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
Applicant’s election without traverse of Group I, claims 1, 4-7 in the reply filed on 3/10/2023 remains acknowledged.
Applicant’s election without traverse of:
(i) aripiprazole (claim 1);
(ii) claim 4 reading on the elected method under (i); and
(iii-a) administering in combination with irradiation (claim 6) during breast cancer treatment (claim 7),
in the reply filed on 3/10/2023 remains acknowledged.
Claims 2-3, 8-12, 14-24 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim.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 3/10/2023.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
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, 13 is/are rejected under 35 U.S.C. 103 as being unpatentable over Cho et al. (KR1020170026115; 2017 Mar 8; cited in a prior Office action); in view of Kim et al. (“Src is the primary target of aripiprazole, an atypical antipsychotic drug, in its anti-tumor action”; 2018; Oncotarget; Vol. 9 (No.5); 5979-5992; published 2017 Dec 8; cited in a prior Office action); Zerp et al.; (“Targeting anti-apoptotic Bcl-2 by AT-101 to increase radiation efficacy: data from in vitro and clinical pharmacokinetic studies in head and neck cancer”; 2015; Radiation Oncology; 10:158; DOI 10.1186/s13014-015-0474-9; cited in a prior Office action); Raju et al. (“Dasatinib, a multi-kinase inhibitor increased radiation sensitivity by interfering with nuclear localization of epidermal growth factor receptor and by blocking DNA repair pathways”; 2012; Radiotherapy and Oncology; 105: 241-249; cited in a prior Office action); and Emi et al. (“Targeted therapy against Bcl-2-related proteins in breast cancer cells”; 2005; Breast Cancer Research; 7:R940-R952; DOI 10.1186/bcr1323; cited in a prior Office action).
An English language machine translation of the KR publication was obtained from WIPO Patentscope (https://patentscope.wipo.int/search/en/detail.jsf?docPN=KR1020170026115, accessed 3/24/2023; cited in a prior Office action). The “translated” version of the Patent Application (filed 7/7/2016) (in English) is relied on for the English language teachings of Cho, supplied by WIPO.
Cho teaches compositions comprising aripiprazole for … treating cancer (Title), [0001]. Methods currently in use for treating cancer include radiation therapy [0002]. Aripiprazole may inhibit Src kinase activity [0013]. Aripiprazole may inhibit the expression of, inter alia, Bcl2 [0014]
It is an object of the present invention to provide a pharmaceutical composition for treating cancer, containing aripiprazole as an active ingredient [0007], [0011], satisfying the recited providing a composition comprising aripiprazole as an active ingredient (claim 1, lines 2-3). Another object of the present invention for
Figure 4 is a diagram showing the effect of aripiprazole on cancer cell proliferation in MDA-MB-231 cells [0021]:
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providing evidence of reduced cell viability as a function of concentration of Aripiprazole in breast cancer cells, having reduced viability as the time increases to 72 hours, at higher concentrations. See also [0047], documenting when aripiprazole was treated (including the MDA-MB-231 cells), the proliferation of cancer cells was inhibited in a concentration-dependent manner. Thus, selection of Applicant elected breast cancer for treatment with Aripiprazole would have been obvious from this data and teachings.
While Cho teaches both Aripiprazole and radiation therapy to treat cancers, such as breast cancer, Cho does not teach the elected combination of radiation irradiation during cancer treatment, required by amended claim 1. Because both are taught for the same purpose, namely treating cancer, it would have been obvious to combine Aripiprazole and radiation therapy, and to use the combination to treat, inter alia, breast cancer, rendering obvious the elected combination treatment.
MPEP 2144.06(I) indicates "It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art." In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980). In the instant case, aripiprazole as a composition, and radiation are each taught to be useful for the same purpose, rendering obvious their combination. See also KSR Rationale (A) Combining prior art elements according to known methods to yield predictable results (MPEP 2143 (I)(A)). Additive effects would have been the predicted results of the combination of aripiprazole plus radiation therapy; i.e., above that of radiation alone, predicted to achieve enhanced radiation sensitivity.
Regarding the recited “enhancing radiation sensitivity” (claim 1), the outcome of induced apoptosis of cancer cells by irradiation with radiation (claim 4) (aripiprazole promotion of apoptosis is taught, [0065]-[0068], just with aripiprazole; this would also be expected to occur when combined with radiation treatment), the composition induces PARP cleavage or DNA fragmentation of cancer cells (claim 5) ([0004] indicates AIF is a sign of caspase-independent apoptosis, and after apoptotic stimulation, it is translocated into the nucleus to induce DNA fragmentation), each of these are considered characteristic of the combination of, absent evidence to the contrary.
