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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 1/7/26 has been entered.
Election/Restrictions and Claim Status
Applicants’ amendments and arguments filed 1/7/26 are acknowledged. Any objection or rejection from the 10/23/25 office action that is not addressed below is withdrawn based on the amendments.
Previously, the species of enfortumab vedotin was elected.
As recognized by the applicant claims 24, 31-37 and 40-43 encompass the elected species.
Claims 27-30 and 38-39 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 5/20/25.
Newly added claims 44-45 read on the elected species.
Claims 1-23 and 25-26 have been canceled.
Claims 24, 31-37 and 40-45 are being examined.
Priority
The priority information is found in the filing receipt dated 1/22/25.
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.
Claims 24, 31-37 and 40-45 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 which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claims 24 and 37 refer to a ‘tumor sample’. Claim 45 refers to a tumor sample from plasma. The instant specification does not use the phrase tumor sample. It is unclear if a tumor sample is merely a sample from a patient with a tumor or if the tumor sample is a sample taken specifically from the tumor itself. None of the dependent claims clarify the claim scope. It is unclear if claims 44-45 are proper dependent claims since a tumor is made of tissue (claim 44) and since a tumor would be expected to include vasculature and plasma (claim 45).
Although unclear, the claims have been interpreted as including no new matter.
Claim Rejections - 35 USC § 103
Claims were previously rejected based on the references cited below. Since the claims have been amended, the rejections are updated to correspond to the instant claims.
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.
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) 24, 31-37 and 40-45 is/are rejected under 35 U.S.C. 103 as being unpatentable over Riester et al. (‘Integrative analysis of 1q23.3 copy-number gain in metastatic urothelial carcinoma’ Clinical Cancer Research v20(7) April 1, 2014 pages 1873-1883; ‘Riester’) in view of Riester et al. supplement (Supplement to ‘Integrative analysis of 1q23.3 copy-number gain in metastatic urothelial carcinoma’ Clinical Cancer Research v20(7) April 1, 2014, pages 1-13; ‘RiesterSupplement’) in view of Challita-Eid et al. (‘Enfortumab vedotin antibody-drug conjugate targeting nectin-4 is a highly potent therapeutic agent in multiple preclinical cancer models’ Cancer Research v76(10) May 15, 2016 pages 3003-3013 as cited with IDS 1/16/25; ‘Challita-Eid’).
Riester teach that urothelial carcinoma of the bladder is associated with copy number alterations and that the copy number alterations were evaluated to identify predictors of poor survival (abstract purpose section). Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875). Riester teach Nanostring as a quantitative measure of expression (page 1876 last paragraph). Riester teach that the PVRL4 gene encodes for Nectin-4 (page 1881 last complete paragraph). Riester teach that PVRL4 may play a pathogenic role in the aggressiveness of urothelial cancer (page 1874 first paragraph). Riester teach that data from other cancers suggest that Nectin-4 is associated with poor outcomes and that high levels of Nectin-4 are associated with poor survival (page 1881 last complete paragraph). Riester refers to copy number gains and amplifications as reported in the supplementary data (page 1881 last complete paragraph). In figures S12-S13, RiesterSupplement teach that copy number gains and amplification increased PVRL4 mRNA levels significantly. Riester states that PVRL4 and another gene displayed the most profound expression changes (page 1876 last paragraph). Riester teach improved survival of urothelial cancer with treatment (14 months versus 6 months) and teach a need for new treatment approaches (page 1873 paragraph connecting columns 1-2).
Riester does not administer a drug conjugate targeting Nectin-4.
