hypertension (Fig 4).
Therefore, it would have been obvious to one having ordinary skill in the art, before the effective filing date of the claimed invention to apply the method of treatment using a vector comprising a polynucleotide encoding a ceramidase which can be used to treat cell damage in lung epithelium and cardiomyocytes as taught by Schuchman to subjects with pulmonary arterial hypertension wherein levels of ceramides are increased as taught by Brittain with a reasonable expectation of success. Brittain teaches that proapoptotic ceramides are increased in the cardiomyocytes of patients having pulmonary arterial hypertension. Brittain further teaches mortality due to right ventricle failure in pulmonary arterial hypertension and pulmonary arterial hypertension associated damage to the right ventricle is supported by the instant specification in Para. [0003]. Since Schuchman teaches that a vector comprising a polynucleotide encoding a ceramidase can be used to promote cell survival in cardiomyocytes as well as lung tissues, a skilled artisan would have been motivated to combine the teachings of Schuchman and Brittain in order to treat cellular damage of both heart and lung tissue in subjects having pulmonary arterial hypertension using a vector comprising a polynucleotide encoding a ceramidase.
The combined teachings of Schuchman and Brittain do not teach wherein the viral vector is an adeno-associated viral vector.
Jooss and Chirmule teach that use of adenovirus vectors for in vivo gene delivery can induce inflammatory responses whereas adeno-associated viral vectors are characterized by their lack of immune response to the transgene (Abstract). Additionally, Jooss and Chirmule teach that use of adenoviral vectors are complicated by the fact that many human subjects have neutralizing antibodies which can prohibit gene transfer (Pg. 956, right column, last full para.) and that use of recombinant adeno-associated vectors (AAV) can avoid an immune response leading to long-term transgene expression which is an advantage over adenoviral vectors (Pg. 957, right column, first full para.). Further, Jooss and Chirmule teach that use of adenovirus vectors is associated with induction of an inflammatory reaction (Pg. 958, left column, first full para.) whereas adeno-associated viral vectors does not induce inflammatory responses (Pg. 958, right column, second full para.)
Therefore, it would have been obvious to one having ordinary skill in the art, before the effective filing date of the claimed invention, to substitute the adenoviral vector as taught by Schuchman with an adeno-associated viral vector as taught by Jooss and Chirmule with a reasonable expectation of success. Jooss and Chirmule teach that use of adeno-associated vectors are able to deliver long-term transgene expression without inducing an immune response and without the inflammatory responses which are negative consequences of the use of adenoviral vectors. Thus, one having ordinary skill in the arts would have been motivated to use the adeno-associated viral vector as taught by Jooss and Chirmule to deliver the polypeptide encoding a ceramidase as taught by Schuchman as a skilled artisan would have recognized that use of an adeno-associated viral vector would lead to stable expression of the ceramidase while avoiding the negative immune and inflammatory responses associated with adenoviral vector use.
With regard to claim 43, Schuchman teaches an acid ceramidase protein which is the product of the Ashah1 gene (Para. [0023], lines 1-2 and 21), which is considered to reasonably read on a polynucleotide encoding ASAH1.
With regard to claim 47, Schuchman teaches wherein the ceramidase treatment is administered by aerosol inhalation (Para. [0048}, line 3).
With regard to claim 48, Schuchman teaches wherein the ceramidase composition can be administered vis intratracheal inoculation (Para. [0047], line 5).
Claim 44 is rejected under 35 U.S.C. 103 as being unpatentable over Schuchman, Brittain, and Jooss and Chirmule as applied to claim 39 above, and further in view of Medin (as above in claim 34).
With regard to claim 44, as detailed above, the combined teachings of Schuchman, Brittain, and Jooss and Chirmule teach use of a ceramidase which is the product of the Asah1 gene (Para. Para. [0023], lines 1-2 and 21), i.e., an ASAH1 ceramidase, for the treatment of damage to lung tissue in subjects having pulmonary arterial hypertension. Schuchman also teaches that the ceramidase may be used to treat Farber disease (Para. [0043]).
The combined teachings of Schuchman, Brittain, and Jooss and Chirmule do not teach wherein the ASAH1 comprises an amino acid sequence which is encoded by SEQ ID NO: 1.
Medin teaches a viral vector which expresses an ASAH1 ceramidase wherein the transgene encoding the ASAH1 comprises SEQ ID NO:8 (Claims 1, 10, and 11) and which can be used to treat Farber disease. SEQ ID NO: 8 as taught by Medin shares 100% homology to instantly claimed SEQ ID NO: 1 (see SEQ ID NO: 1 rni file, result 1, duplicate 1).
Therefore, it would have been obvious to one having ordinary skill in the art, before the effective filing date of the claimed invention, to use the nucleotide sequence encoding ASAH1 having SEQ ID NO: 8, which shares 100% homology with instantly claimed SEQ ID NO:1, as taught by Medin as the sequence encoding ceramidase which is the product of the Asah1 gene as taught by Schuchman with a reasonable expectation of success. While Schuchman teaches use of an ASAH1 polypeptide, Schuchman is silent to the specific nucleic acid sequence which encodes the ASAH1 polypeptide. Since Schuchman teaches their ceramidase could be used to treat Farber disease (Para. 0043]) and Medin teaches a ceramidase having SEQ ID NO: 8 which can be used to treat Farber disease (Col. 10, lines 24-28 and 38-40), a skilled artisan would have been motivated to use SEQ ID NO: 8 as taught by Medin to encode the ASAH1 polypeptide as taught by Schuchman. Furthermore, the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
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.