It is noted that In re Best (195 USPQ 430) and In re Fitzgerald (205 USPQ 594) discuss the support of rejections wherein the prior art discloses subject matter which there is reason to believe inherently includes functions that are newly cited or is identical to a product instantly claimed. In such a situation the burden is shifted to the applicants to "prove that subject matter shown to be in the prior art does not possess characteristic relied on" (205 USPQ 594, second column, first full paragraph).
The Examiner notes that it might be argued that the recited outcome of enhanced radiation sensitivity is not necessarily present in the obvious combination of radiation treatment and aripiprazole provision and administration. If this position were adopted, the following bases each predict enhanced radiation sensitivity from the combination of radiation and aripiprazole, giving the method of the claims:
First, Kim et al teaches, in a similar study to that of Cho, where Aripiprazole (ARP) suppressed cell proliferation of, inter alia, MDA-MB-231 (breast cancer) cells (abstract). ARP reduced the viability of … the breast cancer cell line MDA-MB-231… . Effects were dose and time dependent (Figure 1B, 1C, 1D, and 1E). Depending on treatment time (24 to 48 h), IC50 values for ARP were 17.7 µM to 80.6 µM (Table 1) (5980, 2nd paragraph).
Figure 6 is a schematic of parallel pathways of the antitumorigenic mechanisms of ARP. These include inhibition of Bcl-3, which is also taught by Cho, for ARP.
Zerp teaches targeting anti-apoptotic Bcl-2 by AT-101 increases radiation efficacy, providing data from in vitro and clinical pharmacokinetic studies in head and neck cancer (HNSCC) (title). Overexpression of Bcl-2 family members have been associated with radio- and chemoresistance and poor clinical outcome. Inhibition of anti-apoptotic Bcl-2 represents and appealing strategy to overcome resistance to anti-cancer therapies; the effect of the study was to evaluate combined effects of radiation and the pan-Bcl-2 inhibitor AT-101 in HNSCC in vitro. In addition, we determined human plasma levels of AT-101 obtained from a phase I/II trial, and compared them with the effective in vitro concentrations to substantiate therapeutic opportunities (Abstract/Background). The effect of AT-101, radiation and the combination of apoptosis induction and clonogenic survival in two HNSCC cell lines that express the target proteins (Methods). In vitro results showed that AT-101 enhances radiation-induced apoptosis with CI’s below 1.0, indicating synergy; a radiosensitizing effect was demonstrated (Results). The conclusion was that AT-101 is a competent enhancer of radiation -induced apoptosis in vitro; in addition, radiosensitization was observed at clinically attainable plasma levels; these results support further evaluation of the combination of AT-101 with radiation in Bcl-2-overexpressing tumors. The teachings of Zerp provide a basis, when ARP inhibits Bcl-2 levels, as taught by Cho and Kim, that ARP will also function to sensitize radiation, as occurred by AT-101.
Emi teaches that Bcl-2 confers resistance to apoptosis, thereby reducing the effectiveness of chemotherapy (abstract; Introduction). Four breast cancer cell lines were examined and the effects of, inter alia, antisense (AS) Bcl-2 phosphorothioate oligodeoxyneculeotides (ODNs) on chemosensitivity were tested (Methods). Treatment with AS Bcl-2 ODNs resulted in sequence-specific decrease in protein expression; in MDA-MB-231 cells with AS Bcl-2 increased chemosensitivity to a series of drugs (Results). AS Bcl-2 ODN is a targeted therapy against Bcl-2 protein, which is taught may enhance effects of chemotherapy in patients with breast cancer (Conclusion). Enhancement is shown in Table 1, ranging from 3.1- to 6.5-fold to the 4 chemotherapy drugs tested with MDA-MB-231 breast cancer cells.