Challita-Eid teach that nectin-4 was identified as a target in epithelial cancers (abstract). Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract). Challita-Eid teach that the findings validate nectin-4 as an attractive therapeutic target (abstract). Challita-Eid teach that nectin-4 overexpression in human tumor in breast, bladder, pancreas and lung suggest that a significant proportion of patients may benefit from nectin-4 targeted delivery (page 3012 last paragraph before disclosure of potential conflicts of interest).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of Riester based on the teachings and suggestions of Riester. Since Riester teach that PVRL4 may play a pathogenic role in the aggressiveness of urothelial cancer (page 1874 first paragraph) and RiesterSupplement teach that copy number gains and amplification increased PVRL4 mRNA levels significantly (figures S12-S13) one would have been motivated to identify such subjects. Since Riester teach a need for new treatment approaches (page 1873 paragraph connecting columns 1-2) and teach that PVRL4 may play a pathogenic role in the aggressiveness of urothelial cancer (page 1874 first paragraph) one would have been motivated to use known methods of targeting PVRL4 as taught by Challita-Eid. Specifically, Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Since Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract) one would have been motivated to administer to subjects. One would have had a reasonable expectation of success since Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875). Further, Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract).
In relation to detecting of claim 24, Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString in which mRNA was extracted from tumors (paragraph connecting pages 1874-1875).
In relation to the selecting a patient as in claim 24, Riester teach that urothelial carcinoma of the bladder is associated with copy number alterations and that the copy number alterations were evaluated to identify predictors of poor survival (abstract purpose section). RiesterSupplement teach that copy number gains and amplification (subjects with amplification would have a copy number of more than 2) increased PVRL4 mRNA levels significantly (figures S12-S13). Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875).
In relation to the drug conjugate of claims 24, 31 and 32-34, Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract). Challita-Eid teach that the findings validate nectin-4 as an attractive therapeutic target (abstract). Since Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract) one would have been motivated to administer to subjects.
In relation to claims 35-36, Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract).
In relation to the drug conjugate of claims 37 and 40-42, Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract). Challita-Eid teach that the findings validate nectin-4 as an attractive therapeutic target (abstract). Since Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract) one would have been motivated to administer to subjects.
In relation to the subject diagnosed with a certain copy number as in claim 37, Riester teach that urothelial carcinoma of the bladder is associated with copy number alterations and that the copy number alterations were evaluated to identify predictors of poor survival (abstract purpose section). RiesterSupplement teach that copy number gains and amplification (subjects with amplification would have a copy number of more than 2) increased PVRL4 mRNA levels significantly (figures S12-S13). Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875).
In relation to claim 43, Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract).
In relation to claims 44-45, Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString in which mRNA was extracted from tumors (paragraph connecting pages 1874-1875). Although unclear (see 112 rejection) since a tumor is made of tissue and a tumor would be expected to include vasculature and plasma the claim limitations have been interpreted as being met.
Response to Arguments - 103
Applicant's arguments filed 1/7/26 have been fully considered but they are not persuasive.
Although applicants argue about the teachings of Klumper, it is first noted that the Klumper reference does not appear to be of record. Further, applicants appear to indicate that Klumper is dated 2024 so it is not prior art.
Although applicants argue about teachings that enable prospective patient enrichment, there are no enablement rejections of record. Arguments related to 35 USC 112(a) do not appear to be relevant to a 35 USC 103 rejection.
Although applicants argue about the teachings of the references alone, 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).
Although applicants argue about clinical significance and therapeutic implications, none of the active steps require effective amounts or effective treatments (merely administering for example). Further, Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract). Challita-Eid teach that the findings validate nectin-4 as an attractive therapeutic target (abstract).
Although applicants refer to an unexpected correlation between Nectin-4 copy number and Nectin-4 mRNA expression, Riester teach that the PVRL4 gene encodes for Nectin-4 (page 1881 last complete paragraph). In figures S12-S13, RiesterSupplement teach that copy number gains and amplification increased PVRL4 mRNA levels significantly. Riester states that PVRL4 and another gene displayed the most profound expression changes (page 1876 last paragraph). Thus, it is unclear why applicants assert that such results are unexpected since the results of Riester are consistent with applicants conclusion related to example 6.
