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 .
Objections/Rejections Withdrawn
Rejections and/or objections not reiterated from previous Office Actions are hereby withdrawn. The following rejections and/or objections are either reiterated or newly applied, and constitute the complete set presently being applied to the instant application.
Response to Arguments
35 U.S.C. 103
Applicant's arguments filed 12/1/2025 regarding the claims rejected under 35 U.S.C. 103 have been fully considered but they are not persuasive.
Lisanti teaches administering caveolin-1 (cav-1) peptides to treat pulmonary hypertension, including peptides such as SEQ ID NO: 7 that comprise the instant SEQ ID NO: 2. Although Lisanti does not teach administering SEQ ID NO: 2, it would be obvious to do so in view of Williams, as cited in the previous Office Action.
Lisanti describes how cav-1 and cav-2 deficient mice have abnormalities in pulmonary structure and function as demonstrated by hypercellularity, interstitial fibrosis, thickening of the alveolar septa, and reduced exercise tolerance. Additionally, cav-1 deficient mice develop pulmonary hypertension and right ventricular hypertrophy ([0006]). Thus, Lisanti teaches that cav-1 has a biological connection to both lung damage (i.e., pulmonary fibrosis, as exemplified by the development of interstitial fibrosis and thickening of the alveolar septa) and pulmonary hypertension, which can be treated with cav-1-derived peptides ([0035]).
Williams further describes how the mechanisms underlying lung injury involves cell surface signaling interactions between uPA, uPAR, and cav-1 and, thus, compositions that modulate such interactions could be used in methods for inhibiting apoptosis of injured, diseased, or damaged tissues, for instance, in pulmonary fibrosis ([0001]). Peptides of the invention include, for example, SEQ ID NO: 2 ([0085]).
Thus, Lisanti teaches that loss of cav-1 is involved in the development of both pulmonary fibrosis and pulmonary hypertension, which can be treated with cav-1-derived peptides. Williams further teaches cav-1 peptides such as the instant SEQ ID NO: 2 that can be used to treat pulmonary fibrosis. Based on these teachings, one skilled in the art would be motivated to use the instant SEQ ID NO: 2 in a method of treating pulmonary hypertension because one would recognize that pulmonary hypertension and pulmonary fibrosis share a common underlying biological mechanism; consequently, it follows that since pulmonary fibrosis and pulmonary hypertension can both be treated with cav-1-derived peptides, SEQ ID NO: 2 could be used to treat pulmonary hypertension in addition to pulmonary fibrosis.
Thus, motivation to combine is disclosed and the rejection has been modified herein.
Double patenting
Applicant’s arguments with respect to the rejection(s) of claim(s) under double patenting have been fully considered and are persuasive. Therefore, the rejection has been withdrawn. However, upon further consideration, a new ground(s) of rejection is made in view of the amended claims.
Election/Restrictions
Applicant’s election without traverse of the species SEQ ID NO: 2 in the reply filed on 12/1/2025 is acknowledged.
Claims Status
Claims 83-104 are pending under examination. Claims 85 and 87 were previously withdrawn as non-elected species. Claims 1-82 were previously cancelled. Claims 83-88, 90, 92, 93, and 96 are currently amended. Claims 103 and 104 are new.
Priority
The present Application claims priority to PCT/US2021/028326, filed 4/21/2021, which claims priority to the provisional applications 63/041629, filed 6/19/2020, and 63/013392, filed 4/21/2020. The priority date of 4/21/2020 is acknowledged.
Information Disclosure Statement
The IDS’s submitted on 12/01/2025 and 01/23/2026 are being considered. Any strikethroughs are owed to lack of the document in the file wrapper (it is noted that there were at least two references uploaded that do not have a corresponding entry in either of the IDS’s from 12/1/2025 or 1/23/2026).
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.
Claim(s) 83-104 are rejected under 35 U.S.C. 103 as being unpatentable over Lisanti et al. (US 2009/0068258 A1, filed 8/14/2008, published 3/12/2009), as evidenced by Douschan et al. (Douschan P. Mild Elevation of Pulmonary Arterial Pressure as a Predictor of Mortality. Am J Respir Crit Care Med. 2018 Feb 15;197(4):509-516.), in view of Williams et al. (WO 2020055824, filed 9/10/2019, published 3/19/2020).
Lisanti teaches and claims methods for treating pulmonary hypertension and right ventricular hypertrophy involving administering to a patient an effective amount of a caveolin peptide coupled to a cell permeating compound such as a cell permeating peptide (Abstract, claim 1, [0008]). Lisanti teaches the caveolin peptide SEQ ID NO: 7, which consists of DGIWKASFTTFTVTKYWFYR and comprises the instant SEQ ID NO: 2 ([0021], [0023], [0029]; claims 12, 13, and 28).