Expression levels of Bcl-2 are shown in Figure 1 (a) & (b) for MDA-MB-231 (the same breast cancer cell line discussed by taught by Cho in Figure 4). Emi establishes this breast cancer taught by Cho expresses Bcl-2 protein (anti-apoptosis), reduction of Bcl-2 enhances apoptosis, and that enhancement to chemotherapy occurs when Bcl-2 levels are reduced. The skilled artisan would have reasonably also expected reduction of Bcl-2 levels by aripiprazole, according to the teachings of Cho, and reduction of Bcl-2 levels would have been reasonably predicted to result in increased sensitivity to radiation, based on teachings of Zerp, at least for Bcl-2 expressing cancers, such as MDA-MB-231. Thus, the mechanism of Bcl-2 reduction attributed to Aripiprazole would have reasonably been expected to enhance radiation sensitivity in the obvious combination of radiation + aripiprazole.
Secondly, Kim further teaches purified Src kinase activity is reduced in a ARP concentration dependent manner (Figure 4 B). As summarized in Figure 6, ARP induced apoptosis and suppressed the migration of glioma cells by targeting Src in in vitro and in vivo anti-cancer activities. Currently, several anticancer drugs on the market or under development inhibit Src kinase. One example is dasatinib. Our findings suggest that ARP may be useful as an anticancer drug that directly inhibits Src kinase (5985, right, 2nd paragraph).
Regarding dasatinib, Raju teaches inhibition of epidermal growth factor receptor (EGFR) signaling during radiation led to improvement of tumor control and survival, novel strategies are needed to further improve the outcome of patients with locally advanced head and neck carcinoma. Because EGFR is known to interact with c-Src kinases, the present study investigated dasatinib, an inhibitor of c-Src kinases, for its efficacy in enhancing radiosensitivity of human head and neck squamous cell carcinomas (HNSCC) in vitro and examined the underlying mechanisms for this effect (Abstract/Background). Dasatinib suppressed cell survival of six HNSCC cell lines tested independent of c-Src or EGFR levels but enhanced radiosensitivity of two lines, that had higher levels of EGFR (Results). In conclusion dasatinib induces apoptosis and blocks DNA repair in EGFR-expressing HNSCC cells and improves radiotherapy outcome; these results warrant further investigation using in vivo tumor models for potential translation into clinical testing. Thus, the showing with dasatinib, that this compound is art-recognized as a Src kinase inhibitor, and improves radiotherapy, leads to a reasonable expectation that ARP, as a Src kinase inhibitor, will have a similar improvement of radiation therapy.
The skilled artisan, with recognition that aripiprazole is known to be Src kinase inhibitor, will also be expected to enhance radiation therapy, based on Src kinase inhibition mechanism. Thus, there are 2 unique mechanisms of action, each of which predicts enhanced sensitivity to radiation.
Response to Arguments
As previously stated: The Declaration of Young Bin Lim under 37 CFR 1.132 filed 1/8/2025 is insufficient to overcome the rejection of claims 1, 4-5, 13 based upon Cho et al. (KR1020170026115; 2017 Mar 8; cited in a prior Office action); in view of Kim et al. (“Src is the primary target of aripiprazole, an atypical antipsychotic drug, in its anti-tumor action”; 2018; Oncotarget; Vol. 9 (No.5); 5979-5992; published 2017 Dec 8); Zerp et al.; (“Targeting anti-apoptotic Bcl-2 by AT-101 to increase radiation efficacy: data from in vitro and clinical pharmacokinetic studies in head and neck cancer”; 2015; Radiation Oncology; 10:158; DOI 10.1186/s13014-015-0474-9); Raju et al. (“Dasatinib, a multi-kinase inhibitor increased radiation sensitivity by interfering with nuclear localization of epidermal growth factor receptor and by blocking DNA repair pathways”; 2012; Radiotherapy and Oncology; 105: 241-249); and Emi et al. (“Targeted therapy against Bcl-2-related proteins in breast cancer cells”; 2005; Breast Cancer Research; 7:R940-R952; DOI 10.1186/bcr1323) as set forth above because:
Examiner notes that the elected aripiprazole in combination with radiation in treatment of breast cancer elected species is under examination. A study beyond obviousness of breast cancer has not been conducted. Regarding the Declaration, most of the studies described do not involve any breast cancer. Regarding breast cancer, e (p. 4) argues that MCF-7 (breast cancer) xenografts in mice indicates aripiprazole sensitizes to radiation in vivo. Examiner notes that the claims are not limited to MCF-7 as a breast cancer, and the rejection of record establishes the MDA-MB-231 (breast cancer cell line taught by Cho in Figure 4) expresses Bcl-2; there is a reasonable expectation of sensitization by aripiprazole to radiation via reduction of Bcl-2 expression. Sensitivity to radiation is also predicted based on inhibition of Src kinase. Thus, the observation that aripiprazole sensitizes a specific breast cancer to radiation is not considered to establish an unexpected result.