Although applicants refer to surprising findings related to tumors with high Nectin-4 expression responding to Nectin-4 targeted conjugates, Challita-Eid teach nectin-4 overexpression in human tumor in breast, bladder, pancreas and lung suggest that a significant proportion of patients may benefit from nectin-4 targeted delivery (page 3012 last paragraph before disclosure of potential conflicts of interest). Challita-Eid expressly states that high mRNA expression of nectin 4 make it an ADC (antibody drug conjugate) target (page 3003 last paragraph). Thus, it is unclear why applicants assert that such results are unexpected.
Although applicants argue about the complexity of gene regulation, the factual support for such assertion has not been provided (compare MPEP 2145 I).
Although applicants argue about an expectation of using a reliable biomarker for identifying responsive patients, such language does not seem to appear in the claims. Claims 24 and 37 recite active steps that include administering.
Although applicants argue (including via a previous declaration) that example 6 establishes that increased Nectin-4 copy number variation was associated with elevated Nectin-4 mRNA expression, MPEP 716.02(e) specifically recognizes that evidence of unexpected results must compare the claimed invention with the closest prior art. In the instant case, there appears to be no comparison. However, a comparison can be readily made. Riester teach that the PVRL4 gene encodes for Nectin-4 (page 1881 last complete paragraph). In figures S12-S13, RiesterSupplement teach that copy number gains and amplification increased PVRL4 mRNA levels significantly. Riester states that PVRL4 and another gene displayed the most profound expression changes (page 1876 last paragraph). Thus, the results of Riester are consistent with applicants conclusion related to example 6. MPEP 716.02(b) states that the burden is on the applicant to establish that results are unexpected and significant. The arguments as provided are not adequate to establish that any results are unexpected.
Although applicants argue (including via a previous declaration) that example 9 demonstrates treatment with Nectin-4 targeted drug conjugates correlates with Nectin-4 protein expression, MPEP 716.02(e) specifically recognizes that evidence of unexpected results must compare the claimed invention with the closest prior art. In the instant case, there appears to be no comparison. First, it is noted that Nectin-4 targeted drug conjugates, based on the nature of targeting Nectin-4, would be dependent on Nectin-4 expression. Challita-Eid teach nectin-4 overexpression in human tumor in breast, bladder, pancreas and lung suggest that a significant proportion of patients may benefit from nectin-4 targeted delivery (page 3012 last paragraph before disclosure of potential conflicts of interest). Challita-Eid expressly states that high mRNA expression of nectin 4 make it an ADC (antibody drug conjugate) target (page 3003 last paragraph). Thus, the results of Challita-Eid are consistent with applicants conclusion related to example 9. MPEP 716.02(b) states that the burden is on the applicant to establish that results are unexpected and significant. The arguments as provided are not adequate to establish that any results are unexpected. MPEP 716.02(c) states that expected beneficial results are evidence of obviousness. Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract).
Although applicants argue that Riester teaches away by disclosing that PVRL4 is not a strong predictor of survival, Riester recognizes that identification of drivers of the disease are what is used to yield therapeutic opportunities (page 1882 first complete paragraph). Thus, one would have been motivated to identify the drivers of the disease. Riester teach that PVRL4 may play a pathogenic role in the aggressiveness of urothelial cancer (page 1874 first paragraph). Riester teach that data from other cancers suggest that Nectin-4 is associated with poor outcomes and that high levels of Nectin-4 are associated with poor survival (page 1881 last complete paragraph). Riester refers to copy number gains and amplifications as reported in the supplementary data (page 1881 last complete paragraph). In figures S12-S13, RiesterSupplement teach that copy number gains and amplification increased PVRL4 mRNA levels significantly. Riester states that PVRL4 and another gene displayed the most profound expression changes (page 1876 last paragraph).
Although applicants argue that there is no reasonable expectation of success, MPEP 2143.02 recognizes that conclusive proof of efficacy is not required to show a reasonable expectation of success. Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract). Challita-Eid teach that the findings validate nectin-4 as an attractive therapeutic target (abstract). Challita-Eid teach that nectin-4 overexpression in human tumor in breast, bladder, pancreas and lung suggest that a significant proportion of patients may benefit from nectin-4 targeted delivery (page 3012 last paragraph before disclosure of potential conflicts of interest).