Lisanti further teaches genetic loss of cav-1 in mice causes them to develop pulmonary hypertension and right ventricular hypertrophy as well as abnormalities in pulmonary structure and function demonstrated by hypercellularity, interstitial fibrosis and thickening of the alveolar septa (pulmonary fibrosis), and reduced exercise tolerance ([0006]).
Lisanti does not teach a method of treating pulmonary hypertension in a subject comprising administering an effective amount of a peptide 1) comprising SEQ ID NO: 2 with an N- and/or C-terminal modification or 2) consisting of the amino acid sequence of SEQ ID NO: 2.
Williams teaches compositions comprising caveolin-1 (Cav-1) peptides and methods of using the Cav-1 peptides for the treatment of lung infections or acute chronic lung injury, particularly lung fibrosis (Abstract). Williams teaches that, during lung injury, p53 expression increases, inducing plasminogen activator inhibitor-1 (PAI-1) while inhibiting expression of urokinase-type plasminogen activation (uPA) and its receptor (uPAR), resulting in apoptosis of lung epithelial cells (LECs). The mechanism of injury involves cell surface signaling interactions between uPA, uPAR, caveolin-1 (“Cav-1”) and β1-integrin ([0001]).
Williams further teaches that the addition of N- and/or C-terminal modifications such as a blocking modification can help reduce protein degradation of cav-1 peptides ([0059]).
Thus, regarding claims 83 and 84, Lisanti teaches that loss of cav-1 is involved in the development of both pulmonary fibrosis and pulmonary hypertension, which can be treated with cav-1-derived peptides. Williams teaches a method of treating pulmonary fibrosis comprising administering cav-1 peptides with N- and/or C-terminal modifications that improve their resistance to protein degradation. Based on these teachings, it would be prima facie obvious to modify SEQ ID NO: 7 taught by Lisanti by adding an N- and/or C-terminal modification in order to improve the peptide’s resistance to protein degradation. One skilled in the art would have a reasonable expectation of success as Lisanti established that cav-1-derived peptides could be used to treat both pulmonary fibrosis and pulmonary hypertension, and Williams established a way to improve the stability and longevity of cav-1 peptides through improving their resistance to degradation.
Additionally, Williams also teaches the instant SEQ ID NO: 2 can be used to treat pulmonary fibrosis. Therefore, it also would be obvious to use SEQ ID NO: 2 of Williams in the method of treating pulmonary hypertension taught by Lisanti. One skilled in the art would be motivated to do so because one would recognize that pulmonary hypertension and pulmonary fibrosis share a common underlying biological mechanism; since pulmonary fibrosis and pulmonary hypertension can both be treated with cav-1-derived peptides, it follows that SEQ ID NO: 2 can also be used to treat pulmonary hypertension. One would have a reasonable expectation of success as Lisanti established cav-1 peptides can be used to treat both disorders and Williams established that SEQ ID NO: 2 itself could treat pulmonary fibrosis.
Regarding claim 86, as stated above, Williams teaches the instant SEQ ID NO: 2.
Regarding claims 88-92, as stated above, Williams teaches that modifications to cav-1 peptides can be made to amino acids on the N-terminus, C-terminus, or internally. N-terminal modifications may be, for example, but not limited to acylation or acetylation, and C-terminal modifications can include amidation ([0087]). In certain embodiments, the peptide may comprise a N-terminal modification or a C-terminal modification or both a N- and C-terminal modification ([0006; 0059]).
Regarding claims 93, Lisanti teaches coupling molecules to a 16 amino acid peptide corresponding to the homeodomain of the Drosophila transcription factor antennapedia (AP or penetrin – internalization sequence) has been shown to facilitate their uptake into cultured mammalian cells through a non-endocytic and non-degradative pathway ([0007]). Further, coupling of the Cav-1 scaffolding domain to the AP peptide (AP-Cav or Cavtratin) was shown to facilitate its translocation across the cell membranes and to reduce inflammation, microvascular hyper-permeability and tumor progression in mice (also internalization sequence, see [0007]).
Regarding claims 94 and 95, Lisanti also indicates that a cell permeating compound coupled to a caveolin peptide includes a cell permeating compound coupled to a caveolin peptide directly or via a linker as well as synthesized sequences of a cell permeating compound and a caveolin peptide. The order of the sequence or coupling can be either first cell permeating compound (CPC) then caveolin peptide (Cav) or first caveolin peptide then cell permeating compound, i.e. either CPC-Cav or Cav-CPC ([0020]).
