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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 5/1/2026 has been entered.
Objections/Rejections Withdrawn
Rejections and/or objections not reiterated from previous Office Actions are hereby withdrawn.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
Applicant's arguments filed 5/1/2026, with respect to the claim rejections under 35 U.S.C. 103, have been fully considered but they are not persuasive.
The Applicant’s position is that 1) Brown would have led a person of ordinary skill in the art to expect that the efficacy of a peptide vaccine would be reduced after tumor resection and instead would guide one away from the presently claimed invention, 2) Brown only teaches local administration of immune adjuvant therapy, 3) Brown does not teach or suggest administering the presently claimed peptide vaccine in the post-operative setting, much less with a reasonable expectation of achieving the claimed therapeutic benefit, 4) the present application demonstrates that the claimed post-operative peptide administration produces striking and unexpected therapeutic effects, and 5) a person of ordinary skill in the art would not have had a reasonable expectation of success in using the claimed peptide vaccine after surgery to suppress metastasis.
Regarding 1), as stated in the Final Office Action dated 12/1/2025, Brown teaches that there is a gradual decline of dendritic cells (DC) after removal of the tumor that lasts for several days; during the first ~10 days post-surgery. Brown indicates that the decline in DCs is likely due to removal of the antigen source - the tumor. Consequently, one skilled in the art would recognize that administering a new source of antigen, such as through a peptide vaccine as instantly claimed, could sustain DCs and facilitate antigen presentation to CD8+ cells, thereby promoting their treatment of cancer cells, particularly recurrent or metastatic ones may have been missed during surgery.
Further, based on the broadest reasonable interpretation, post-surgery is inclusive of any time after surgery has occurred. Thus, the teachings of Brown continue to apply here; Applicant acknowledges as much in the Remarks, stating “Brown can be understood as suggesting that the brief period immediately after surgery-before cross-presentation fully declines-might permit some adjuvant intervention to enhance an already-existing immune response." (Pg 5, second paragraph from the bottom of the page).
Regarding 2), the instant claims are drawn to a method of administration of a peptide comprising 4 linked CTL peptides following surgery as a method to treat SART2-positive malignancies. Per the broadest reasonable interpretation, administration is inclusive of any mode or means of administration - including local administration; see Advisory Action dated 3/25/2026. Thus, the teachings of Brown continue to apply.
Regarding 3), in response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
Further, there is a reasonable expectation of success based upon the combined teachings of Brown and Fuyaka as Fukaya teaches the peptides claimed are capable of treating cancer.
Regarding 4), per MPEP 716.02(C)(II), “Expected beneficial results are evidence of obviousness of a claimed invention, just as unexpected results are evidence of unobviousness thereof." In re Gershon, 372 F.2d 535, 538, 152 USPQ 602, 604 (CCPA 1967).”
Moreover, per MPEP 716.02(B)(III), “Evidence of unexpected properties may be in the form of a direct or indirect comparison of the claimed invention with the closest prior art which is commensurate in scope with the claims. See In re Boesch, 617 F.2d 272, 205 USPQ 215 (CCPA 1980).
In the instant case, Figure 5 demonstrates a significant reduction in pulmonary lung metastases upon administration with the instant SEQ ID NO: 24. However, Applicants have merely demonstrated a method of treating cancer with the instant SEQ ID NO: 24, which is known in the art and taught by Fuyaka, which is the closest prior art. Because one would reasonably expect that a peptide known to treat cancer could treat cancer metastasis and because Fuyaka had previously demonstrated such peptides can treat cancer effectively, these results are not unexpected.
Regarding 5), Fukaya teaches a method of treating cancer, described above. Per the broadest reasonable interpretation, treating cancer includes treating cancer metastasis. Therefore, this argument is not found persuasive.