Although applicants argue about HER2 and companion diagnostics, it is first noted that the instant claims do not appear to relate to HER2 or companion diagnostics. Further, any factual support for such assertions has not been provided (compare MPEP 2145 I).
Further, MPEP 716.01(c) states that with respect to opinion testimony that the examiner must consider: “the nature of the matter sought to be established, the strength of any opposing evidence, the interest of the expert in the outcome of the case, and the presence or absence of factual support for the expert’s opinion”. In the instant case it appears that the nature of the matter sought is to establish unexpected results to overcome the 103 rejection. With respect to the strength of the opposing evidence, the teachings of the references are discussed in detail above. With respect to interest of the expert, the affidavit is signed by an instant inventor who presumably has a vested interest in the outcome of the case. With respect to the presence or absence of factual support, there appears to be no comparison to the prior art (see MPEP 716.02(e)). Thus there is no bases to conclude unexpected results.
Further, MPEP 716.02(d) states that any unexpected results are to be commensurate in scope with the claimed invention. Claims 24 and 37 broadly refer to ‘patient’ which encompasses any type of subject (human, dog, ape, etc.) and broadly refer to tumor which encompasses any type of tumor. In addition, claims 24 and 37 broadly refer to ‘drug conjugate targeting Nectin-4’ which is broad with respect to the type of drug.
The affidavit under 37 CFR 1.132 filed 9/29/25 is insufficient to overcome the rejection of the claims under 103 as set forth above because: MPEP 716.02(b) recognizes that the burden is on the applicant to establish that results are unexpected and MPEP 716.02(e) refers to comparing to the prior art. In view of the foregoing, when all of the evidence is considered, the totality of the rebuttal evidence of nonobviousness fails to outweigh the evidence of obviousness.
Although applicants argue about hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
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 24, 31-37 and 40-45 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-21 of U.S. Patent No. 11,453,702 (702) in view of Riester et al. (‘Integrative analysis of 1q23.3 copy-number gain in metastatic urothelial carcinoma’ Clinical Cancer Research v20(7) April 1, 2014 pages 1873-1883; ‘Riester’) in view of Riester et al. supplement (Supplement to ‘Integrative analysis of 1q23.3 copy-number gain in metastatic urothelial carcinoma’ Clinical Cancer Research v20(7) April 1, 2014, pages 1-13; ‘RiesterSupplement’) in view of Challita-Eid et al. (‘Enfortumab vedotin antibody-drug conjugate targeting nectin-4 is a highly potent therapeutic agent in multiple preclinical cancer models’ Cancer Research v76(10) May 15, 2016 pages 3003-3013 as cited with IDS 1/16/25; ‘Challita-Eid’).
702 recites treating a cancer in a patient having an increased copy number variation of Nectin-4 comprising administering to the patient a compound (claim 20) specifically a patient with bladder cancer (claim 21).
702 does not specifically recite how much of an increase in copy number variation nor does 702 recite an antibody drug conjugate.
Riester teach that urothelial carcinoma of the bladder is associated with copy number alterations and that the copy number alterations were evaluated to identify predictors of poor survival (abstract purpose section). Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875). Riester teach Nanostring as a quantitative measure of expression (page 1876 last paragraph). Riester teach that the PVRL4 gene encodes for Nectin-4 (page 1881 last complete paragraph). Riester teach that PVRL4 may play a pathogenic role in the aggressiveness of urothelial cancer (page 1874 first paragraph). Riester teach that data from other cancers suggest that Nectin-4 is associated with poor outcomes and that high levels of Nectin-4 are associated with poor survival (page 1881 last complete paragraph). Riester refers to copy number gains and amplifications as reported in the supplementary data (page 1881 last complete paragraph). In figures S12-S13, RiesterSupplement teach that copy number gains and amplification increased PVRL4 mRNA levels significantly. Riester states that PVRL4 and another gene displayed the most profound expression changes (page 1876 last paragraph). Riester teach improved survival of urothelial cancer with treatment (14 months versus 6 months) and teach a need for new treatment approaches (page 1873 paragraph connecting columns 1-2).
