DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Election/Restrictions and Claim Status
Applicants’ amendments and arguments filed 11/10/25 are acknowledged. Any objection or rejection from the 5/8/25 office action that is not addressed below is withdrawn based on the amendments.
Previously, Group 3 and the species of PKHB1 were elected.
Claims 7-9 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 12/27/23.
Claims 2-3, 6 and 10-11 have been canceled.
Claims 1, 4-5 and 12 are being examined.
Priority
The priority information is provided in the filing receipt dated 9/27/21.
Claim Rejections - 35 USC § 103
Claims were previously rejected based on the references cited below. Since the claims have been amended, the rejection is updated to correspond to the instant claims.
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claim(s) 1, 4-5 and 12 is/are rejected under 35 U.S.C. 103 as being unpatentable over Martinez-Torres et al. (as cited with IDS 4/26/21; ‘Martinez-Torres’) in view of Kokhaei et al. (‘Apoptotic tumor cells are superior to tumor cell lysate, and tumor cell RNA in induction of autologous T cell response in B-CLL’ Leukemia v18 2004 pages 1810-1815; ‘Kokhaei’).
Martinez-Torres teach the PKHB1 peptide and sequence (k-R-F-Y-V-V-M-W-K-k) (page
4 first complete paragraph). Martinez-Torres teach peptides that induce programmed cell death in chronic lymphocytic leukemia B cells (abstract). Martinez-Torres teach injection of PKHB1 to mice with MEC-1 cells (page 7 first complete paragraph) where MEC-1 is a CLL (chronic lymphocytic leukemia) cell line (page 18 first paragraph). Martinez-Torres teach decreased tumor growth with PKHB1 treatment in vivo (page 18 first paragraph). Martinez-Torres teach that PKHB1 induced PCD in CLL cells and induced toxicity in ~49% of the CLL cells (figure 1 and 2nd complete paragraph on page 8). Martinez-Torres teach that blood samples from CLL patients were provided (page 7 last paragraph).
Martinez-Torres does not teach administration of cancer cells.
Kokhaei teach B cell chronic lymphocytic leukemia is an ideal target for immunotherapy (abstract). Kokhaei teach using tumor cells and tumor cell lysates in an autologous setting (abstract). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy (abstract). Kokhaei also teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2). Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of Martinez-Torres because Martinez-Torres teach peptides that are highly effective in treating chronic lymphocytic leukemia B cells (conclusions page 2). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy for B cell chronic lymphocytic leukemia (abstract). Since both references teach methods of treating chronic lymphocytic leukemia B cells the idea of combining the teachings flows logically from their having been individually taught in the art. For ease of administration, one would have been motivated to combine the cells and peptide prior to administration. Since Kokhaei also teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2) one would have also been motivated to administer cell lysates with the peptide. One would have had a reasonable expectation of success since Martinez-Torres teach decreased tumor growth with PKHB1 treatment in vivo (page 18 first paragraph). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy (abstract).
In relation to the peptide of claims 1 and 4, Martinez-Torres teach the PKHB1 peptide
and sequence (k-R-F-Y-V-V-M-W-K-k) (page 4 first complete paragraph) which is the elected
peptide.
In relation to collecting a cancer cell, Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’) which are leukemia cells.
In relation to the cancer cell of claims 1 and 5, Kokhaei teach using tumor cells and tumor cell lysates in an autologous setting (abstract). Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’) which are leukemia cells.
In relation to the contacting and administering of claim 1, for ease of administration, one would have been motivated to combine the cells and peptide prior to administration. Martinez-Torres expressly teach injection of PKHB1 (page 7 first complete paragraph).
In relation to the individual of clam 1, Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’).
In relation to ‘of inducing immunogenic cell death’ and ‘wherein immunogenic cell death is characterized’ in claim 1, such phrase is an intended use (see MPEP 2111.02). With respect to ‘whereby immunogenic cell death of one or more cancer cells of the cancer is induced’, Martinez-Torres teach the PKHB1 peptide and sequence (k-R-F-Y-V-V-M-W-K-k) (page 4 first complete paragraph) which is the elected peptide. Such peptide would function as claimed since a compound and its properties are inseparable (MPEP 2112.01 II).
In relation to claim 12, Kokhaei teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2).
Response to Arguments – 103
Applicant's arguments filed 11/10/25 have been fully considered but they are not persuasive with respect to the rejection set forth above.