As discussed in MPEP 716.02(c), "Expected beneficial results are evidence of obviousness of a claimed invention, just as unexpected results are evidence of unobviousness thereof." In re Gershon, 372 F.2d 535, 538, 152 USPQ 602, 604 (CCPA 1967) (resultant decrease of dental enamel solubility accomplished by adding an acidic buffering agent to a fluoride containing dentifrice was expected based on the teaching of the prior art). This finding does not establish anything unexpected.
Regarding f & g, synthetic lethality is argued for the MCF-7 cells. Examiner notes that an apoptosis increase is predicted for MDA-MB-231 breast cancer, via each of the mechanisms of action relied on in the rejection basis.
Examiner notes that while the Declaration argues Aripiprazole does not radiosensitize cells through alteration of BCL2, the Declaration does not test MDA-MB-231, and conclusions based on a different breast cancer cell line do not necessarily establish the mechanism by which treatment based on MDA-MB-231 would occur.
In fact, the argument of the Declaration is in direct conflict with Kim, which tested ARP being applied to a series of cancer lines, including MDA-MB-231, and reduction of Bcl-2 protein and mRNA levels is clearly reported (abstract). Thus, the conclusion of the Declaration is in conflict with Kim data. This would reasonably be taken in that the observation of the Declaration cannot be applied generically, nor for the specific MDA-MB-231 breast cancer cells the rejection relies on. Examiner again notes there is no limitation in the claims that limits breast cancer to MCF-7 type cells, or those for which there is no BLC2 involvement (or involving NOXA, per h of the Declaration). Amended claim 1 recites 13 alternative cancer types, only one of these being a generic breast cancer. And there appears to be differences between MDA-MB-231 and MCF-7 breast cancer cells.
Examiner notes that treatment by Emi with an agent antisense to Bcl-2 results in reduction of Bcl-2 antiapoptotic protein levels (Emi, R951, Conclusion paragraph), in addition to the Bcl-2 reduction specifically recognized by Kim. The inhibition of Bcl-2 suggested by Cho and taught by Kim by aripiprazole is also predicted to enhance apoptosis, and sensitize MDA-MB-231 to radiation.
While the arguments of Young Bin Lim seem to be premised on observations for MCF-7 being applicable to all breast cancers, review of Emi demonstrates that 4 unique breast cancers have differential responses: One determining factor might be the differential expression of Bcl-2 and Bcl-xL in breast cancer cells. Overexpression of Bcl-2 is observed more frequently than overexpression of Bcl-xL (70% versus 40%) in breast cancer tissue, which suggests a more important role for Bcl-2 in conferring drug resistance (Emi, R951, Conclusion paragraph). Thus, a showing for one cancer, that does not even correspond to the breast cancer cell line taught by the prior art, cannot be relied on for the full scope of treatments of breast cancers (one embodiment of amended claim 1).
The Examiner notes that synergy has been established by some of the evidence presented in the Lim Declaration, as is argued by Applicant. However, there are two bases in the applied rejection that predict synergy, at least for MDA-MB-231 type breast cancer. While it is possible that a unique mechanism of action is demonstrated by the declaration, at least for MCF-7 breast cancer, it has not been established that this is generically applicable to breast cancers, or that the arguments made in the Declaration apply to MDA-MB-231 (or alternative types of breast cancers, treated by aripiprazole and radiation combinations).
Nonetheless, the evidence only shows synergy for limited sets of combinations, Appendix B-4 for MCF-7 appears to demonstrate synergy for: DNA Fragmentation in MCF-7 for 20 µM Ari and 2.5-5 Gy IR, is accompanied by a reported CI demonstrating synergy. While arguments are made about enhancing radiation sensitivity (synergy between IR and Ari), the Examiner does not see other evidence that is applicable to breast cancer. For instance, Appendix B-2, which provides CI data for 6 cancers, does not present any evidence applicable to any breast cancer (even MCF-7 is not shown). Appendix B6 does not present data for Ari without IR in breast cancer; thus, this evidence is not construed to support argument of synergy applicable to the elected cancer. The evidence from Cho indicates a concentration dependence of Ari alone. Thus, B6 data are inconclusive about synergy on MCF-7. Thus, the evidence supports only a very narrow range of a combination of IR and Ari concentrations. None of the claims recite any doses of either aripiprazole or radiation.