Challita-Eid teach that nectin-4 was identified as a target in epithelial cancers (abstract). Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract). Challita-Eid teach that the findings validate nectin-4 as an attractive therapeutic target (abstract). Challita-Eid teach that nectin-4 overexpression in human tumor in breast, bladder, pancreas and lung suggest that a significant proportion of patients may benefit from nectin-4 targeted delivery (page 3102 last paragraph before disclosure of potential conflicts of interest).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 702 based on the teachings and suggestions of 702. Since 702 refers to increased copy number of Nectin-4 (claim 20) one would have been motivated to incorporate the teachings and suggestions of Riester. Since Riester teach that PVRL4 may play a pathogenic role in the aggressiveness of urothelial cancer (page 1874 first paragraph) and RiesterSupplement teach that copy number gains and amplification increased PVRL4 mRNA levels significantly (figures S12-S13) one would have been motivated to identify such subjects. Since Riester teach a need for new treatment approaches (page 1873 paragraph connecting columns 1-2) and teach that PVRL4 may play a pathogenic role in the aggressiveness of urothelial cancer (page 1874 first paragraph) one would have been motivated to use known methods of targeting PVRL4 as taught by Challita-Eid. Specifically, Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Since Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract) one would have been motivated to administer to subjects. One would have had a reasonable expectation of success since Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875). Further, Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract).
In relation to the detecting of claim 24, Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString in which mRNA was extracted from tumors (paragraph connecting pages 1874-1875).
In relation to the selecting a patient as in claim 24, 702 recites a patient having increased copy number variation (claim 20). Riester teach that urothelial carcinoma of the bladder is associated with copy number alterations and that the copy number alterations were evaluated to identify predictors of poor survival (abstract purpose section). RiesterSupplement teach that copy number gains and amplification (subjects with amplification would have a copy number of more than 2) increased PVRL4 mRNA levels significantly (figures S12-S13). Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875).
In relation to the drug conjugate of claims 24, 31 and 32-34, Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract). Challita-Eid teach that the findings validate nectin-4 as an attractive therapeutic target (abstract). Since Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract) one would have been motivated to administer to subjects.
In relation to claims 35-36, Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract).
In relation to the drug conjugate of claims 37 and 40-42, Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract). Challita-Eid teach that the findings validate nectin-4 as an attractive therapeutic target (abstract). Since Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract) one would have been motivated to administer to subjects.
In relation to the subject diagnosed with a certain copy number as in claim 37, Riester teach that urothelial carcinoma of the bladder is associated with copy number alterations and that the copy number alterations were evaluated to identify predictors of poor survival (abstract purpose section). RiesterSupplement teach that copy number gains and amplification (subjects with amplification would have a copy number of more than 2) increased PVRL4 mRNA levels significantly (figures S12-S13). Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875).
In relation to claim 43, Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract).
In relation to claims 44-45, Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString in which mRNA was extracted from tumors (paragraph connecting pages 1874-1875). Although unclear (see 112 rejection) since a tumor is made of tissue and a tumor would be expected to include vasculature and plasma the claim limitations have been interpreted as being met.
Claims 24, 31-37 and 40-45 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-24 of U.S. Patent No. 11,180,531 (531) in view of Riester et al. (‘Integrative analysis of 1q23.3 copy-number gain in metastatic urothelial carcinoma’ Clinical Cancer Research v20(7) April 1, 2014 pages 1873-1883; ‘Riester’) in view of Riester et al. supplement (Supplement to Integrative analysis of 1q23.3 copy-number gain in metastatic urothelial carcinoma’ Clinical Cancer Research v20(7) April 1, 2014, pages 1-13; ‘RiesterSupplement’) in view of Challita-Eid et al. (‘Enfortumab vedotin antibody-drug conjugate targeting nectin-4 is a highly potent therapeutic agent in multiple preclinical cancer models’ Cancer Research v76(10) May 15, 2016 pages 3003-3013 as cited with IDS 1/16/25; ‘Challita-Eid’).