Although applicants argue that the claims have been amended, the amended claims are addressed above.
Although applicants argue about the teachings of the references alone, 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). The specific teachings of the references and how the claim limitations are met are discussed in detail above.
Although applicants argue about immunogenic cell death, claim 1 recites ‘of inducing immunogenic cell death’ which is an intended use (see MPEP 2111.02). With respect to ‘whereby immunogenic cell death of one or more cancer cells of the cancer is induced’, Martinez-Torres teach the PKHB1 peptide and sequence (k-R-F-Y-V-V-M-W-K-k) (page 4 first complete paragraph) which is the elected peptide. Such peptide would function as claimed since a compound and its properties are inseparable (MPEP 2112.01 II).
Although applicants argue that there is no motivation to combine and no expectation of success, it would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of Martinez-Torres because Martinez-Torres teach peptides that are highly effective in treating chronic lymphocytic leukemia B cells (conclusions page 2). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy for B cell chronic lymphocytic leukemia (abstract). Since both references teach methods of treating chronic lymphocytic leukemia B cells the idea of combining the teachings flows logically from their having been individually taught in the art.
Although applicants argue about DAMPs, the active methods steps of claim 1 include collecting, contacting and administering which are met for the reasons set forth above. There is no requirement that any DAMP level is to be measured. Martinez-Torres teach the PKHB1 peptide and sequence (k-R-F-Y-V-V-M-W-K-k) (page 4 first complete paragraph) which is the elected peptide. Such peptide would function as claimed since a compound and its properties are inseparable (MPEP 2112.01 II).
Although applicants argue about unexpected results and example 9 and figures 20-24, it is first noted that there does not appear to be any example 9 in the instant specification.
Figures 20-21 appear to relate to administration of peptide alone (example 2 page 41). Martinez-Torres teach decreased tumor growth with PKHB1 treatment in vivo (page 18 first paragraph). Martinez-Torres teach that PKHB1 induced PCD in CLL cells and induced toxicity in ~49% of the CLL cells (figure 1 and 2nd complete paragraph on page 8). MPEP 716.02(c) II recognizes that expected beneficial results are evidence of obviousness.
Figures 22-24 appear to relate to administration of tumor cell lysate alone (page 44). Kokhaei teach B cell chronic lymphocytic leukemia is an ideal target for immunotherapy (abstract). Kokhaei teach using tumor cells and tumor cell lysates in an autologous setting (abstract). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy (abstract). Kokhaei also teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2). MPEP 716.02(c) II recognizes that expected beneficial results are evidence of obviousness.
MPEP 716.02(b) recognizes that the burden is on the applicant to establish results are unexpected and significant. No explanation has been provided other than a mere assertion. Further, as noted above each of the treatments individually was known to have beneficial effects. Although MPEP 716.02(a) recognizes situations in which evidence of a greater than expected results can be made, there is no such evidence in this case. The examples are not commensurate in scope with the claimed invention (see MPEP 716.02(d)) since they seem to relate to administration of peptide or cell lysate (not combinations) and since they relate to a specific peptide and cancer cell type. There is no adequate basis to conclude unexpected results.
Although applicants argue about a teaching away, no particular citation is provided thus the argument is unclear. MPEP 2123 expressly recognizes that alternative embodiments constitute prior art and refers to situations in which ‘A known or obvious composition does not become patentable simply because it has been described as somewhat inferior to some other product’.
Although applicants argue about induction of ICD and the lysate of claim 12, MPEP 2144 IV recognizes that the reason or motivation to modify the reference can be for a different purpose. One of the active method steps of claim 1 is ‘administering’. Kokhaei teach using tumor cells and tumor cell lysates in an autologous setting (abstract). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy (abstract). Kokhaei also teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2).
Double Patenting
Claims were previously rejected under double patenting. Since the claims have been amended the rejections are updated to correspond to the instant claims.
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, 4-5 and 12 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-9 of U.S. Patent No. 10759843 (843) in view of Martinez-Torres et al. (as cited with IDS 4/26/21; ‘Martinez-Torres’) in view of Kokhaei et al. (‘Apoptotic tumor cells are superior to tumor cell lysate, and tumor cell RNA in induction of autologous T cell response in B-CLL’ Leukemia v18 2004 pages 1810-1815; ‘Kokhaei’).
