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 .
THIS IS A SECOND NON-FINAL OFFICE ACTION.
Election/Restrictions, Earlier Claim Status, and Updated as to New Claims
Applicant's election with traverse of “the V1 peptide, disclosed as SEQ ID NO:13, with no additional structure” in the reply filed on 12/6/24 is acknowledged. The traversal is on the ground(s) that “the groups are closely related in subject matter and could be searched and examined simultaneously without placing a serious burden on the Examiner.” This is not found persuasive because while explicitly disclosed specific sequences for which there is data afford one type of examination, where there is a relatively broad genus claimed, such as in instant claim 1 where the transition “comprise” indicates any length of peptide or protein falling with ‘netrin 1 compound’ meaning to either or both sides of SEQ ID NO:1, and the variability of SEQ ID NO:1 is substantial given the alternatives and opportunities for some X positions to be absent (thus a sequence from 8 to 11 amino acids in length), the examination of all possible outcomes, including as to whether they would have the claimed therapeutic effect, places a serious and undue burden on the examiner.
The requirement is still deemed proper and is therefore made FINAL.
The applicant in the 12/6/24 Response to Species Election stated that “Claims 1-13 read on the elected species. This is not correct because the election clearly stated “no additional structure.” Claim 2 requires the additional structure of an attached ethylene oxide compound, so it not subject to examination based on the elected species.
Claim 2 is withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected species, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 12/6/24.
Claim status: claims 1 and 3-13 were under examination, and claim 2 has been withdrawn.
As to new claims 14-16, dependent claims 15 and 16, depending from claim 1, as best understood1 are directed to species other than the elected species, SEQ ID NO:13, which does not comprise a “cysteine at the fourth amino acid position” nor an ethylene oxide compound, as to claim 15, nor any D-amino acids as to claim 16, and claims 15 and 16 therefore are withdrawn as being directed to non-elected species.
Updated Claim Status (per 10/2/25 claims)
Claims 1-16 are pending, this including new claims 14-16.
Claim 2 is withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected species, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 12/6/24.
Claims 15 and 16 are withdrawn as being directed to non-elected species.
Claims 1 and 3-14 are pending and under examination.
Claims 1 and 3-14 are rejected.
Priority
The instant application, filed 11/29/2021 is a National Stage entry of PCT/US2020/034484 , International Filing Date: 05/26/2020
PCT/US2020/034484 Claims Priority from Provisional Application 62854870 , filed 05/30/2019.
Information Disclosure Statement
The Examiner has considered the reference(s) provided in the 10/2/25 Information Disclosure Statement, and provides a signed and dated copy of such herewith.
Claim Objections
Response to Arguments
Applicant’s arguments, see page 6, and claim amendments, filed 10/2/25, with respect to the objections to claims 6 and 9-12, have been fully considered and are persuasive. The objections to claims 6 and 9-12 have been withdrawn.
Claim Interpretation – updated as to amendments including new claims 14-16
The claims terms are given their broadest reasonable interpretation (“[T]he ordinary and customary meaning of a claim term is the meaning that the term would have to a person of ordinary skill in the art in question at the time of the invention, i.e., as of the effective filing date of the patent application.” Phillips v. AWH Corp., 75 USPQ2d 1321, 1326 (Fed. Cir. 2005) (en banc).) The broadest reasonable interpretation of the claims must also be consistent with the interpretation that those skilled in the art would reach.” MPEP 2111, with reference to In re Cortright, 49 USPQ2d 1464, 1468.
Claim 1 is directed to a method of treating, reducing, or inhibiting a hyperlipidemia condition in a subject, wherein the subject has been diagnosed with a hyperlipidemia condition, (added 10/2/25) which comprises administering to the subject one or more netrin 1 compound, wherein the one or more netrin 1 compound(s) comprise SEQ ID NO: 1 as follows: X1-X2-X3-C-X4-X5-X6-X7-T-X8-G (SEQ ID NO: 1), with each variable X1 through X8 having alternative amino acids set forth in the claim.
“A hyperlipidemia condition” is interpreted to “refer[s] to conditions resulting from or related to hyperlipidemia” and include “hyperlipidemia, hypercholesterolemia, obesity, fatty liver, fatty deposits in arteries, arterial macrophage infiltration, atherosclerotic lesions, monocyte migration, vascular smooth muscle cell migration, monocyte adhesion to endothelial cells, neointimal formation, and restenosis,” para 44.
The condition termed “atherosclerosis” is interpreted to be a hyperlipidemia condition at least based on the inclusion in the above listing of “fatty deposits in arteries” and “atherosclerotic lesions,” this further clearly supported by instant claim 7’s inclusion of “fat deposits in arteries and “atherosclerotic lesions”.
A “netrin 1 compound” is defined in the specification as follows:
[0045] As used herein, “netrin-1 compounds” refer to the full-length human netrin-1 protein (GI 148613884), proteins having at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 99% sequence identity to the full-length human netrin-1 protein, and netrin-1 peptides. Netrin-1 compounds may or may not exhibit the same or similar activity as the full-length human netrin-1 protein. Nevertheless, in some embodiments, a netrin-1 compound, e.g., a netrin-1 peptide, exhibits substantially similar activity as the full-length human netrin-1 protein. In some embodiments, a netrin-1 compound, e.g., a netrin-1 peptide, exhibits significantly better activity and/or a different biological activity as the full-length human netrin-1 protein.