MPEP 716.02(d) indicates unexpected results must be commensurate in scope with the claims which the evidence is offered to support. For the elected breast cancer, this is not the case for any rejected claim, even if the evidence were considered to be unexpected (not the position adopted, because enhanced radiation is predicted by the rejection basis for 2 unique mechanistic considerations; see MPEP 716.02(c), which makes clear expected results are evidence of obviousness). Thus, evidence cannot be taken to be commensurate in scope with any rejected claim.
Regarding the 2nd Declaration of Young Bin Lim, filed 7/14/2025, Supplemental Ex 1 is argued to show aripiprazole treatment alone did not affect tumor growth. This is clearly in conflict with the evidence of the rejection from Cho:
Figure 4 is a diagram showing the effect of aripiprazole on cancer cell proliferation in MDA-MB-231 cells [0021]:
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providing evidence of reduced cell viability as a function of concentration of Aripiprazole in breast cancer cells, having reduced viability as the time increases to 72 hours, at higher concentrations.
The Young Bin Lim example clearly conflicts with aripiprazole cell viability concentration dependence. This is clearly demonstrative that the evidence does not correspond to tests comparing the closest prior art, based on Aripiprazole and MDA-MB-231 breast adenocarcinoma studies.
The declaration continues to discuss synergy in tumor volume when aripiprazole and IR is studied, relative to IR alone.
Regarding the studies of tumor growth in head and neck cancer, this cancer is not under examination.
Supplemental Example 2 studies synergistic effect of aripiprazole and IR on BT-474 breast cancer cells.
Examiner again notes that these studies do not provide any evidence for MDA-MB-231 breast cancer cells, on which the rejection relies, and is predictive of enhancing radiation sensitivity.
Applicant argues that Cho and Kim do not teach aripiprazole as a Bcl-2 inhibitor in MDA-MB-231 cells. The inhibition of Bcl2 by aripiprazole is clear from claim 4 of Cho
Regarding Zerp, the Examiner acknowledges that AT-101 added after radiation increases radiation efficiency, but not with or before. Even so, reliant on the Cis below 1.0 to demonstrate synergy, Zerp clearly characterizes this behavior as “AT-101 is a competent enhancer of radiation induced apoptosis”; i.e., reading on the requirement of claim 1, enhancing radiation sensitivity. The use of aripiprazole, taught to decrease Bcl-2, would have reasonably been expected to enhance radiation sensitivity when combined with radiation for treating MDA-MB-231.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The 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/process/file/efs/guidance/eTD-info-I.jsp.
Claims 1, 4-5, 13 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 6-8, 13-15 of copending Application No. 17/937778 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claim sets have substantially similar elements, the copending claims recite the elected species of the instant claims, rendering obvious the same subject matter in each claim set.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Applicant again improperly requests this provisional rejection be held in abeyance.
The Examiner notes that MPEP 804 (I) (B) (1) indicates:
A complete response to a nonstatutory double patenting rejection (also called an "obviousness-type" or ODP rejection) is either a reply by applicant showing that the claims subject to the rejection are patentably distinct from the reference claims or the filing of a terminal disclaimer in accordance with 37 CFR 1.321 in the pending application(s) with a reply to the Office action (see MPEP § 1490 for a discussion of terminal disclaimers). Such a response is required even when the nonstatutory double patenting rejection is provisional.
…
As filing a terminal disclaimer, or filing a showing that the claims subject to the rejection are patentably distinct from the reference application’s claims, is necessary for further consideration of the rejection of the claims, such a filing should not be held in abeyance. Only objections or requirements as to form not necessary for further consideration of the claims may be held in abeyance until allowable subject matter is indicated.
Neither argument that the claims are patentably distinct over each other, nor the filing of a terminal disclaimer reply options have been pursued. Applicant is cautioned that a request to hold the provisional ODP rejection in abeyance or drop the provisional rejection is still not considered a complete response.
Conclusion
No claim is allowed.
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to TIMOTHY P THOMAS whose telephone number is (571)272-8994. The examiner can normally be reached M-Th 6:30-5:00.
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TIMOTHY P. THOMAS
Primary Examiner
Art Unit 1614
/TIMOTHY P THOMAS/Primary Examiner, Art Unit 1614