531 recites treating a cancer patient having an increased copy number variation of Nectin-4 comprising administering to the patient a compound (claim 24).
531 does not specifically recite how much of an increase in copy number variation nor does 531 recite an antibody drug conjugate.
Riester teach that urothelial carcinoma of the bladder is associated with copy number alterations and that the copy number alterations were evaluated to identify predictors of poor survival (abstract purpose section). Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875). Riester teach Nanostring as a quantitative measure of expression (page 1876 last paragraph). Riester teach that the PVRL4 gene encodes for Nectin-4 (page 1881 last complete paragraph). Riester teach that PVRL4 may play a pathogenic role in the aggressiveness of urothelial cancer (page 1874 first paragraph). Riester teach that data from other cancers suggest that Nectin-4 is associated with poor outcomes and that high levels of Nectin-4 are associated with poor survival (page 1881 last complete paragraph). Riester refers to copy number gains and amplifications as reported in the supplementary data (page 1881 last complete paragraph). In figures S12-S13, RiesterSupplement teach that copy number gains and amplification increased PVRL4 mRNA levels significantly. Riester states that PVRL4 and another gene displayed the most profound expression changes (page 1876 last paragraph). Riester teach improved survival of urothelial cancer with treatment (14 months versus 6 months) and teach a need for new treatment approaches (page 1873 paragraph connecting columns 1-2).
Challita-Eid teach that nectin-4 was identified as a target in epithelial cancers (abstract). Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract). Challita-Eid teach that the findings validate nectin-4 as an attractive therapeutic target (abstract). Challita-Eid teach that nectin-4 overexpression in human tumor in breast, bladder, pancreas and lung suggest that a significant proportion of patients may benefit from nectin-4 targeted delivery (page 3102 last paragraph before disclosure of potential conflicts of interest).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 531 based on the teachings and suggestions of 531. Since 531 refers to increased copy number of Nectin-4 (claim 24) one would have been motivated to incorporate the teachings and suggestions of Riester. Since Riester teach that PVRL4 may play a pathogenic role in the aggressiveness of urothelial cancer (page 1874 first paragraph) and RiesterSupplement teach that copy number gains and amplification increased PVRL4 mRNA levels significantly (figures S12-S13) one would have been motivated to identify such subjects. Since Riester teach a need for new treatment approaches (page 1873 paragraph connecting columns 1-2) and teach that PVRL4 may play a pathogenic role in the aggressiveness of urothelial cancer (page 1874 first paragraph) one would have been motivated to use known methods of targeting PVRL4 as taught by Challita-Eid. Specifically, Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Since Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract) one would have been motivated to administer to subjects. One would have had a reasonable expectation of success since Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875). Further, Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract).
In relation to detecting of claim 24, Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString in which mRNA was extracted from tumors (paragraph connecting pages 1874-1875).
In relation to the selecting a patient as in claim 24, 531 recites a patient having increased copy number variation (claim 24). Riester teach that urothelial carcinoma of the bladder is associated with copy number alterations and that the copy number alterations were evaluated to identify predictors of poor survival (abstract purpose section). RiesterSupplement teach that copy number gains and amplification (subjects with amplification would have a copy number of more than 2) increased PVRL4 mRNA levels significantly (figures S12-S13). Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875).
In relation to the drug conjugate of claims 24, 31 and 32-34, Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract). Challita-Eid teach that the findings validate nectin-4 as an attractive therapeutic target (abstract). Since Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract) one would have been motivated to administer to subjects.
In relation to claims 35-36, Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract).
In relation to the drug conjugate of claims 37 and 40-42, Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract). Challita-Eid teach that the findings validate nectin-4 as an attractive therapeutic target (abstract). Since Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract) one would have been motivated to administer to subjects.