[0046] As used herein, a “netrin-1 peptide” refers to a peptide or protein that comprises, consists essentially of, or consists of SEQ ID NO: 1 as follows:
TABLE-US-00002 X1-X2-X3-C-X4-X5-X6-X7-T-X8-G (SEQ ID NO: 1)
wherein
[0047] X1 is Ala, Asn, Cys, D-Cys, Ser, or Thr, preferably X1 is Cys, Ser, or Thr;
[0048] X2 is present or absent, and if present, X2 is Ala, Asp, Ile, Leu, Met, Phe, Pro, Trp, or Val, preferably X2 is Leu or Pro;
[0049] X3 is present or absent, and if present, X3 is Asn, Arg, Asp, Cys, Gln, Glu, Gly, Ser, Thr, or Tyr, preferably X3 is Asn or Asp;
[0050] X4 is Arg, His, or Lys, preferably X4 is Arg or Lys;
[0051] X5 is Arg, Asp, Glu, His, Lys, Phe, Trp, or Tyr, preferably X5 is Asn, Asp, or His;
[0052] X6 is Asn, Cys, Gln, Gly, Ser, Thr, Tyr, or Val, preferably X6 is Asn or Gly;
[0053] X7 is present or absent, and if present, X7 is Asn, Gly, His, Ile, Thr, or Val, preferably X7 is Val; and
[0054] X8 is present or absent, and if present, X8 is Ala, Asn, Ile, Leu, Met, Phe, Pro, Thr, Trp, or Val, preferably X8 is Ala; and
[0055] wherein X2, X3, or both X2 and X3 are present.
Please note that within the scope of a netrin 1 compound is a netrin 1 peptide, which can be any protein that comprises a sequence meeting the requirements of SEQ ID NO:1, and the latter can be as short as 8 amino acids, and as claim 1 is amended up to 61 amino acids in length.
Please also note that the preferably language has been removed by amendment of claims 10/2/25, and a length limitation also has been added.
MPEP 2103 states in part, “Language that suggests or makes optional but does not require steps to be performed or does not limit a claim to a particular structure does not limit the scope of a claim or claim limitation.” Further, MPEP 2111.04 states in part, “Claim scope is not limited by claim language that suggests or makes optional but does not require steps to be performed, or by claim language that does not limit a claim to a particular structure.”
Regarding new claim 14, an independent claim, the use of the language “wherein the one or more netrin-1 compound(s) is a peptide having an amino acid sequence that comprises” followed by a list of SEQ ID Numbers, interpreting “having” in light of the specification as an open transition, such as para 59 of the corresponding PGPUB No. 20220226434, see MPEP 2111.03 IV, is interpreted to mean that the genus of peptides encompassed in claim 14 can include peptides with additional amino acid residues, amino acid isomers, and/or amino acid analogs at the N-terminus, the C-terminus, or both of any of the listed sequences. The examiner notes that this contrasts with the claim 1 newly introduced “wherein the one or more netrin compound(s) is 8-61 amino acids long.” The one or more netrin compound(s) that are administered in claim 14 are not so bounded in length.
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.
Response to Arguments
Applicant’s arguments, see page 6, filed 10/2/25, and claim amendments, with respect to the rejection of Claims 1 and 4-13 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 have been fully considered and are persuasive. The rejection of claims 1 and 4-13 Claims 1 and 4-13 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 has been withdrawn.
Claim Rejections - 35 USC § 112 – Including rejection of newly added claim 14
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Response to Arguments
Applicant's arguments filed 10/2/25have been fully considered but they are not persuasive.
Although applicant amended claim 1 to narrow the size range of the netrin-1 compounds to 8 to 61 amino acids long, only a small number of compounds within such genus were evaluated, see Fig. 2. The examiner has found no data that support what is claimed for other compounds set forth in the specification on pages 28-29, nor data from what appears to be prophetic examples paras 124 to 153, other than preliminary data, para 131 and Figure 9.
Regarding claim 5, now constrained per claim 1 to a netrin-1 compound 8 to 61 amino acids long, is nonetheless directed to comprising an amino acid sequence that has at least 90% sequence identity to SEQ ID NO:9, this being 604 amino acids in length. There is insufficient direction as to what portion of this, limited to 8 to 61 amino acids long by claim 1, and having up to 10% modifications from that portion of SEQ ID NO:9, possesses the required properties to achieve the claimed method.
The examiner respectfully reminds the applicant that the number of variables in claim 1’s SEQ ID NO:1, results in a large and diverse number of species encompassed by the claim 1 genus that is administered for treating, inhibiting or reducing a hyperlipidemia condition.
Claims 1 and 3-14 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Regarding the requirement for adequate written description of chemical entities, Applicant's attention is directed to the MPEP §2163. In particular, Regents of the University of California v. Eli Lilly & Co., 119 F.3d 1559, 1568 (Fed. Cir. 1997), cert. denied, 523 U.S. 1089, 118 S. Ct. 1548 (1998), holds that an adequate written description requires a precise definition, such as by structure, formula, chemical name, or physical properties, "not a mere wish or plan for obtaining the claimed chemical invention." Eli Lilly, 119 F.3d at 1566.