843 recites methods for treating cancer by administering PKHB1 for leukemia (claim 1) specifically B-chronic lymphocyte leukemia (claim 3). 843 recites contacting tumor cells with PKHB1 (claim 5).
843 does not teach administration of a cancer cell.
Martinez-Torres teach the PKHB1 peptide and sequence (k-R-F-Y-V-V-M-W-K-k) (page
4 first complete paragraph). Martinez-Torres teach peptides that induce programmed cell death in chronic lymphocytic leukemia B cells (abstract). Martinez-Torres teach injection of PKHB1 to mice with MEC-1 cells (page 7 first complete paragraph) where MEC-1 is a CLL (chronic lymphocytic leukemia) cell line (page 18 first paragraph). Martinez-Torres teach decreased tumor growth with PKHB1 treatment in vivo (page 18 first paragraph). Martinez-Torres teach that PKHB1 induced PCD in CLL cells and induced toxicity in ~49% of the CLL cells (figure 1 and 2nd complete paragraph on page 8). Martinez-Torres teach that blood samples from CLL patients were provided (page 7 last paragraph).
Kokhaei teach B cell chronic lymphocytic leukemia is an ideal target for immunotherapy (abstract). Kokhaei teach using tumor cells and tumor cell lysates in an autologous setting (abstract). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy (abstract). Kokhaei also teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2). Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 843 because 843 recites a specific peptide and uses thereof (claims 1-3). Thus one would have been motivated to use the peptide according to known methods. Martinez-Torres teach peptides comprising RFYVVMWK (page 4 first complete paragraph) and known uses thereof. Thus one would have been motived to use the peptide of 843 in such method. Further, Martinez-Torres teach advantages of the PKHB1 peptide in stability (page 20 first complete paragraph) so one would have been motivated to use the PKHB1 peptide. One would have had a reasonable expectation of success since methods of contacting were known and since Martinez-Torres teach advantageous effects. Further, Martinez-Torres teach peptides that are highly effective in treating chronic lymphocytic leukemia B cells (conclusions page 2). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy for B cell chronic lymphocytic leukemia (abstract). Since both references teach methods of treating chronic lymphocytic leukemia B cells the idea of combining the teachings flows logically from their having been individually taught in the art. For ease of administration, one would have been motivated to combine the cells and peptide prior to administration. Since Kokhaei also teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2) one would have also been motivated to administer cell lysates with the peptide. One would have had a reasonable expectation of success since Martinez-Torres teach decreased tumor growth with PKHB1 treatment in vivo (page 18 first paragraph). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy (abstract).
In relation to the peptide of claims 1 and 4, Martinez-Torres teach the PKHB1 peptide
and sequence (k-R-F-Y-V-V-M-W-K-k) (page 4 first complete paragraph) which is the elected
peptide.
In relation to collecting a cancer cell, Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’) which are leukemia cells.
In relation to the cancer cell of claim 1 and 5, Kokhaei teach using tumor cells and tumor cell lysates in an autologous setting (abstract). Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’) which are leukemia cells.
In relation to the contacting and administering of claim 1, for ease of administration, one would have been motivated to combine the cells and peptide prior to administration. Martinez-Torres expressly teach injection of PKHB1 (page 7 first complete paragraph).
In relation to the individual of clam 1, Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’).
In relation to ‘of inducing immunogenic cell death’ and ‘wherein immunogenic cell death is characterized’ in claim 1, such phrase is an intended use (see MPEP 2111.02). With respect to ‘whereby immunogenic cell death of one or more cancer cells of the cancer is induced’, Martinez-Torres teach the PKHB1 peptide and sequence (k-R-F-Y-V-V-M-W-K-k) (page 4 first complete paragraph) which is the elected peptide. Such peptide would function as claimed since a compound and its properties are inseparable (MPEP 2112.01 II).
In relation to claim 12, Kokhaei teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2).
Claims 1, 4-5 and 12 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-9 of U.S. Patent No. 11306124 (124) in view of Martinez-Torres et al. (as cited with IDS 4/26/21; ‘Martinez-Torres’) in view of Kokhaei et al. (‘Apoptotic tumor cells are superior to tumor cell lysate, and tumor cell RNA in induction of autologous T cell response in B-CLL’ Leukemia v18 2004 pages 1810-1815; ‘Kokhaei’).
124 recites a peptide that is PKTD10 which comprises R-F-Y-V-V-M-W-K (claim 9). 124 recites methods of administering a peptide specifically for cancer (claims 5-6).
