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 .
The Applicants’ Amendment to the Claims filed on April 13, 2026 is entered.
The Applicants’ Amendment to the Specification filed on April 13, 2026 is entered.
Claims 1, 4, and 7-28 are pending.
Claims 4 and 9-28 are withdrawn.
Claims 1 and 7-8 are under examination.
Election/Restrictions
Applicant’s election without traverse of invention Group I (i.e., claims 1 and 7-8) in the reply filed on 12/01/2025 is as previously acknowledged.
Priority
This US18/029, 174 filed on 03/29/2023 which is a 371 of PCT/EP2021/076844 filed on 09/29/2021 which claims US priority benefit of US Provisional 63/085,77 filed on 09/30/2020. The Filing Receipt received on 10/11/2023 is controlling.
Response to Amendment
All objections and rejections made in the previous office action and not repeated in this office action are withdrawn in view of the Applicant’s submission filed on April 13, 2026.
Claim Rejections - 35 USC § 102 – updated for amendment
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 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.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claim interpretation: Claims are drawn to a method comprising the active method step of providing endothelial cells with a source of autophagy inhibiting amino acids, wherein said autophagy inhibiting amino acids are alanine (A), glutamine (Q), glycine (G), valine (V), leucine (L), isoleucine (I), proline (P) and arginine (R). The intended use “for reducing cytoskeleton reorganization” is not generally provided weight for purpose of applying prior art especially because this intended use language in the preamble is not further connected to active method step in the body of the claim.
Currently amended claims 1 and 7-8 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by WO 2008/100140 to Khan et al published August 21, 2008 (IDS). This is new grounds of rejection.
Regarding claim 1, WO 2008/100140 discloses (cf. Examples) that administration of LQGV, AQGV and LAGV after the induction of hemorrhagic shock in rats reduced TNF-alpha and IL-6 plasma levels, which is associated with reduced TNF-[alpha] and IL-6 mRNA transcript levels in the liver, indicating their therapeutic potential with beneficial effects on systemic inflammation, thereby reducing organ integrity/function, which is associated with severe hemorrhagic shock; also salts of the said peptides such as salts of maleic acid, tartaric acid and citric acid are disclosed (cf. [0028]). Rat models received a single bolus intravenous injection of 10 mg/kg LQGV, AQGV, or LAGV. (See para 0068). The bolus injection meets the limitation of providing to the endothelial layer of a blood vessel. Such treatment reduced pro-inflammatory cytokine plasma levels (para 0076).
Regarding claim 7, Khan et al administer the peptides LQGV, AQGV, or LAGV.
Regarding claim 8, the peptides LQGV, AQGV, or LAGV meet the limitation of 100% amino acids being ala (A), glutamine (Q), glycine (G), valine (V), or leucine (L).
Claims 1 and 7-8 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by US 2008/171094 to Benner et al (published July 17, 2008).
Regarding claims 1 and 7-8 Benner et al describes providing cells by intravenous injection a source of autophagy inhibiting amino acids, specifically the peptides: LAGV, AQGV, VLPALPQ or LQGV. (See para 0072-73, 0093-0097; Examples, Figs. 7-11.) Benner et al show providing these peptides had beneficial activity on the imiquimod induced skin lesions in mice, an animal model for burn patients; also salts of the said peptides such as salts of maleic acid, tartaric acid and citric acid are disclosed (see para 0070). Benner et al disclose that severe stress induces endothelial cell adhesion molecules on the surface of endothelial cell. Benner et al discloses administering hCG-related peptides LAGV for treating hemorrhagic shock and showed reduced inflammatory response (para 108-109). Intravenous administration meets the limitation of providing endothelial cells with the therapeutic peptides.
Regarding amended claims 7, Benner et al discloses the source is a peptide (see Examples, Figs. 7-11).
Regarding amended claim 8, Benner et al disclose the peptide sources LAGV, AQGV, VLPALPQ or LQGV which consist solely of amino acids selected from the group of alanine (A), glutamine (Q), glycine (G), valine (V), leucine (L), isoleucine (I), proline (P) and arginine (R).
Thus, Benner et al anticipates claims 1 and 7-8 as presently written.
Response to Arguments regarding the rejections under 35 U.S.C. 102(a)(1)
The applicants’ arguments filed on April 13, 2026 have been fully considered but are unpersuasive. The applicants argue that claim 1 has been restricted to a method for "reducing cytoskeleton reorganization." Further, the applicants argue that the “remaining claims are dependent on claim 1, and thus contain all of the limitations of claim 1”. In addition, the applicants argue that Brenner does not disclose “in any way reduction of cytoskeleton reorganization”. Thus, the applicants argue that Brenner does not disclose all of the limitations of claim 1 and claims dependent therefrom.
However, this argument is unpersuasive because the limitation “for reducing cytoskeleton reorganization” is intended use which is recited only in the claim preamble and thus is not generally afforded patentable weight for purpose of applying prior art as explained in the body of the rejections just above.
Double Patenting – updated for amendment
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.