Regarding claim 96, Lisanti teaches that preferably the cell permeating compound is a cell permeating peptide. Preferably, the cell permeating peptide is one or more of GRKKRRQRRRPPQ (SEQ ID NO: 6 of Lisanti) or RQIKIWFQNRRMKWKK (SEQ ID NO: 2 of Lisanti). Williams further teaches that Cav-1 peptides may further comprise a cell-binding domain or cell penetrating peptide (CPP). One such CPP taught is SEQ ID NO: 25 of Williams, which consists of GIGAVLKVLTTGLPALISWIKRKRQQ ([0007], [0168]).
Regarding claims 97 and 98, Lisanti teaches that pulmonary hypertension includes 1) primary pulmonary hypertension, which is inherited or occurs for unknown reasons, and 2) secondary pulmonary hypertension, which occurs because of another condition such as heart attack, collagen vascular disease, congenital systemic to pulmonary shunts, portal hypertension, HIV infection, PH of the newborn, and intake of drugs or toxin (anorexigens; [0004]). The instant specification teaches that Group 1 pulmonary hypertension is associated with the narrowing of the small blood vessels in the lungs, i.e. pulmonary arterial hypertension and includes cases where the underlying cause of the narrowing is not known; familial or heritable pulmonary hypertension; pulmonary arterial hypertension caused by certain drugs or toxins; and pulmonary arterial hypertension associated with other conditions such as connective tissue disease like scleroderma or lupus, congenital heart problems, high blood pressure in the liver, HIV, certain infections like schistosomiasis, and sickle cell anemia ([0153]).
Regarding claim 99, Lisanti teaches that pulmonary hypertension includes primary pulmonary hypertension, which is inherited or occurs for unknown reasons. The instant specification also teaches that pulmonary arterial hypertension with no apparent cause is known as primary pulmonary hypertension ([0150]).
Regarding claim 100, Lisanti teaches a method of treatment of a subject with pulmonary hypertension. As evidenced by Douschan et al., mean pulmonary arterial (artery) pressure is typically defined as greater than or equal to 25 mm Hg. Thus, individuals being treated for pulmonary hypertension would necessarily have a mean pulmonary artery pressure greater than 19 mm Hg.
Regarding claims 101 and 102, Lisanti teaches that the cell permeating compound coupled to caveolin peptide can be administered systematically, for example, by intraperitoneal injection, intramuscular injection, subcutaneously injection or intravenous injection or by inhalation using, for example, and aerosol nebulizer (instillation; [0031]).
Regarding claim 103, as stated above, Lisanti teaches that peptides of the invention can be formulated as aerosol nebulizer.
Regarding claim 104, as stated above, Lisanti and Williams teach SEQ ID NO: 7, which comprises the instant SEQ ID NO: 2, and can possess an N- and/or C-terminal modification.
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 83, 84, 88-92, and 97-104 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3, 4, 8, 9, and 10-13 of U.S. Patent No. 12,497,431 B2 (US ‘431; formerly copending Application No. 18/460,215) in view of Lisanti et al. (US 2009/0068258 A1, filed 8/14/2008, published 3/12/2009). Although the claims at issue are not identical, they are not patentably distinct from each other because they contain overlapping subject matter.
Claim 1 of US ‘431 recites a peptide comprising an amino acid sequence KASFTTFTVTKGS (SEQ ID NO: 4), wherein SEQ ID NO: 4 reads on a peptide comprising the instant SEQ ID NO: 2. Dependent claims include additional species of SEQ ID NO: 4 (claims 3 and 4), N- and/or C-terminal modifications (claims 8 and 9), and pharmaceutical compositions and formulations thereof (claims 10-13).
US ‘431 does not teach using the aforementioned peptides in a method of treating pulmonary hypertension.
As described above, Lisanti also teaches treating pulmonary hypertension in a subject in need thereof, comprising administering a cav-1 peptide comprising SEQ ID NO: 2.
Therefore, it would be prima facie obvious to one of ordinary skill in the art to incorporate the teachings of Lisanti into US ‘431, thereby arriving at the instant invention. One skilled in the art would have a reasonable expectation of success as Lisanti teaches using cav-1 peptides comprising SEQ ID NO: 2 to treat pulmonary hypertension. Thus, the claims are obvious in view of US ‘431.
Claims 83, 84, 86, and 88-96 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 57-61 of copending Application No. 19/083,757 (‘757, reference application; claim set filed 6/24/2025) in view of Lisanti et al. (US 2009/0068258 A1, filed 8/14/2008, published 3/12/2009) and Williams et al. (WO 2020055824, filed 9/10/2019, published 3/19/2020). Although the claims at issue are not identical, they are not patentably distinct from each other because they contain overlapping subject matter.
Claim 57 recites a dry powder composition comprising particles, wherein the particles comprise a peptide comprising an amino acid sequence of FTTFTVT (SEQ ID NO: 2) or a pharmaceutically acceptable salt thereof, wherein the peptide does not comprise an amino acid sequence of KASFTTFTVTKGS (SEQ ID NO: 4), wherein the dry powder composition is formulated for use in a dry powder inhaler. SEQ ID NO: 2 of copending application No. ‘757 is identical to the instant SEQ ID NO: 2.