124 does not specifically recite in vitro administration or administration of a cancer cell.
Martinez-Torres teach the PKHB1 peptide and sequence (k-R-F-Y-V-V-M-W-K-k) (page
4 first complete paragraph). Martinez-Torres teach peptides that induce programmed cell death in chronic lymphocytic leukemia B cells (abstract). Martinez-Torres teach injection of PKHB1 to mice with MEC-1 cells (page 7 first complete paragraph) where MEC-1 is a CLL (chronic lymphocytic leukemia) cell line (page 18 first paragraph). Martinez-Torres teach decreased tumor growth with PKHB1 treatment in vivo (page 18 first paragraph). Martinez-Torres teach that PKHB1 induced PCD in CLL cells and induced toxicity in ~49% of the CLL cells (figure 1 and 2nd complete paragraph on page 8). Martinez-Torres teach that blood samples from CLL patients were provided (page 7 last paragraph).
Kokhaei teach B cell chronic lymphocytic leukemia is an ideal target for immunotherapy (abstract). Kokhaei teach using tumor cells and tumor cell lysates in an autologous setting (abstract). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy (abstract). Kokhaei also teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2). Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 124 because 124 recites a specific peptide (claim 9). Thus one would have been motivated to use the peptide according to known methods. Martinez-Torres teach peptides comprising RFYVVMWK (page 4 first complete paragraph) and known uses thereof. Thus one would have been motived to use the peptide of 124 in such method. Further, Martinez-Torres teach advantages of the PKHB1 peptide in stability (page 20 first complete paragraph) so one would have been motivated to use the PKHB1 peptide. One would have had a reasonable expectation of success since methods of contacting were known and since Martinez-Torres teach advantageous effects. Further, Martinez-Torres teach peptides that are highly effective in treating chronic lymphocytic leukemia B cells (conclusions page 2). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy for B cell chronic lymphocytic leukemia (abstract). Since both references teach methods of treating chronic lymphocytic leukemia B cells the idea of combining the teachings flows logically from their having been individually taught in the art. For ease of administration, one would have been motivated to combine the cells and peptide prior to administration. Since Kokhaei also teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2) one would have also been motivated to administer cell lysates with the peptide. One would have had a reasonable expectation of success since Martinez-Torres teach decreased tumor growth with PKHB1 treatment in vivo (page 18 first paragraph). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy (abstract).
In relation to the peptide of claims 1 and 4, Martinez-Torres teach the PKHB1 peptide
and sequence (k-R-F-Y-V-V-M-W-K-k) (page 4 first complete paragraph) which is the elected
peptide.
In relation to collecting a cancer cell, Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’) which are leukemia cells.
In relation to the cancer cell of claims 1 and 5, Kokhaei teach using tumor cells and tumor cell lysates in an autologous setting (abstract). Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’) which are leukemia cells.
In relation to the contacting and administering of claim 1, for ease of administration, one would have been motivated to combine the cells and peptide prior to administration. Martinez-Torres expressly teach injection of PKHB1 (page 7 first complete paragraph).
In relation to the individual of clam 1, Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’).
In relation to ‘of inducing immunogenic cell death’ and ‘wherein immunogenic cell death is characterized’ in claim 1, such phrase is an intended use (see MPEP 2111.02). With respect to ‘whereby immunogenic cell death of one or more cancer cells of the cancer is induced’, Martinez-Torres teach the PKHB1 peptide and sequence (k-R-F-Y-V-V-M-W-K-k) (page 4 first complete paragraph) which is the elected peptide. Such peptide would function as claimed since a compound and its properties are inseparable (MPEP 2112.01 II).
In relation to claim 12, Kokhaei teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2).
Claims 1, 4-5 and 12 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-5 of U.S. Patent No. 11759496 (496) in view of Martinez-Torres et al. (as cited with IDS 4/26/21; ‘Martinez-Torres’) in view of Kokhaei et al. (‘Apoptotic tumor cells are superior to tumor cell lysate, and tumor cell RNA in induction of autologous T cell response in B-CLL’ Leukemia v18 2004 pages 1810-1815; ‘Kokhaei’).
496 recites a peptide that comprise RFYVVMWK (claims 1-2).
496 does not teach a specific method in the claims nor does 496 recite the instantly elected species.