In relation to the subject diagnosed with a certain copy number as in claim 37, Riester teach that urothelial carcinoma of the bladder is associated with copy number alterations and that the copy number alterations were evaluated to identify predictors of poor survival (abstract purpose section). RiesterSupplement teach that copy number gains and amplification (subjects with amplification would have a copy number of more than 2) increased PVRL4 mRNA levels significantly (figures S12-S13). Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875).
In relation to claim 43, Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract).
In relation to claims 44-45, Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString in which mRNA was extracted from tumors (paragraph connecting pages 1874-1875). Although unclear (see 112 rejection) since a tumor is made of tissue and a tumor would be expected to include vasculature and plasma the claim limitations have been interpreted as being met.
Claims 24, 35-37 and 43-45 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 45-64 of copending Application No. 18802865 (reference application; ‘865’). Although the claims at issue are not identical, they are not patentably distinct from each other.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
865 recites a method of measuring Nectin-4 copy number in a tissue sample from a patient having a tumor, selecting the patient having a Nectin-4 copy number of more than two and administering a drug conjugate targeting Nectin-4 (claim 45). 865 specifically recites bladder cancer (claim 54).
In relation to claims 24 and 37, 865 reciters a method of measuring (i.e. detecting) Nectin-4 copy number in a tissue sample from a patient having a tumor, selecting the patient having a Nectin-4 copy number or more than two and administering a drug conjugate targeting Nectin-4 (claim 45).
In relation to claims 35-36 and 43, 865 specifically recites bladder cancer (claim 54).
In relation to claims 44-45, 865 recites a tissue sample from a tumor (claim 46).
Claims 24, 31-37 and 40-45 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 45-63 of copending Application No. 18802865 (865) in view of Riester et al. (‘Integrative analysis of 1q23.3 copy-number gain in metastatic urothelial carcinoma’ Clinical Cancer Research v20(7) April 1, 2014 pages 1873-1883; ‘Riester’) in view of Riester et al. supplement (Supplement to Integrative analysis of 1q23.3 copy-number gain in metastatic urothelial carcinoma’ Clinical Cancer Research v20(7) April 1, 2014, pages 1-13; ‘RiesterSupplement’) in view of Challita-Eid et al. (‘Enfortumab vedotin antibody-drug conjugate targeting nectin-4 is a highly potent therapeutic agent in multiple preclinical cancer models’ Cancer Research v76(10) May 15, 2016 pages 3003-3013 as cited with IDS 1/16/25; ‘Challita-Eid’).
This is a provisional nonstatutory double patenting rejection.
865 recites a method of measuring Nectin-4 copy number in a tissue sample from a patient having a tumor, selecting the patient having a Nectin-4 copy number of more than two and administering a drug conjugate targeting Nectin-4 (claim 45). 865 specifically recites bladder cancer (claim 54).
865 does not specifically recite an antibody drug conjugate.
Riester teach that urothelial carcinoma of the bladder is associated with copy number alterations and that the copy number alterations were evaluated to identify predictors of poor survival (abstract purpose section). Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875). Riester teach Nanostring as a quantitative measure of expression (page 1876 last paragraph). Riester teach that the PVRL4 gene encodes for Nectin-4 (page 1881 last complete paragraph). Riester teach that PVRL4 may play a pathogenic role in the aggressiveness of urothelial cancer (page 1874 first paragraph). Riester teach that data from other cancers suggest that Nectin-4 is associated with poor outcomes and that high levels of Nectin-4 are associated with poor survival (page 1881 last complete paragraph). Riester refers to copy number gains and amplifications as reported in the supplementary data (page 1881 last complete paragraph). In figures S12-S13, RiesterSupplement teach that copy number gains and amplification increased PVRL4 mRNA levels significantly. Riester states that PVRL4 and another gene displayed the most profound expression changes (page 1876 last paragraph). Riester teach improved survival of urothelial cancer with treatment (14 months versus 6 months) and teach a need for new treatment approaches (page 1873 paragraph connecting columns 1-2).