Moreover, Fukaya defines the term “treatment and/or prevention of cancer” to refer to prevention of the development/recurrence of cancer, suppression of the progression/exacerbation of cancer, or the improvement of cancer conditions (Col. 13, lines 23-27). One skilled in the art would reasonably recognize that “suppression of the progression/exacerbation of cancer” reads on metastasis.
Thus, the teachings of Fukaya provide a reasonable expectation of success.
Collectively, the arguments set forth in 1)-5) above are insufficient to overcome the outstanding obviousness rejection, which has been maintained/modified herein.
Applicant’s arguments with respect to the rejections under double patenting have been considered but are moot because the double patenting rejections do not rely on the teachings of Fuyaka or Brown. Thus, they have been maintained/modified herein.
Claim Status
Claims 1, 4-6, and 9-13 are pending. Claims 2-3 and 7-8 are cancelled.
Priority
The Application is the 371 of PCT/JP2020/048667, filed on 12/25/20, and claims foreign priority to JP2019-236947 filed 12/26/19. The translation JP2019-236947, filed on 3/2/26 is acknowledged. The priority date of 12/26/19 is acknowledged.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claim(s) 1, 4-6, and 9-13 are rejected under 35 U.S.C. 103 as being unpatentable over Fukaya et al. (US10,137,183 B2, filed 10/20/14, published 11/27/18) in view of Brown et al. (Loss of antigen cross-presentation after complete tumor resection is associated with the generation of protective tumor-specific CD8(+) T-cell immunity. Oncoimmunology. 2012 Oct 1;1(7):1084-1094.).
Fukaya teaches a cancer antigen peptide that can be administered to a wide range of cancer patients in the form of a peptide vaccine for cancer without the need for HLA typing and regardless of the HLA types of patients. Such a peptide having 4 linked CTL epitopes is obtained by linking 4 CTL epitope peptides selected from among CTL epitope peptides derived from tumor antigen molecules that are reported to have the capacity for CTL induction via linkers (Abstract).
Fukaya teaches the peptides SEQ ID NO: 1-18, referred to as PEP1-18, respectively, which correspond to and are identical to the instant SEQ ID NO: 1-18 (Sequence Listing, Col. 25-51). Specific peptides comprising SEQ ID NO: 4-6 and 9, wherein the peptides are connected via linkers and SEQ ID NO: 4 is present at the C-terminus, include PEP5-(L)-PEP6-(L)-PEP9-(L)-PEP4; PEP9-(L)-PEP5-(L)-PEP6-(L)-PEP4; PEP6-(L)-PEP5-(L)-PEP9-(L)-PEP4; PEP6-(L)-PEP9-(L)-PEP5-(L)-PEP4; PEP9-(L)-PEP6-(L)-PEP5-(L)-PEP4; PEP5-(L)-PEP9-(L)-PEP6-(L)-PEP4 (Col. 3, line 45; Col. 9, line 33; Claim 4).
Fukaya claims a method for treating cancer comprising administering to a cancer patient the peptide or a pharmaceutical composition containing it (claim 13). These peptides can be included in pharmaceutical compositions as an active ingredient used for cancer immunotherapy (Col. 12, lines 58-62). Fukaya further teaches that the dosage of the pharmaceutical composition according to the present invention can be adequately adjusted in accordance with factors such as the conditions/severity of cancer to be treated, the age of the patient, or the body weight of the patient (amount effective for treatment; Col. 15, lines 17-32).
Fukaya defines the term “treatment and/or prevention of cancer” to refer to prevention of the development/recurrence of cancer, suppression of the progression/exacerbation of cancer, or the improvement of cancer conditions (Col. 13, lines 23-27); “suppression of the progression/exacerbation of cancer” reads on cancer metastasis.
Fukaya also teaches that SEQ ID NO: 5 is derived from SART2 (Table 2). Such CTL epitope peptides derived from tumor antigen molecules are peptides that result from decomposition of tumor antigens within tumor cells that are then bound to HLA class I molecules and presented on the cell surface, which can be recognized by a tumor-specific CTL and/or induce and/or activate-tumor specific CTLs ([0095]), thus making it obvious to treat SART2-expressing cells with the aforementioned polypeptides.