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Claims 29-30, 33-34, 37-40, 43-44, and 47-48 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2, 5-6, and 9-10 of U.S. Patent No. 11,618,893 B2 (found in IDS dated 11/03/2025). Although the claims at issue are not identical, they are not patentably distinct from each other because instant claims 29-30, 33-34, 37-40, 43-44, and 47-48 are generic to claims 1-10 of U.S. Patent No. 11,618,893 B2. Therefore, claims 1-2, 5-6, and 9-10 of U.S. Patent No. 11,618,893 B2 anticipate and fall entirely within the scope of instant claims 29-30, 33-34, 37-40, 43-44, and 47-48.
Instant claim 29 is drawn to a method of treating damage to pulmonary tissue comprising selecting a selecting a subject having pulmonary tissue damage resulting from pulmonary arterial hypertension and administering to the subject a therapeutic amount of “an viral vector” comprising a polynucleotide encoding a ceramidase and instant claim 37, which depends from claim 29, further limits the viral vector as an adeno-associated viral vector. Similarly, instant claim 39 is drawn to method of treating damage to pulmonary tissue comprising selecting a subject having pulmonary tissue damage resulting from pulmonary arterial hypertension and administering to the subject a therapeutic amount of an adeno-associated viral vector comprising a polynucleotide encoding a ceramidase. Claim 1 of U.S. Patent No. 11,618,893 B2 is drawn to a method of treating damage to pulmonary tissue comprising selecting a subject having pulmonary tissue damage resulting from pulmonary arterial hypertension and administering to the subject a therapeutic amount of an Anc80 viral vector comprising a polynucleotide encoding a ceramidase. As the Anc80 viral vector of U.S. Patent No. 11,618,893 B2 is a species of the viral vector and adeno-associated viral vector as instantly claimed in claims 29, 37, and 39; instant claims 29, 37, and 39 are anticipated by claim 1 of U.S. Patent No. 11,618,893 B2 and therefore not patentably distinct.
Instant claim 30, which depends from the method of instant claim 29 as detailed above, and instant claim 40, which depends from the method of instant claim 39 as detailed above, are drawn to the methods wherein the ceramidase is an acid ceramidase and wherein said ceramidase is an ASAH1, an ASAH2, an ASAH2B, an ASAH2C, an ACER1, an ACER2, or an ACER3. Claims 2 and 5 of U.S. Patent No. 11,618,893 B2 are drawn to the method of reference claim 1 as detailed above wherein the ceramidase is an acid ceramidase and wherein said ceramidase is an ASAH1, an ASAH2, an ASAH2B, an ASAH2C, an ACER1, an ACER2, or an ACER3. Thus instant claims 30 and 40 are not patentably distinct from claims 2 and 5 of U.S. Patent No. 11,618,893 B2.
Instant claim 34, which depends from the method of instant claim 29 as detailed above, and instant claim 44, which depends from the method of instant claim 39 as detailed above, are drawn to the methods wherein the polynucleotide encodes an ASAH1 and the ASAH1 comprises an amino acid sequence encoded for by SEQ ID NO: 1. Claim 6 of U.S. Patent No. 11,618,893 B2 are drawn to the method of reference claim 1 as detailed above wherein the polynucleotide encodes an ASAH1 and the ASAH1 comprises an amino acid sequence encoded for by the nucleotide sequence of SEQ ID NO: 1. Instant SEQ ID NO: 1 shares 100% homology to SEQ ID NO: 1 of U.S. Patent No. 11,618,893 B2 (see Result 1 of SEQ ID NO: 1 .rni file, search results dated 11/03/2025). Thus, instant claims 34 and 44 are not patentably distinct from claim 6 of U.S. Patent No. 11,618,893 B2.
Instant claim 38, which depends from the method of instant claim 29 as detailed above, and instant claim 48, which depends from the method of instant claim 39 as detailed above, are drawn to the methods wherein administering is intra-tracheal. Claim 10 of U.S. Patent No. 11,618,893 B2 which depends from reference claim 1 as detailed above, is drawn to the method wherein administering is intra-tracheal. Thus, instant claims 38 and 48 are not patentably distinct from claim 10 of U.S. Patent No. 11,618,893 B2.
Instant claim 47, which depends from the method of instant claim 39 detailed above, is drawn to the method wherein the viral vector is aerosolized. Claim 9 of U.S. Patent No. 11,618,893 B2 which depends from reference claim 1 as detailed above, is drawn to the method wherein the Anc80 is aerosolized. As the Anc80 viral vector of U.S. Patent No. 11,618,893 B2 is a species of the adeno-associated viral vector as instantly claimed in claim 39, instant claim 47 is not patentably distinct from claim 9 of U.S. Patent No. 11,618,893 B2.
Conclusion
No claims are allowed.
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/ERIN V PAULUS/Examiner, Art Unit 1631
/ARTHUR S LEONARD/Examiner, Art Unit 1631