Applicant is alerted that "a sufficient description of a genus ... requires the disclosure of either a representative number of species falling within the scope of the genus or structural features common to the members of the genus so that one of skill in the art can ‘visualize or recognize’ the members of the genus." AriadPharms., Inc. v. EliLilly & Co., 598 F.3d 1336, 1350 (Fed. Cir. 2010). A "generic claim may define the boundaries of a vast genus of chemical compounds, and yet the question may still remain whether the specification, including original claim language, demonstrates that the applicant has invented species sufficient to support a claim to a genus." Id. at 1349. “[M]erely drawing a fence around a perceived genus is not a description of the genus.” AbbVie Deutschland GmbH & Co., KG v. Janssen Biotech, Inc., 759 F.3d 1285, 1300 (Fed. Cir. 2014). “One needs to show that one has truly invented the genus, i.e., that one has conceived and described sufficient representative species encompassing the breadth of the genus.” Id. “Otherwise, one has only a research plan, leaving it to others to explore the unknown contours of the claimed genus.” Id.
In the instant case, the entire genus of claim 1’s one or more nectin-1 compound(s), although now limited to 8 to 61 amino acids in length, are not adequately represented by a representative number of species having been shown to possess the properties to achieve what is claimed in the claim 1 method. The number of variables in claim 1’s SEQ ID NO:1, results in a large and diverse number of species encompassed by the claim 1 genus that is administered for treating, inhibiting or reducing a hyperlipidemia condition. There is insufficient guidance, structure-function teachings, or other relevant disclosures as to what modifications, including as to the numerous combinations of variables at the positions of claim 1’s SEQ ID NO:1, are made within the structurally allowed limitations that result in achieving what is claimed in the claim 1 method, or in the dependent claims 9-12.
Additionally, as to claim 14’s one or more nectin-1 compound(s), which comprise an amino acid sequence that comprises any one of the claim 14-listed SEQ ID Numbers but can extend to the N- and/or C-terminus of any of these with any number and type of additional amino acids, are claimed to be administered to treat, reduce, or inhibit a hyperlipidemia condition, wherein the subject has been diagnosed with a hyperlipidemia condition, the latter as defined pertaining to a range of conditions.
Although applicant may consider that the listed SEQ ID Numbers provide a structural feature common to the members of the genus, 1) given the alternatives at multiple positions and resultant structural and physicochemical differences among these sequences, and 2) given the lack of evaluations of a range of species that would adequately represent the full scope of the genus, the examiner concludes that this is not the case, and the presence of the listed SEQ ID Numbers in the claimed genus does not present a genus such that one of skill in the art can 1) ‘visualize or recognize’ the members of the genus, and 2) understand that they all (or at least most of them) possess a structure that will result in achieving the claimed method when administered. Please also note that SEQ ID NO:9, listed in claim 14, is 604 amino acids long, and the administered claimed peptide genus encompasses this peptide (per the specification this term includes proteins) with additional amino acids at one or both of its N- and C- termini. These are reasonably expected to perform differently from a short peptide such as of 9 to 11 amino acids in length, or other short peptides, at least based on ability to penetrate cell membranes, effects of proteases, and passage through the kidneys, yet there are no evaluations of this subgenus of the claimed genus nor of other longer peptides encompassed by claim 14.
As to what is provided in the application as filed, the specification and figures provide very limited data on several nectin-1 peptides, nectin-1 and a combination of V1 and V2 peptides; these are NOT representative of the genus of claim 1 nor of claim 14. See all figures and pages 32-35. “Expected results” and/or apparently prophetic descriptions/examples are provided from page 35 through page 40, this section ending with the statement, “Taken together, these data would indicate that amplification of netrin-1 signaling, by either increasing endogenous expression of netrin-1 or administration of exogenous netrin-1 compounds, is important for vascular protection.” This is not the cornerstone of demonstration of possession, especially for a diverse genus that is claimed to be administered.
The description requirement of the patent statute requires a description of an invention, not an indication of a result that one might achieve if one made that invention. See In re Wilder, 736, F.2d 1516, 1521, 222 USPQ 369, 372-73 (Fed. Cir. 1984) (affirming rejection because the specification does "little more than outlin[e] goals appellants hope the claimed invention achieves and the problems the invention will hopefully ameliorate.") Accordingly, even considering the knowledge in the art at the time of filing, based on the disclosures and data in the application as filed, and the diverse genus, it is deemed that the specification fails to provide adequate written description for the genus of claim 1, nor of the broader claim 14 genus, nor of claims depending from claim 1, and does not reasonably convey to one skilled in the relevant art that the inventor(s), at the time the application was filed, had possession of the entire scope of the claimed invention.
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.
Response to Arguments
Applicant's arguments filed 10/2/25 have been fully considered but they are not persuasive.
On page 9 applicant argues that “Nothing in Cai teaches or suggests that netrin-1 compounds may be successfully used for treating hyperlipidemia.” Applicant is not claiming only treating hyperlipidemia. What is claimed is treating, reducing or inhibiting a hyperlipidemia condition, which includes atherosclerosis, see Claim Interpretation above. Cai clearly teaches administering its peptides to treat atherosclerosis, see inter alia para 145 which begins, “Embodiment 19. A method of treating, inhibiting, or reducing vascular diseases involving vascular injury such as atherosclerosis …”, see also Cai para 147. Applicant’s argument and assertion is clearly unpersuasive given what applicant claims and defines, and what Cai explicitly teaches.
Any assertions in the Remarks pertaining to alleged deficiencies of Fostermann and/or Stansbury are moot in that these references are no longer applied to the rejections.
Arguments against the rejection of claim 13 based on references other than CUMC are addressed above or moot. CUMC is applied for the indicated teachings regarding when the hyperlipidemia condition “is the result of a high-fat diet”, not on any particular drug taught to be administered. Also, the examiner reiterates that what is claimed to be treated, reduced or inhibited is a hyperlipidemia condition, see Claim Interpretation, not only hyperlipidemia as applicant in the Remarks repeatedly asserts.