Fukaya does not explicitly teach administering the above polypeptides after surgery.
Brown describes the impact of tumor resection on the tumor-specific T-cell response (Abstract). Brown states that in situ tumor ablation creates a source of antigens and an immune response that is enhanced by immunotherapy but also notes that there is a decline in dendritic cells (DCs) that cross-present tumor antigens over ~10 days post-surgery. Presumably, the complete removal of the tumor removes the source of antigens and the duration of post-surgery antigen presentation is then limited by the half-life of the remaining antigen-bearing dendritic cells. The initial persistence of cross-presentation in the draining nodes after primary resection suggests a possible window of opportunity for locally delivered immune adjuvant therapy into the resection bed (Pg 1090, left column, both paragraphs).
In summary, Fukaya teaches a method for treating SART2 malignancies comprising administering to a cancer patient a 4 CTL epitope linked peptide comprising SEQ ID NO: 4-6 and 9. Brown teaches that DCs that cross-present tumor antigens decline gradually after tumor resection but could be bolstered by locally delivered immune adjuvant therapy into the resection bed as the decline is related to removal of the antigen source – the tumor.
Based on these teachings, regarding claim 1, it would be prima facie obvious to use the method of Fukaya after surgery. One skilled in the art would be motivated to do so in order to increase the number of DCs that recognize the tumor antigen so they can target any cancerous cells that remain after surgery. One skilled in the art would have a reasonable expectation of success as it was already established that post-surgical adjuvant therapy can help modulate the immune system to more effectively treat cancer.
Moreover, per MPEP 2144.06(I), it is obvious to combine equivalents known for the same purpose: "It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art." In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) (citations omitted). By logical extension, it is obvious to combine two therapies – surgery to remove a cancerous tumor followed by administration of a peptide vaccine adjuvant therapy – each separately beneficial for treating cancer into one method of treating cancer.
Regarding claim 4, Fukaya teaches the peptide comprising or consisting of PEP5-(L)-PEP9-(L)-PEP6-(L)-PEP4, wherein PEP4-6 and 9 are equivalent to SEQ ID NO: 4-6 and 9 respectively, (Col. 3, line 45; Col. 9, line 33; Claims 1 and 4).
Regarding claims 5 and 6, Fukaya additionally teaches the use of other linkers to connect 4 CTL epitope peptides together, including amino acid linkers such as arginine trimer, arginine tetramer, lysine dimer, lysine trimer, lysine tetramer, glycine dimer, glycine trimer, glycine tetramer, glycine pentamer, glycine hexamer, alanine-alanine-tyrosine (AAY), isoleucine-leucine-alanine (ILA)k, and arginine-valine-lysine-arginine (RVKR), with an arginine dimer or trimer being preferable (Col. 8, lines 39-52).
Regarding claim 9, Fukaya teaches SEQ ID NO: 27, which is identical to the instant SEQ ID NO: 24 (Table 3; Sequence Listing).
Regarding claims 10 and 11, as stated above, Fukaya defines the term “treatment and/or prevention of cancer” to refer to prevention of the development/recurrence of cancer, suppression of the progression/exacerbation of cancer, or the improvement of cancer conditions (Col. 13, lines 23-27); “suppression of the progression/exacerbation of cancer” reads on cancer metastasis.
Regarding claims 12 and 13, Fukaya further discloses embodiments wherein the peptide having 4 linked epitopes may consist of hydrophilic amino acids linked to the N terminus that may be composed of arginine trimer or arginine tetramer composed of three or four arginine residues linked to each other (Col. 4, lines 18-25).