Martinez-Torres teach the PKHB1 peptide and sequence (k-R-F-Y-V-V-M-W-K-k) (page
4 first complete paragraph). Martinez-Torres teach peptides that induce programmed cell death in chronic lymphocytic leukemia B cells (abstract). Martinez-Torres teach injection of PKHB1 to mice with MEC-1 cells (page 7 first complete paragraph) where MEC-1 is a CLL (chronic lymphocytic leukemia) cell line (page 18 first paragraph). Martinez-Torres teach decreased tumor growth with PKHB1 treatment in vivo (page 18 first paragraph). Martinez-Torres teach that PKHB1 induced PCD in CLL cells and induced toxicity in ~49% of the CLL cells (figure 1 and 2nd complete paragraph on page 8). Martinez-Torres teach that blood samples from CLL patients were provided (page 7 last paragraph).
Kokhaei teach B cell chronic lymphocytic leukemia is an ideal target for immunotherapy (abstract). Kokhaei teach using tumor cells and tumor cell lysates in an autologous setting (abstract). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy (abstract). Kokhaei also teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2). Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 496 because 496 recites a specific peptide (claim 2). Thus one would have been motivated to use the peptide according to known methods. Martinez-Torres teach peptides comprising RFYVVMWK (page 4 first complete paragraph) and known uses thereof. Thus one would have been motived to use the peptide of 496 in such method. Further, Martinez-Torres teach advantages of the PKHB1 peptide in stability (page 20 first complete paragraph) so one would have been motivated to use the PKHB1 peptide. One would have had a reasonable expectation of success since methods of contacting were known and since Martinez-Torres teach advantageous effects. Further, Martinez-Torres teach peptides that are highly effective in treating chronic lymphocytic leukemia B cells (conclusions page 2). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy for B cell chronic lymphocytic leukemia (abstract). Since both references teach methods of treating chronic lymphocytic leukemia B cells the idea of combining the teachings flows logically from their having been individually taught in the art. For ease of administration, one would have been motivated to combine the cells and peptide prior to administration. Since Kokhaei also teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2) one would have also been motivated to administer cell lysates with the peptide. One would have had a reasonable expectation of success since Martinez-Torres teach decreased tumor growth with PKHB1 treatment in vivo (page 18 first paragraph). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy (abstract).
In relation to the peptide of claims 1 and 4, Martinez-Torres teach the PKHB1 peptide
and sequence (k-R-F-Y-V-V-M-W-K-k) (page 4 first complete paragraph) which is the elected
peptide.
In relation to collecting a cancer cell, Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’) which are leukemia cells.
In relation to the cancer cell of claims 1 and 5, Kokhaei teach using tumor cells and tumor cell lysates in an autologous setting (abstract). Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’) which are leukemia cells.
In relation to the contacting and administering of claim 1, for ease of administration, one would have been motivated to combine the cells and peptide prior to administration. Martinez-Torres expressly teach injection of PKHB1 (page 7 first complete paragraph).
In relation to the individual of clam 1, Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’).
In relation to ‘of inducing immunogenic cell death’ and ‘wherein immunogenic cell death is characterized’ in claim 1, such phrase is an intended use (see MPEP 2111.02). With respect to ‘whereby immunogenic cell death of one or more cancer cells of the cancer is induced’, Martinez-Torres teach the PKHB1 peptide and sequence (k-R-F-Y-V-V-M-W-K-k) (page 4 first complete paragraph) which is the elected peptide. Such peptide would function as claimed since a compound and its properties are inseparable (MPEP 2112.01 II).
In relation to claim 12, Kokhaei teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2).
Claims 1, 4-5 and 12 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of U.S. Patent No. 9198949 (949) in view of Martinez-Torres et al. (as cited with IDS 4/26/21; ‘Martinez-Torres’) in view of Kokhaei et al. (‘Apoptotic tumor cells are superior to tumor cell lysate, and tumor cell RNA in induction of autologous T cell response in B-CLL’ Leukemia v18 2004 pages 1810-1815; ‘Kokhaei’).
949 recites a peptide of sequence RFYVVMWK (claim 1).
949 does not teach a specific method in the claims nor does 949 recite the instantly elected species.