Claims 1, 3-8 and 14 are rejected under 35 U.S.C. 103 as being unpatentable over US 2017/0210780, inventors Cai and Li, published 7/27/17 (“Cai”), in view of Insull, The American Journal of Medicine (2009) 122, S3–S14 (“Insull”).
Claim 1 is directed to a method of treating, reducing, or inhibiting a hyperlipidemia condition in a subject, wherein the subject has been diagnosed with a hyperlipidemia condition, which comprises administering to the subject one or more netrin 1 compound, wherein the one or more netrin 1 compound comprise, consist essentially of, or consist of SEQ ID NO: 1 as follows: X1-X2-X3-C-X4-X5-X6-X7-T-X8-G (SEQ ID NO: 1), with each variable X1 through X8 having alternative amino acids set forth in the claim, the compounds limited to lengths of 8 to 61 amino acids.
The elected species is SEQ ID NO:13, which is 54 amino acids in length, is identical with positions 285 through 338 of Netrin-1 protein, and comprises the instant claim 1 SEQ ID NO:1 sequence as a portion of it as follows:
CKCNGHAARCVRDRDDSLVCDCRHNTAGPECDRCKPFHYDRPWQRATAREANEC, the underlined SEQ ID NO:1 portion applying when X1=C, X2 is absent, X3=D, X4=R, X5=H, X6=N, X7 is absent, and X8=A. (Please note that the italicized C, T and G are found in instant SEQ ID NO:1 as fixed, not as variables.)
Cai teaches “A method of treating, inhibiting, or reducing vascular diseases involving vascular injury such as atherosclerosis and hypertension which comprises contacting blood vessels with one or more peptides according to Embodiments 1-5 or the composition according to Embodiment 7 or Embodiment 8 systematically or locally; attenuating vascular smooth muscle cell migration and proliferation with one or more peptides according to Embodiments 1-5 or the composition according to Embodiment 7 or Embodiment 8 via DCC-dependent signaling; or both,” para 145, see also para 147.
Cai specifically identifies among its embodiments a peptide corresponding to its SEQ ID NO:1, which is identical to instant SEQ ID NO:13:
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850
810
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,
see paras 8, 9, and claims 1 and 8.
With regard to the subsequence CDCRHNTAG within instant SEQ ID NO:13 and falling with the scope of SEQ ID NO:1 of instant claim 1 as its V1-9aa, its SEQ ID NO:4 this shown from bottom right of Cai page 10, below para 100, which also shows its SEQ ID NO:1 (~ instant SEQ ID NO:13) as its V1:
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271
284
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.
Because Cai teaches that its peptides treat atherosclerosis, a hyperlipidemia condition, Cai teaches administering its SEQ ID NO:1, the same as instant elected SEQ ID NO:13, to treat a hyperlipidemia condition.
Cai does not explicitly teach the newly added limitation of claim 1, wherein the subject has been diagnosed with a hyperlipidemia condition.
Insull clearly teaches the advantages of diagnosing atherosclerosis, particularly at earlier reversible stages, and then treating the atherosclerosis (excerpts below with examiner-added emphases):
From page S3:
The clinical practitioner’s goal for atherosclerosis is to treat it effectively. The purpose of this article is to introduce the pathology of atherosclerotic lesions to provide a rational basis for their clinical management. For each human individual, the natural history of the pathology of arterial lesion development lasts >40 years.1,2 Treatments such as diet modification, exercise, and drugs that affect plasma lipids and hypertension may induce changes in the clinical manifestations and in the natural pathology of plaques and arteries.
From page S4:
The continuous development of atherosclerosis usually is described in 2 ways that are different but complementary: (1) as an extended series of histologic processes and changes, and (2) as a shorter series of different classes of lesions that are grossly visible to the unaided eye. Together, these approaches enhance our understanding of atherosclerosis. Both are clinically useful when combined with clinical imaging of plaques for diagnosing each individual patient’s stage of atherosclerosis and risks, and for selecting appropriate therapy.
From page S5:
Upon entry, monocytes transform into macrophages, take up lipids as multiple small inclusions, and become foam cells. The degree of lipid accumulation is critical for early-stage diagnosis of atherosclerosis. Isolated foam cells, multiple layers of foam cells, and isolated extracellular pools of lipid are not considered atherosclerosis. These early changes are microscopic and may progress to gross visibility. These lipid changes can be reversed. Atherosclerosis is believed to start when the lipid accumulation appears as confluent extracellular lipid pools and extracellular lipid cores with decreased cellularity.
From S8 to S9:
Hypothetical sequences of plaque development can be reasonably proposed because pathology studies now have outlined the complete sequence of development of major plaques from pathologic intimal thickening to fatty streaks, through fibrous cap atheromas, to plaques associated with sudden cardiac death.2,12,20 The hypothetical developmental sequences in Figure 3 are based on identification of precursor plaques for the 4 classes of sudden death by the logical criterion that they possess closely similar histopathologies.12 For the clinical practitioner who is managing the individual patient, this sequence can serve as a useful guide to the choice of plaque imaging method, the plaque diagnosis, the plaque prognosis, and the choice of therapy.