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1, 4-6, and 9-13 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-9 and 11-13 of U.S. Patent No. US 10,137,183 B2 (‘183; published 11/27/18). 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 US ‘183 recites a peptide having the general formula: A-(L)-B-(L)-C-(L)-D wherein (L) is a linker and wherein A, B, C, and D consist of a total of four CTL epitope peptides and are independently selected from the group consisting of: PEP1 as represented by SEQ ID NO: 1; PEP2 as represented by SEQ ID NO: 2; PEP4 as represented by SEQ ID NO: 4; PEP5 as represented by SEQ ID NO: 5; PEP6 as represented by SEQ ID NO: 6; PEP7 as represented by SEQ ID NO: 7; PEP8 as represented by SEQ ID NO: 8; PEP9 as represented by SEQ ID NO: 9; PEP10 as represented by SEQ ID NO: 10; PEP13 as represented by SEQ ID NO: 13; PEP15 as represented by SEQ ID NO; 15; PEP17 as represented by SEQ ID NO: 17; and PEP18 as represented by SEQ 18 NO: 18; and wherein
(a) the peptide comprises PEP2 at the C terminus but not when the peptide comprises PEP7 at the N terminus followed by PEP8; or (b) the peptide comprises PEP4 at the C terminus; or (c) the peptide comprises PEP10 at the C terminus; or (d) the peptide comprises PEP5 at the C terminus preceded by PEP6; or (e) the peptide-consists of PEP5, PEP6, PEP9, and PEP18, and wherein the peptide optionally comprises hydrophilic amino acids at the N terminus or C terminus to improve solubility of the peptide.
Dependent claims include wherein the CTL epitope peptides are 4 non-redundant peptides selected from the group consisting of PEP1, PEP2, PEP4, PEP5 , PEP6, PEP7, PEP8, PEP9, PEP10, PEP13, PEP15, PE17, and PEP18 (claim 2); the peptide is selected from the group consisting of: (i) the peptide comprising PEP2 at the C terminus and also 3 CTL epitope peptides selected from the group consisting of PEP1, PEP7, PEP5, and PEP13 but not when the peptide comprises PEP7 at the N terminus followed by PEP8; (ii) the peptide consisting of PEP4 at the C terminus and also PEP5, PEP6, and PEP9; (iii) the peptide consisting of PEP10 at the C terminus and also 3 CTL epitope peptides selected from the group consisting of PEP1, PEP13, PEP15, PEP17, and PEP18; (iv) the peptide consisting of PEP5 at the C terminus preceded by PEP6, also PEP1 and PEP7; and (v) the peptide consisting of PEP9 at the C terminus and also PEP5, PEP6, and PEP18 (claim 3); the ordered arrangement of the peptide from the N terminus is selected from the group consisting of: PEP5-(L)-PEP6-(L)-PEP5-(L)-PEP4 ;PEP9-(L)-PEP5-(L)-PEP6-(L)-PEP4; PEP6-(L)-PEP5-(L)-PEP9-(L)-PEP4; PEP6-(L)-PEP9-(L)-PEP5-(L)-PEP4; PEP9-(L)-PEP6-(L)-PEP5-(L)-PEP4; PEP5-(L)-PEP9-(L)-PEP6-(L) PEP4; PEP1-(L)-PEP7-(L)-PEP8-(L)-PEP2; PEP1-(L)-PEP8-(L)-PEP7-(L)-PEP2; PEP7-(L)-PEP1-(L)-PEP8-(L)-PEP2; PEP8-(L)-PEP7-(L)-PEP1-(L)-PEP2; PEP8-(L)-PEP1-(L)-PEP7-(L)-PEP2; PEP7-(L)-PEP13-(L)-PEP8-(L)-PEP2; PEP8-(L)-PEP 13-(L)-PEP7-(L)-PEP2; PEP13-(L)-PEP7-(L)-PEP8-(L)-PEP2; PEP8-(L)-PEP7-(L)-PEP13-(L)-PEP2; PEP13-(L)-PEP8-(L)-PEP7-(L)-PEP2; PEP13-(L)-PEP15-(L)-PEPI 