Dependent claims include species of the peptide (claims 58-60) and the peptide comprises a CPP (claim 61).
Copending Application No. ‘757 does not teach using the aforementioned peptides in a method of treating pulmonary hypertension.
As described above, Lisanti teaches that loss of cav-1 leads to the development of conditions such as pulmonary fibrosis and pulmonary hypertension; Lisanti also teaches treating pulmonary hypertension in a subject in need thereof, comprising administering a cav-1 peptide comprising SEQ ID NO: 2. Williams teaches modifying cav-1 peptides comprising SEQ ID NO: 2 through addition of an N- and or C-terminal modification to improve the peptide’s resistance to protein degradation.
Therefore, it would be prima facie obvious to one of ordinary skill in the art to incorporate the teachings of Lisanti and Williams into copending Application No. 757, thereby arriving at the instant invention. One skilled in the art would have a reasonable expectation of success as Lisanti teaches using cav-1 peptides to treat pulmonary hypertension and Williams teaches modification of cav-1 peptides through the addition of an N- and/or C-terminal modifications. Thus, the claims are obvious in view of copending Application No. 757.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 83, 84, and 86 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of U.S. Patent No. 12,280,088 B2 (‘088) in view of Lisanti et al. (US 2009/0068258 A1, filed 8/14/2008, published 3/12/2009). Although the claims at issue are not identical, they are not patentably distinct from each other because they contain overlapping subject matter.
Independent claim 1 of copending U.S. Patent No. ‘088 recites a dry powder composition comprising particles, wherein the particles comprise a peptide consisting of FTTFTVT (SEQ ID NO: 2) or a pharmaceutically acceptable salt thereof, wherein the particles have a median particle diameter of less than 5μm, wherein the dry powder composition does not comprise a pharmaceutically acceptable carrier or excipient; and wherein the dry powder composition is formulated for use in a dry powder inhaler. The claimed peptide SEQ ID NO: 2 of U.S. Patent No. ‘088 is identical to the instant SEQ ID NO: 2.
US ‘088 does not teach using the aforementioned peptides in a method of treating pulmonary hypertension.
As described above, Lisanti teaches that loss of cav-1 leads to the development of conditions such as pulmonary hypertension; Lisanti also teaches treating pulmonary hypertension in a subject in need thereof, comprising administering a cav-1 peptide comprising the above SEQ ID NO: 2.
Therefore, it would be prima facie obvious to one of ordinary skill in the art to incorporate the teachings of Lisanti into US ‘088, thereby arriving at the instant invention. One skilled in the art would have a reasonable expectation of success as Lisanti teaches using cav-1 peptides to treat pulmonary hypertension. Thus, the claims are obvious in view of US ‘088.
Claims 83, 84, 86, 88-92, and 104 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 28-32, 35-40, and 42-45 of copending Application No. 19/388,100 (‘100, reference application; claim set filed 1/26/2026) in view of Lisanti et al. (US 2009/0068258 A1, filed 8/14/2008, published 3/12/2009).
Claim 28 of copending Application No. ‘100 recites a recombinant caveolin-1 peptide comprising an amino acid sequence of FTTFTVT (SEQ ID NO: 2), wherein the recombinant caveolin-1 peptide increases viability of alveolar epithelial cells wherein the recombinant caveolin-1 peptide does not comprise the amino acid sequence of DGIWKASFTTFTVTKYWFYR of the caveolin-1 protein (SEQ ID NO: 1).
Dependent claims include additional species of SEQ ID NO: 2 (claims 29-32, 37-40), the caveolin-1 peptide comprises N- and/or C-terminal modifications (claims 35 and 36), a composition thereof (claims 42-45).
Copending Application No. ‘100 does not teach using the aforementioned peptides in a method of treating pulmonary hypertension.
As described above, Lisanti also teaches treating pulmonary hypertension in a subject in need thereof, comprising administering a cav-1 peptide comprising the above SEQ ID NO: 2.
Therefore, it would be prima facie obvious to one of ordinary skill in the art to incorporate the teachings of Lisanti into copending Application No. ‘100, thereby arriving at the instant invention. One skilled in the art would have a reasonable expectation of success as Lisanti teaches using such peptides to treat pulmonary hypertension. Thus, the claims are obvious in view of copending Application No. ‘100.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
No claim is allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Sara E Konopelski Snavely whose telephone number is (571)272-1841. The examiner can normally be reached Monday - Friday 9-6pm EST.
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/SARA E KONOPELSKI SNAVELY/Examiner, Art Unit 1658
/FRED H REYNOLDS/Primary Examiner, Art Unit 1658