Based upon the above teachings of Insull, which clearly identify diagnosing atherosclerosis in a human individual subject as an important step, to be followed by treatment of such subject, one of ordinary skill in the art would very reasonably understand that before administering to a subject a therapeutic peptide such as one of those particularly taught by Cai to be useful for treating atherosclerosis, see above, such subject reasonably would have been diagnosed with atherosclerosis, this clearly, per Claim Interpretation and also as made clear in Insull, being a hyperlipidemia condition (e.g., from S4, “Atherosclerosis develops progressively through continuous evolution of arterial wall lesions centered on the accumulation of cholesterol-rich lipids and the accompanying inflammatory response.”). Stated another way, it is reasonable that one of ordinary skill in the art would diagnose a subject as having atherosclerosis before administering a treatment, such as that of Cai, to treat such hyperlipidemia condition.
Considering the teachings and data in Cai in view of Insull, one of ordinary skill in the art would have understood at the time of the instant application filing that the elected SEQ ID NO:13 peptide would reasonably treat a subject who had been diagnosed with atherosclerosis, a hyperlipidemia condition, to reduce or inhibit atherosclerosis by such action (as noted, and noting again, atherosclerosis being a hyperlipidemia condition, see Claim Interpretation above). The rationale is simply to apply a known therapeutic peptide to a role in therapy that it could reasonably achieve based on prior art teachings. There would have been a reasonable expectation of success based on such teachings.
Accordingly, claim 1, as well as claim 3, specifically reciting SEQ ID NO:13, claim 4, SEQ ID NO:13 within the 8-60 range, claim 5, SEQ ID NO:13 having 100 percent sequence identity with SEQ ID NO:9 between the latter sequence’s 285-338 positions, claim 6, in view of Cai also teaching administering pharmaceutical compositions comprising its V1 peptide, see para 10, claims 7 and 8, each of which includes “fat deposits in arteries” and “atherosclerotic lesions”, would have been obvious over Cai in view of Insull.
Claims 9-12 would have been obvious because administering the same compound to the same population - having atherosclerosis, a hyperlipidemia condition, would reasonably be expected to have the same result.
New claim 14 would have been obvious on the same bases as claim 1, claim 14 encompassing peptides also in the genus of claim 1, and specifically including SEQ ID NO:13.
Claim 13 is rejected under 35 U.S.C. 103 as being unpatentable over US 2017/0210780, inventors Cai and Li, published 7/27/17 (“Cai”), in view of Insull, The American Journal of Medicine (2009) 122, S3–S14 (“Insull”), as applied to claim 1, and further in view of CUMC article “New Link Between High-Fat Diet and Atherosclerosis Identified”, downloaded from the Internet 6/3/25, dated 10/8/12, 4 pages (CUMC, previously provided).
The rejection of claim 1 is set forth above.
Although Cai teaches administering its SEQ ID NO:1 netrin-1 peptide equivalent to instant SEQ ID NO:13 to treat atherosclerosis, a hyperlipidemia condition, Cai does not explicitly address the effect of its netrin-1 peptides, including that corresponding to instant SEQ ID NO:13, on when the hyperlipidemia condition “is the result of a high-fat diet” (this pertaining to the cause of the hyperlipidemia condition).
The level of skill in the art is high.
Claim 13 states that the hyperlipidemia of claim 1 “is the result of a high-fat diet.” The specification states, “As used herein, a “high fat diet” refers to a diet in which at least about 40% of a subject's daily caloric intake are fat calories (i.e., calories from fat),” para 32.
CUMC clearly teaches that a diet high in saturated fat raises levels of endothelial lipase, an enzyme associated with the development of atherosclerosis, page 1. Based on this teaching, one of ordinary skill in the art would reasonably understand that the atherosclerosis of a population of subjects having atherosclerosis would reasonably include subjects whose atherosclerosis condition “is the result of a high-fat diet.” Given treating the subjects in the same population, Cai administering its SEQ ID NO:1 netrin-1 peptide, the same as instant SEQ ID NO:13 netrin-1 peptide, reasonably would include treating atherosclerosis when this hyperlipidemia condition was caused by a high-fat diet such as that taught in CUMC. Additionally, treating a subject with the same compound would have the same result for the same population, see MPEP 2112.01 II and 2112.02 II.
Accordingly, claim 13 is rejected as obvious.
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.
Response to Arguments
Applicant's arguments filed 10/2/25 have been fully considered but they are not persuasive.
Applicant, page 11, argues against the previously applied references in that they do not teach the newly added limitation. This is unpersuasive because a new reference, Insull, is added to the rejections below to address this new limitation. Please also note that the newly added limitation states, “wherein the subject has been diagnosed with a hyperlipidemia condition.”
Any assertions in the Remarks on pages 11-13 pertaining to alleged deficiencies of Fostermann and/or Stansbury are moot in that these references are no longer applied to the rejections.
Claims 1, 3-8 and 14-16 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4-6, 8, 10 of U.S. Patent No. 10550163 (Reference patent) in view of Insull, The American Journal of Medicine (2009) 122, S3–S14 (“Insull”).
Instant claim 1 is set forth above.
In Sun Pharmaceutical Industries Ltd. v. Eli Lilly and Co., 95 USPQ2d 1797 (Fed. Cir. 2010), the Court determined that claims of a later patent were held invalid for obviousness-type double patenting when the earlier patent claimed a compound and disclosed its utility in its specification, and later patent claimed a method of using the compound for a use described in the specification of the earlier patent.
Reference patent claims 1, 4-6, 8, 10 encompass instantly claimed peptides of claim 1, and include the instant elected sequence (as reference patent SEQ ID NO:1).
Reference patent teaches administering one or more of such peptides to treat atherosclerosis, see paras 145 and 147, and see also paras 8 and 9 as to specifically administering its SEQ ID NO:1.