Currently amended claims 1, and 7-8 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 9, and 19-26 of copending Application No. 17/995,692 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because instant claims are anticipated by the copending claims. This is new grounds of rejection.
Regarding instant claim 1, copending claim 9 recites a method comprising providing to the endothelial layer of a blood vessel of the subject a pharmaceutically acceptable solution comprising a peptide consisting of ref SEQ ID NO: 3 or ref SEQ ID NO:3. Reference SEQ ID NO:2 is the peptide AQGV (Ala Gln Gly Val). Reference SEQ ID NO: 3 is the peptide LQGV (Leu Gln Gly Val).
Regarding instant claim 7, copending claim 9 recites that the source of the amino acids is a peptide consisting of reference SEQ ID NO:2 and SEQ ID NO:3.
Regarding instant claim 8, copending claim 9 recites that the source of the amino acids is a peptide consisting of reference SEQ ID NO:2 and SEQ ID NO:3. Reference SEQ ID NO:2 is the peptide AQGV (Ala Gln Gly Val) and reference SEQ ID NO: 3 is the peptide LQGV (Leu Gln Gly Val). Each of the reference peptides meets the limitation of instant claims of having an amino acid sequence comprising 100% amino acids being ala (A), glutamine (Q), glycine (G), valine (V), or leucine (L).
The intended use “for reducing cytoskeleton reorganization” is not generally provided weight for purpose of applying prior art especially because this intended use language in the preamble is not further connected to active method step in the body of the claim. Thus, instant claims 1, and 7-8 are anticipated by reference claims.
Currently amended claims 1, and 7-8 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 61-63 of copending Application No. 17/639,018 (reference application) in view of US 2008/171094 to Benner et al (published July 17, 2008). This is new grounds of rejection.
Although the claims at issue are not identical, they are not patentably distinct from each other because instant claims are rendered obvious over the combination of copending claims 61 and 63 in view of Benner et al.
Regarding instant claims 1, and 7-8, copending claim 62 recites a method of reducing autophagy in a subject by administering the pharmaceutical formulation of copending claim 58 to the subject. Copending claim 63 recites a method of modifying vascular permeability in a subject by administering the pharmaceutical of claim 58. Claim 61 depends from claim 58 and recites the preferred embodiment of a peptide source of LQGV which has 100% autophagy inhibiting amino acids.
Co-pending claims differ from presently amended claims because while they recite administering the peptide source of LQGV which has 100% autophagy inhibiting amino acids to a subject for reducing autophagy in the subject and for modifying vascular permeability in a subject, they do not explicitly recite providing endothelial cells with such peptide source.
Benner et al describes providing cells by intravenous injection a source of autophagy inhibiting amino acids, specifically the peptides: LAGV, AQGV, VLPALPQ or LQGV. (See para 0072-73, 0093-0097; Examples, Figs. 7-11.) Benner et al show providing these peptides had beneficial activity on the imiquimod induced skin lesions in mice, an animal model for burn patients; also salts of the said peptides such as salts of maleic acid, tartaric acid and citric acid are disclosed (see para 0070). Benner et al disclose that severe stress induces endothelial cell adhesion molecules on the surface of endothelial cell. Benner et al discloses administering hCG-related peptides LAGV for treating hemorrhagic shock and showed reduced inflammatory response (para 108-109). Intravenous administration meets the limitation of providing endothelial cells with the therapeutic peptides. It would have been prima facie obvious to provide the therapeutic peptides of the copending claims by intravenous injection for providing the peptides to endothelial cells for the rationale that the claims are for reducing autophagy in a subject by administering the pharmaceutical formulation and for modifying vascular permeability in a subject;
Further it would have been prima facie obvious to use the pharmaceutical composition of copending claim 61 in the method of copending claim 63 because each of these claims depends from the same base claim 58.
Thus, the combination of copending claims 61-63 in view of Benner et al renders obvious instant claims 1 and 7-8.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Response to Arguments regarding Double Patenting
The applicants’ arguments filed on April 13, 2026 have been fully considered but are unpersuasive. The applicants argue that the “amended claims have been limited to a reduction of cytoskeletal reorganization of endothelial cells”. Further, the applicants argue that “[n]one of the current claims of co-pending US Application No. 17/639,018 read on reduction of cytoskeletal reorganization of endothelial cells, rendering the double patenting rejections moot”. However, this argument is unpersuasive because the limitation “for reducing cytoskeleton reorganization” is intended use which is recited only in the claim preamble and thus is not generally afforded patentable weight for purpose of applying prior art as explained in the body of the rejections just above.
Conclusion
No claim is allowed.
Related prior art which may be applied in a future office action if appropriate: Kahn et al (WO 2005/046569; May 26, 2005).
THIS ACTION IS MADE FINAL. 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 CATHERINE S HIBBERT whose telephone number is (571)270-3053. The examiner can normally be reached M-F 8:00-5:00.
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CATHERINE S. HIBBERT
Primary Examiner
Art Unit 1658
/CATHERINE S HIBBERT/ Primary Examiner, Art Unit 1658
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