8-(L)-PEP10 ; PEP 13-(L)-PEP 18-(L)-PEP15-(L)-PEP10; PEP15-(L)-PEP13-(L)-PEP18-(L)-PEP10; PEP15-(L)-PEP18-(L)-PEP13-(L)-PEP10; PEP18-(L)-PEP13-(L)-PEP15-(L)-PEP10; PEP18-(L)-PEP15-(L)-PEP13-(L)-PEP10; PEP1-(L)-PEP15-(L)-PEP18-(L)-PEP10; PEP1-(L)-PEP18-(L)-PEP15-(L)-PEP10; PEP15-(L)-PEP1-(L)-PEP18-(L)-PEP10; PEP15-(L)-PEP18-(L)-PEP1-(L)-PEP10; PEPI 8-(L)-PEP1-(L)-PEP15-(L)-PEP10; PEP18-(L)-PEP15-(L)-PEP1-(L)-PEP10; PEP15-(L)-PEP17-(L)-PEP13-(L)-PEP10; PEP15-(L)-PEP13-(L)-PEP17-(L)-PEP10; PEP17-(L)-PEP15-(L)-PEP13-(L)-PEP10; PEP17-(L) -PEP13-(L)-PEP15-(L)-PEP10; PEP13-(L) -PEP17-(L)-PEP15-(L)-PEP10; PEP13-(L)-PEP15-(L)-PEP17-(L)-PEP10; PEP6-(L)-PEP18-(L)-PEP5-(L)-PEP9; PEP6-(L)-PEP5-(L)-PEP18-(L)-PEP9; PEP1-(L)-PEP7-(L)-PEP6-(L)-PEP5; or PEP7-(L)-PEP1-(L)-PEP6-(L)-PEP5 (claim 4); the linker is an amino acid linker (claim 5); the amino acid linker is an arginine dimer or an arginine trimer (claim 6); the hydrophilic amino acids are located at the N terminus (claim 7); the hydrophilic amino acids comprise an arginine trimer or an arginine tetramer (claim 8); the peptide consist of the amino acid sequence as shown in SEQ ID NO: 22-66 (claim 9); a pharmaceutical composition comprising, as an active ingredient, the peptide according to claim 1 (claim 11); a pharmaceutical composition comprising two or more distinct peptides according to claim 1 (claim 12); and a method for treating cancer comprising administering to a cancer patient the peptide or the pharmaceutical composition (claim 13).
Claims 1, 4-6, and 9-13 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4-8, 11-12, and 14 of U.S. Patent No. US 12,251,447 B2 (‘447; published 3/18/25). 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 US ‘447 recites a combined formulation comprising a peptide having 4 linked epitopes comprising 4 CTL epitope peptides linked via linkers and a PD-1 pathway antagonist in combination, wherein the PD-1 pathway antagonist is at least one selected from the group consisting of an anti-PD-1 antibody, an anti-PD-L1 antibody, and an anti-PD-L2 antibody, wherein the peptide having 4 linked epitopes comprises: the epitope peptide as shown in SEQ ID NO: 5, the epitope peptide as shown in SEQ ID NO: 6, the epitope peptide as shown in SEQ ID NO: 9, and one epitope peptide selected from the group consisting of the epitope peptide as shown in SEQ ID NO: 2, the epitope peptide as shown in SEQ ID NO: 4 and the 15 epitope peptide as shown in SEQ ID NO: 10, at the C terminus wherein the 4 linked epitopes are linked via linkers, wherein the peptide optionally further comprises a peptide sequence consisting of hydrophilic amino acids, wherein the linker is an arginine dimer composed of wherein the linker is an arginine dimer composed of two arginine residues linked to each other, wherein the peptide sequence consisting of hydrophilic amino acids is linked to the N terminus and is composed of an arginine trimer composed of three arginine residues linked to each other or an arginine tetramer composed of four arginine residues linked to each other.