Because reference patent teaches that its peptides treat atherosclerosis, a hyperlipidemia condition, reference patent teaches administering its SEQ ID NO:1, the same as instant elected SEQ ID NO:13, to treat a hyperlipidemia condition.
The reference patent does not explicitly teach the newly added limitation of claim 1, wherein the subject has been diagnosed with a hyperlipidemia condition.
Insull clearly teaches the advantages of diagnosing atherosclerosis, particularly at earlier reversible stages, and then treating the atherosclerosis (excerpts below with examiner-added emphases):
From page S3:
The clinical practitioner’s goal for atherosclerosis is to treat it effectively. The purpose of this article is to introduce the pathology of atherosclerotic lesions to provide a rational basis for their clinical management. For each human individual, the natural history of the pathology of arterial lesion development lasts >40 years.1,2 Treatments such as diet modification, exercise, and drugs that affect plasma lipids and hypertension may induce changes in the clinical manifestations and in the natural pathology of plaques and arteries.
From page S4:
The continuous development of atherosclerosis usually is described in 2 ways that are different but complementary: (1) as an extended series of histologic processes and changes, and (2) as a shorter series of different classes of lesions that are grossly visible to the unaided eye. Together, these approaches enhance our understanding of atherosclerosis. Both are clinically useful when combined with clinical imaging of plaques for diagnosing each individual patient’s stage of atherosclerosis and risks, and for selecting appropriate therapy.
From page S5:
Upon entry, monocytes transform into macrophages, take up lipids as multiple small inclusions, and become foam cells. The degree of lipid accumulation is critical for early-stage diagnosis of atherosclerosis. Isolated foam cells, multiple layers of foam cells, and isolated extracellular pools of lipid are not considered atherosclerosis. These early changes are microscopic and may progress to gross visibility. These lipid changes can be reversed. Atherosclerosis is believed to start when the lipid accumulation appears as confluent extracellular lipid pools and extracellular lipid cores with decreased cellularity.
From S8 to S9:
Hypothetical sequences of plaque development can be reasonably proposed because pathology studies now have outlined the complete sequence of development of major plaques from pathologic intimal thickening to fatty streaks, through fibrous cap atheromas, to plaques associated with sudden cardiac death.2,12,20 The hypothetical developmental sequences in Figure 3 are based on identification of precursor plaques for the 4 classes of sudden death by the logical criterion that they possess closely similar histopathologies.12 For the clinical practitioner who is managing the individual patient, this sequence can serve as a useful guide to the choice of plaque imaging method, the plaque diagnosis, the plaque prognosis, and the choice of therapy.
Based upon the above teachings of Insull, which clearly identify diagnosing atherosclerosis in a human individual subject as an important step, to be followed by treatment of such subject, one of ordinary skill in the art would very reasonably understand that before administering to a subject a therapeutic peptide such as one of those particularly taught by the reference patent to be useful for treating atherosclerosis, see above, such subject reasonably would have been diagnosed with atherosclerosis, this clearly, per Claim Interpretation and also as made clear in Insull, being a hyperlipidemia condition (e.g., from S4, “Atherosclerosis develops progressively through continuous evolution of arterial wall lesions centered on the accumulation of cholesterol-rich lipids and the accompanying inflammatory response.”). Stated another way, it is reasonable that one of ordinary skill in the art would diagnose a subject as having atherosclerosis before administering a treatment, such as that of the reference patent, to treat such hyperlipidemia condition.
Considering the teachings and composition claims of the reference patent, in view of Insull, one of ordinary skill in the art would have understood at the time of the instant application filing that the elected SEQ ID NO:13 peptide, as well as many other peptides encompassed by instant claim 1, would reasonably treat a subject who had been diagnosed with atherosclerosis, a hyperlipidemia condition, to reduce or inhibit atherosclerosis by such action (as noted, and noting again, atherosclerosis being a hyperlipidemia condition, see Claim Interpretation above). The rationale is simply to apply a known therapeutic peptide to a role in therapy that it could reasonably achieve based on prior art teachings. There would have been a reasonable expectation of success based on such teachings.
Accordingly, claim 1, as well as claim 3, specifically reciting SEQ ID NO:13, claim 4, SEQ ID NO:13 within the 8-60 range, claim 5, SEQ ID NO:13 having 100 percent sequence identity with SEQ ID NO:9 between the latter sequence’s 285-338 positions, claim 6, in view of reference patent also teaching administering pharmaceutical compositions comprising its V1 peptide, see para 10, claims 7 and 8, each of which includes “fat deposits in arteries” and “atherosclerotic lesions”, are rejected over the reference patent claims and teachings in view of Insull.
Claims 9-12 would have been obvious because administering the same compound to the same population - having atherosclerosis, a hyperlipidemia condition, would reasonably be expected to have the same result.
New claim 14 would have been obvious on the same bases as claim 1, claim 14 encompassing peptides also in the genus of claim 1, and specifically including SEQ ID NO:13.
In summary, given that the reference patent discloses the same utility in its specification encompassed by the instant claims, where the instant application claims a method of using the same compounds for the same use described in the specification of the earlier patent, to treat atherosclerosis, the indicated instant claims are properly rejected under this section.
Claim 13 is rejected on the ground of nonstatutory double patenting as being unpatentable over claim 11 of U.S. Patent No. 10550163 (Reference patent) in view of Insull, The American Journal of Medicine (2009) 122, S3–S14 (“Insull”), as applied to claim 1, and further in view of CUMC article “New Link Between High-Fat Diet and Atherosclerosis Identified”, downloaded from the Internet 6/3/25, dated 10/8/12, 4 pages (CUMC).