Martinez-Torres teach the PKHB1 peptide and sequence (k-R-F-Y-V-V-M-W-K-k) (page
4 first complete paragraph). Martinez-Torres teach peptides that induce programmed cell death in chronic lymphocytic leukemia B cells (abstract). Martinez-Torres teach injection of PKHB1 to mice with MEC-1 cells (page 7 first complete paragraph) where MEC-1 is a CLL (chronic lymphocytic leukemia) cell line (page 18 first paragraph). Martinez-Torres teach decreased tumor growth with PKHB1 treatment in vivo (page 18 first paragraph). Martinez-Torres teach that PKHB1 induced PCD in CLL cells and induced toxicity in ~49% of the CLL cells (figure 1 and 2nd complete paragraph on page 8). Martinez-Torres teach that blood samples from CLL patients were provided (page 7 last paragraph).
Kokhaei teach B cell chronic lymphocytic leukemia is an ideal target for immunotherapy (abstract). Kokhaei teach using tumor cells and tumor cell lysates in an autologous setting (abstract). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy (abstract). Kokhaei also teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2). Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 949 because 949 recites a specific peptide (claim 1). Thus one would have been motivated to use the peptide according to known methods. Martinez-Torres teach peptides comprising RFYVVMWK (page 4 first complete paragraph) and known uses thereof. Thus one would have been motived to use the peptide of 949 in such method. Further, Martinez-Torres teach advantages of the PKHB1 peptide in stability (page 20 first complete paragraph) so one would have been motivated to use the PKHB1 peptide. One would have had a reasonable expectation of success since methods of contacting were known and since Martinez-Torres teach advantageous effects. Further, Martinez-Torres teach peptides that are highly effective in treating chronic lymphocytic leukemia B cells (conclusions page 2). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy for B cell chronic lymphocytic leukemia (abstract). Since both references teach methods of treating chronic lymphocytic leukemia B cells the idea of combining the teachings flows logically from their having been individually taught in the art. For ease of administration, one would have been motivated to combine the cells and peptide prior to administration. Since Kokhaei also teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2) one would have also been motivated to administer cell lysates with the peptide. One would have had a reasonable expectation of success since Martinez-Torres teach decreased tumor growth with PKHB1 treatment in vivo (page 18 first paragraph). Kokhaei teach that apoptotic tumor cells (Apo-DC) induced beneficial responses and suggest loading with apoptotic bodies as a suitable approach for immunotherapy (abstract).
In relation to the peptide of claims 1 and 4, Martinez-Torres teach the PKHB1 peptide
and sequence (k-R-F-Y-V-V-M-W-K-k) (page 4 first complete paragraph) which is the elected
peptide.
In relation to collecting a cancer cell, Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’) which are leukemia cells.
In relation to the cancer cell of claims 1 and 5, Kokhaei teach using tumor cells and tumor cell lysates in an autologous setting (abstract). Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’) which are leukemia cells.
In relation to the contacting and administering of claim 1, for ease of administration, one would have been motivated to combine the cells and peptide prior to administration. Martinez-Torres expressly teach injection of PKHB1 (page 7 first complete paragraph).
In relation to the individual of clam 1, Kokhaei teach that blood was collected from B-CLL patients (page 1810 section ‘Patients’).
In relation to ‘of inducing immunogenic cell death’ and ‘wherein immunogenic cell death is characterized’ in claim 1, such phrase is an intended use (see MPEP 2111.02). With respect to ‘whereby immunogenic cell death of one or more cancer cells of the cancer is induced’, Martinez-Torres teach the PKHB1 peptide and sequence (k-R-F-Y-V-V-M-W-K-k) (page 4 first complete paragraph) which is the elected peptide. Such peptide would function as claimed since a compound and its properties are inseparable (MPEP 2112.01 II).
In relation to claim 12, Kokhaei teach that the use of cell lysates resulted in beneficial IFN-gamma secreting T cells (figure 4 and page 1813 paragraph connecting columns 1-2).
Response to Arguments – Double Patenting
Applicant's arguments filed 11/10/25 have been fully considered but they are not persuasive with respect to the rejections set forth above.
Although applicants argue that the claims have been amended, the amended claims are addressed above.
Although applicants argue about the teachings of the patents alone, 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). The specific teachings of the references and how the claim limitations are met are discussed in detail above.
Although applicants refer to arguments above, such arguments are not found persuasive for the reasons set forth above.
Conclusion
Applicant's amendment necessitated any new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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RONALD T. NIEBAUER
Primary Examiner
Art Unit 1658
/RONALD T NIEBAUER/Examiner, Art Unit 1658