Independent claim 4 recites method for treating a cancer in a patient by administering a peptide having 4 linked epitopes comprising 4 CTL epitope peptides linked via linkers and a PD-1 pathway antagonist, wherein the PD-1 pathway antagonist is at least one selected from the group consisting of an anti-PD-1 antibody, an anti-PD-L1 antibody, and an anti-PD-L2 antibody, wherein the peptide having 4 linked epitopes comprises: the epitope peptide as shown in SEQ ID NO: 5, the epitope peptide as shown in SEQ ID NO: 6, the epitope peptide as shown in SEQ ID NO: 9, and one epitope peptide selected from the group consisting of the epitope peptide as shown in SEQ ID NO: 2, the epitope peptide as shown in SEQ ID NO: 4 and the epitope peptide as shown in SEQ ID NO: 10, at the C terminus wherein the 4 linked epitopes are linked via linkers, wherein the peptide optionally further comprises a peptide sequence consisting of hydrophilic amino acids, wherein the linker is an arginine dimer composed of two arginine residues linked to teach other, wherein the peptide sequence consisting of hydrophilic amino acids is linked to the N terminus and is composed of an arginine trimer composed of three arginine residues linked to each other or an arginine tetramer composed of four arginine residues linked to each other.
Dependent claims include wherein the peptide having 4 linked epitopes is shown in SEQ ID NO: 24, 25, or 26 (which are identical to the instant SEQ ID NO: 24, 25, and 25; claim 5); the PD-1 antibody species (claims 6 and 7); the peptide having 4 linked epitopes is administered to the patient before administration of the PD-1 pathway antagonist, simultaneously with administration of the PD-1 pathway antagonist, or after administration of the PD-1 pathway antagonist (claim 8).
Independent claim 11 recites a method for enhancing the antitumor effect of a PD-1 pathway antagonist, comprising administering a peptide having 4 linked epitopes to a patient, wherein the PD-1 pathway antagonist is at least one selected from the group consisting of an anti-PD-1 antibody, an anti-PD-L1 antibody, and an anti-PD-L2 antibody, wherein the peptide having 4 linked epitopes comprises: the epitope peptide as shown in SEQ ID NO: 5, the epitope peptide as shown in SEQ ID NO: 6, the epitope peptide as shown in SEQ ID NO: 9, and one epitope peptide selected from the group consisting of the epitope peptide as shown in SEQ ID NO: 2, the epitope peptide as shown in SEQ ID NO: 4 and the epitope peptide as shown in SEQ ID NO: 10, at the C terminus wherein the 4 linked epitopes are linked via linkers, wherein the peptide optionally further comprises a peptide sequence consisting of hydrophilic amino acids, wherein the linker is an arginine dimer composed of two arginine residues linked to each other, wherein the peptide sequence consisting of hydrophilic amino acids is linked to the N terminus and is composed of an arginine trimer composed of three arginine residues linked to each other or an arginine tetramer composed of four arginine residues linked to each other.
Dependent claims include wherein the peptide having 4 linked epitopes is administered to the patient before administration of the PD-1 pathway antagonist, simultaneously with administration of the PD-1 pathway antagonist, or after administration of the PD-1 pathway antagonist (claim 12); and wherein the method comprises administering a peptide having the sequence of SEQ ID NO: 24, a peptide having the sequence of SEQ ID NO: 44, and a peptide having the sequence of SEQ ID NO; 45, as a mixture (claim 14).
Conclusion
No claim is allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Sara Konopelski Snavely whose telephone number is (571)272-1841. The examiner can normally be reached Monday - Friday 9-6pm EST.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Melissa L Fisher can be reached at 571-270-7430. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/SARA E KONOPELSKI SNAVELY/Examiner, Art Unit 1658
/Melissa L Fisher/Supervisory Patent Examiner, Art Unit 1658
Prosecution Insights