Challita-Eid teach that nectin-4 was identified as a target in epithelial cancers (abstract). Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract). Challita-Eid teach that the findings validate nectin-4 as an attractive therapeutic target (abstract). Challita-Eid teach that nectin-4 overexpression in human tumor in breast, bladder, pancreas and lung suggest that a significant proportion of patients may benefit from nectin-4 targeted delivery (page 3102 last paragraph before disclosure of potential conflicts of interest).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 865 based on the teachings and suggestions of 865. Since 865 refers to increased copy number of Nectin-4 (claim 45) one would have been motivated to incorporate the teachings and suggestions of Riester. Since Riester teach that PVRL4 may play a pathogenic role in the aggressiveness of urothelial cancer (page 1874 first paragraph) and RiesterSupplement teach that copy number gains and amplification increased PVRL4 mRNA levels significantly (figures S12-S13) one would have been motivated to identify such subjects. Since Riester teach a need for new treatment approaches (page 1873 paragraph connecting columns 1-2) and teach that PVRL4 may play a pathogenic role in the aggressiveness of urothelial cancer (page 1874 first paragraph) one would have been motivated to use known methods of targeting PVRL4 as taught by Challita-Eid. Specifically, Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Since Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract) one would have been motivated to administer to subjects. One would have had a reasonable expectation of success since Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875). Further, Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract).
In relation to the detecting of claim 24, Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString in which mRNA was extracted from tumors (paragraph connecting pages 1874-1875).
In relation to the selecting a patient as in claim 24, 865 recites a patient having increased copy number variation (claim 20). Riester teach that urothelial carcinoma of the bladder is associated with copy number alterations and that the copy number alterations were evaluated to identify predictors of poor survival (abstract purpose section). RiesterSupplement teach that copy number gains and amplification (subjects with amplification would have a copy number of more than 2) increased PVRL4 mRNA levels significantly (figures S12-S13). Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875).
In relation to the drug conjugate of claims 24, 31 and 32-34, Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract). Challita-Eid teach that the findings validate nectin-4 as an attractive therapeutic target (abstract). Since Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract) one would have been motivated to administer to subjects.
In relation to claims 35-36, Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract).
In relation to the drug conjugate of claims 37 and 40-42, Challita-Eid teach that a antibody drug conjugate named enfortumab vedotin comprises a human anti-nectin 4 antibody conjugated to MMAE that targets nectin-4 (abstract). Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract). Challita-Eid teach that the findings validate nectin-4 as an attractive therapeutic target (abstract). Since Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract) one would have been motivated to administer to subjects.
In relation to the subject diagnosed with a certain copy number as in claim 37, Riester teach that urothelial carcinoma of the bladder is associated with copy number alterations and that the copy number alterations were evaluated to identify predictors of poor survival (abstract purpose section). RiesterSupplement teach that copy number gains and amplification (subjects with amplification would have a copy number of more than 2) increased PVRL4 mRNA levels significantly (figures S12-S13). Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString (paragraph connecting pages 1874-1875).
In relation to claim 43, Challita-Eid teach that enfortumab vedotin significantly inhibited the growth of 4 tumour types (breast, bladder, pancreatic and lung) (abstract).
In relation to claims 44-45, Riester teach that copy number data was obtained from patients with urothelial carcinoma (abstract experimental design section) specifically by using NanoString in which mRNA was extracted from tumors (paragraph connecting pages 1874-1875). Although unclear (see 112 rejection) since a tumor is made of tissue and a tumor would be expected to include vasculature and plasma the claim limitations have been interpreted as being met.
Response to Arguments – Double Patenting
Applicant's arguments filed 1/7/26 have been fully considered but they are not persuasive.
Although applicants argue about reasons discussed above, as set forth above the reasons are not persuasive.
Further, Claims 24, 35-37 and 43-45 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 45-64 of copending Application No. 18802865 (reference application; ‘865’). The arguments above do not in any way address Application No. 18802865.
Conclusion
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RONALD T. NIEBAUER
Primary Examiner
Art Unit 1658
/RONALD T NIEBAUER/Examiner, Art Unit 1658
Prosecution Insights