The rejection of claim 1 is set forth above.
Although reference patent claims and disclosure teach as well as suggest administering its peptides, including its SEQ ID NO:1 netrin-1 peptide, equivalent to instant SEQ ID NO:13, to treat atherosclerosis, a hyperlipidemia condition, it does not explicitly address the effect of its netrin-1 peptides when the hyperlipidemia condition (atherosclerosis) “is the result of a high-fat diet” (this pertaining to the cause of the hyperlipidemia condition).
The level of skill in the art is high.
Claim 13 states that the hyperlipidemia of claim 1 “is the result of a high-fat diet.” The specification states, “As used herein, a “high fat diet” refers to a diet in which at least about 40% of a subject's daily caloric intake are fat calories (i.e., calories from fat),” para 32.
CUMC clearly teaches that a diet high in saturated fat raises levels of endothelial lipase, an enzyme associated with the development of atherosclerosis, page 1. Based on this teaching, one of ordinary skill in the art would reasonably understand that the atherosclerosis of a population of subjects having atherosclerosis would reasonably include subjects whose atherosclerosis condition “is the result of a high-fat diet.” Given treating the subjects in the same population, the reference patent claimed peptides when used for treating atherosclerosis, reasonably would include treating atherosclerosis when this hyperlipidemia condition was caused by a high-fat diet such as that taught in CUMC. Additionally, treating a subject with the same compound would have the same result for the same population, see MPEP 2112.01 II and 2112.02 II.
Accordingly, claim 13 is rejected under this section.
Claims 1, 3-12 and 14 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3, 5-7, 22 and 23 of copending Application No. 17286857 (reference application), in view of Insull, The American Journal of Medicine (2009) 122, S3–S14 (“Insull”), as evidenced by Robbins et al., CHEST, vol. 136, no. 1, JULY, 2009, pp 31-36 (Robbins).
For compact prosecution, this rejection extends beyond the elected species.
Reference application claim 1 encompasses instant SEQ ID Numbers 5 and 6, which are identical to reference application SEQ ID Numbers 5 and 6, these found in reference application claims 3, 22 and 23.
Reference application claim 7 is directed to a method of treating, reducing or inhibiting pulmonary hypertension in a subject, comprising administering to the subject a therapeutically effective amount of one or more peptides according to claim 1, such peptides clearly including peptides encompassed by the instant claims 1 and 3-12 and 14.
Because as evidenced by Robbins, pages 31-32, patients diagnosed with Pulmonary venous hypertension (PVH) due to diastolic dysfunction (DD), a substantial subset of pulmonary hypertension (PH), nearly all had multiple features of metabolic syndrome (MS), the latter including ‘characteristics’ listed in Table 1 on page 33 and associated strongly with PVH, as well as another type of PH, PAH, these characteristics/diagnoses/conditions including obesity (based on BMI), hyperlipidemia, and coronary heart disease (associated with instant claim 9’s fat deposits in arteries) would reasonably be treated by administering the same compound to the same population or portion of the population that overlaps with the population treated by the instant claim methods. Because as evidenced by Robbins the conditions treated by the reference claim 7 and the instant claims treat co-morbidities, given that the same conditions, such as PVH or PAH and an instant claimed hyperlipidemia condition, can exist in the same person, the active step of each claim, of the reference application and the instant application, treats both respective conditions. On these bases instant claims 1 and 3-12 and 14 administer the same compounds as administered by the reference application that treat the same populations as the reference claims.
The reference patent application does not explicitly teach the newly added limitation of claim 1, wherein the subject has been diagnosed with a hyperlipidemia condition.
Insull clearly teaches the advantages of diagnosing atherosclerosis, particularly at earlier reversible stages, and then treating the atherosclerosis (excerpts below with examiner-added emphases):
From page S3:
The clinical practitioner’s goal for atherosclerosis is to treat it effectively. The purpose of this article is to introduce the pathology of atherosclerotic lesions to provide a rational basis for their clinical management. For each human individual, the natural history of the pathology of arterial lesion development lasts >40 years.1,2 Treatments such as diet modification, exercise, and drugs that affect plasma lipids and hypertension may induce changes in the clinical manifestations and in the natural pathology of plaques and arteries.
From page S4:
The continuous development of atherosclerosis usually is described in 2 ways that are different but complementary: (1) as an extended series of histologic processes and changes, and (2) as a shorter series of different classes of lesions that are grossly visible to the unaided eye. Together, these approaches enhance our understanding of atherosclerosis. Both are clinically useful when combined with clinical imaging of plaques for diagnosing each individual patient’s stage of atherosclerosis and risks, and for selecting appropriate therapy.
From page S5:
Upon entry, monocytes transform into macrophages, take up lipids as multiple small inclusions, and become foam cells. The degree of lipid accumulation is critical for early-stage diagnosis of atherosclerosis. Isolated foam cells, multiple layers of foam cells, and isolated extracellular pools of lipid are not considered atherosclerosis. These early changes are microscopic and may progress to gross visibility. These lipid changes can be reversed. Atherosclerosis is believed to start when the lipid accumulation appears as confluent extracellular lipid pools and extracellular lipid cores with decreased cellularity.
From S8 to S9:
Hypothetical sequences of plaque development can be reasonably proposed because pathology studies now have outlined the complete sequence of development of major plaques from pathologic intimal thickening to fatty streaks, through fibrous cap atheromas, to plaques associated with sudden cardiac death.2,12,20 The hypothetical developmental sequences in Figure 3 are based on identification of precursor plaques for the 4 classes of sudden death by the logical criterion that they possess closely similar histopathologies.12 For the clinical practitioner who is managing the individual patient, this sequence can serve as a useful guide to the choice of plaque imaging method, the plaque diagnosis, the plaque prognosis, and the choice of therapy.
Based upon the above teachings of Insull, which clearly identify diagnosing atherosclerosis in a human individual subject as an important step, to be followed by treatment of such subject, one of ordinary skill in the art would very reasonably understand that before administering to a subject a therapeutic peptide such as one of those particularly taught by the reference patent to be useful for treating atherosclerosis, see above, such subject reasonably would have been diagnosed with atherosclerosis, this clearly, per Claim Interpretation and also as made clear in Insull, being a hyperlipidemia condition (e.g., from S4, “Atherosclerosis develops progressively through continuous evolution of arterial wall lesions centered on the accumulation of cholesterol-rich lipids and the accompanying inflammatory response.”). Stated another way, it is reasonable that one of ordinary skill in the art would diagnose a subject as having atherosclerosis before administering a treatment, such as that of the reference patent, to treat such hyperlipidemia condition.
Considering the teachings and composition claims of the reference patent, in view of Insull, one of ordinary skill in the art would have understood at the time of the instant application filing that the elected SEQ ID NO:13 peptide, as well as many other peptides encompassed by instant claim 1, would reasonably treat a subject who had been diagnosed with atherosclerosis, a hyperlipidemia condition, to reduce or inhibit atherosclerosis by such action (as noted, and noting again, atherosclerosis being a hyperlipidemia condition, see Claim Interpretation above). The rationale is simply to apply a known therapeutic peptide to a role in therapy that it could reasonably achieve based on prior art teachings. There would have been a reasonable expectation of success based on such teachings.
Accordingly, claim 1, as well as claim 3, where its SEQ ID Numbers 5 and 6 are identical to reference application SEQ ID Numbers 5 and 6, claim 4, reference application SEQ ID Numbers 5 and 6 within the 8-60 range, claim 5, reference application SEQ ID Numbers 5 and 6 within 90 percent sequence identity with SEQ ID NO:9, claim 6, given that reference application claim 6 encompasses SEQ ID Numbers 5 and 6 when in combination, so in the form of a pharmaceutical composition, claims 7 and 8, each of which includes “fat deposits in arteries” and “atherosclerotic lesions”, are rejected over the reference patent claims and teachings in view of Insull.
Claims 9-12 would have been obvious because administering the same compound to the same population - having atherosclerosis, a hyperlipidemia condition, would reasonably be expected to have the same result.
New claim 14 would have been obvious on the same bases as claim 1, claim 14 encompassing peptides also in the genus of claim 1, and specifically including SEQ ID Nos. 5 and 6, the same as in the reference application claims 3, 22 and 23.
In summary, claims 1, 3-12 and 14 are provisionally rejected on the ground of nonstatutory double patenting.
This is a provisional nonstatutory double patenting rejection.
Claim 13 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3, 5, 7, and 22 of copending Application No. 17286857 (reference application), in view of Insull, The American Journal of Medicine (2009) 122, S3–S14 (“Insull”), as evidenced by Robbins et al., CHEST, vol. 136, no. 1, JULY, 2009, pp 31-36 (Robbins), as applied to claim 1 above, and further in view of CUMC article “New Link Between High-Fat Diet and Atherosclerosis Identified”, downloaded from the Internet 6/3/25, dated 10/8/12, 4 pages (CUMC).
The rejection of claim 1 is set forth above.
Reference patent application claims and disclosure do not explicitly address the effect of its netrin-1 peptides when the hyperlipidemia condition (atherosclerosis) “is the result of a high-fat diet” (this pertaining to the cause of the hyperlipidemia condition).
The level of skill in the art is high.
Claim 13 states that the hyperlipidemia of claim 1 “is the result of a high-fat diet.” The specification states, “As used herein, a “high fat diet” refers to a diet in which at least about 40% of a subject's daily caloric intake are fat calories (i.e., calories from fat),” para 32.
CUMC clearly teaches that a diet high in saturated fat raises levels of endothelial lipase, an enzyme associated with the development of atherosclerosis, page 1. Based on this teaching, one of ordinary skill in the art would reasonably understand that the atherosclerosis of a population of subjects having atherosclerosis would reasonably include subjects whose atherosclerosis condition “is the result of a high-fat diet.” Given treating the subjects in the same population, the reference patent claimed peptides when used for treating atherosclerosis, reasonably would include treating atherosclerosis when this hyperlipidemia condition was caused by a high-fat diet such as that taught in CUMC. Additionally, treating a subject with the same compound would have the same result for the same population, see MPEP 2112.01 II and 2112.02 II.
Accordingly, claim 13 is rejected under this section.
Conclusion
No claim is allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JOSEPH FISCHER whose telephone number is (571)270-7925. The examiner can normally be reached on Monday to Friday, 9:00 AM to 5:00 PM, however noting that the examiner will not normally be working on Wednesday-Friday and on Monday/Tuesday on alternating weeks, but will promptly answer messages upon his return to work.
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/JOSEPH FISCHER/Primary Examiner, Art Unit 1658
1 The examiner is interpreting the use of “may” in claims 15 and 16 as referring to alternative limitations within each claim; to interpret “may” as optional at least would render these claims subject to a 35 USC 112d/112 paragraph 4 rejection as not further limiting, which appears to the examiner to not be the intention in setting forth these new claims.
Prosecution Insights