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 .
Priority
The present Application, filed December 19, 2023, is a continuation of International Patent Application No. PCT/US2022/034383, filed June 21, 2022, which claims the benefit of U.S. Provisional Patent Application No. 63/202,770, filed June 23, 2021.
Status of the Claims
In the amendment filed August 30, 2024, claims 1, 3, 8, 10, and 13 are canceled and new claims 14-24 are added. Claims 2, 4-7, 9, and 11 are amended. Claims 2, 4-7, 9, 11-12, and 14-24 are currently pending.
Information Disclosure Statement
The information disclosure statement (IDSs) submitted on August 30, 2024, January 14, 2025, and April 14, 2026 are acknowledged.
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claim 5 fails to recite eligible subject matter:
Claim 5 is rejected under 35 U.S.C. § 101 because the claimed invention is directed to a natural phenomenon without significantly more. The claim recites an alleged method of treating cancer in a subject, the method having an ultimate step of selecting a treatment protocol for he subject on the basis of a determination of whether the subject is sensitized to treatment with azenosertib. This step describes a mental process represents an abstract idea, namely a mental process that “can be performed in the human mind, or by a human using a pen and paper.” CyberSource Corp. v. Retail Decisions, Inc., 654 F.3d 1366, 1372 (Fed. Cir. 2011). Such “methods which can be performed mentally, or which are the equivalent of human mental work, are unpatentable abstract ideas the ‘basic tools of scientific and technological work’ that are open to all.’” CyberSource at 1371.
This judicial exception is not integrated into a practical application because it does not meet any of the criteria of a practical application. For example, the recited method does not effect a transformation of a particular article to a different state or thing, and does not generally apply the judicial exception in a meaningful way beyond linking it to a particular technological environment. Despite the preambular recitation of a method of treating cancer, no actual treatment is accomplished by the method as recited. Instead, the judicial exception – the “selection” of a treatment protocol – is itself the application, as it is the ultimate and only result of the method. As such, the judicial exception is not integrated into a practical application for subject matter eligibility purposes.
The claim also does not include additional elements that are sufficient to amount to significantly more than the judicial exception because the additional steps are merely conventional activity. Apart from the judicial exception, the method comprises a step of determining whether the subject is sensitized to treatment with azenosertib, this step comprising sub-steps of (i) obtaining or having obtained a biological sample from the subject, and (ii) performing or having performed at least one assay on the biological sample to determine if the subject has altered function of CCNE1. Obtaining biological samples for analysis is a thoroughly conventional activity (see, for example, the non-patent publication, Biological sample collection and processing for molecular epidemiological studies, Mutation Res., 543, pgs. 217-234 (2003) by Holland et al.); and a variety of techniques amenable to evaluating alterations in CCNE1 function are known in the art (see, for example, the non-patent publication, Detection of CCNE1/URI (19q12) amplification by in situ hybridisation is common in high grade and type II endometrial cancer, Oncotarget, 8, pgs. 14794-14805 (2016) by Noske et al.), such that this step is likewise fairly conventional. Furthermore, both steps are recited at such a high level of generality that neither could be regarded as constituting significantly more than the judicial exception. Alice Corp. Pty. Ltd. v. CLS Bank Int'l, 573 U.S. 208, 225 (2014).
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 2, 4-5, 7, 9, 11–12, 14–21, and 23-24 are indefinite:
Claims 2, 4–5, 7, 9, 11–12, 14–21, and 23-24 are rejected under 35 U.S.C. § 112(b) as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor regards as the invention.
Claims 2, 4, and 5 are indefinite for reciting an “altered function of CCNE1,” because a person of ordinary skill in the art could not reasonably determine the metes and bounds of this phrase. First, there is no method described in the claims or spec for determining whether CCNE1 function is altered. Further to this point, while one could perform certain tests, such as determining whether a sample had undergone CCNE1 gene amplification, this would not necessarily determine whether any alteration to CCNE1 activity had occurred. Second, there is no recited mechanism, direction, magnitude, or specificity of CCNE1 function alteration. For example, it would be unclear whether a condition that had a nonspecific, indirect effect on CCNE1 activity constitutes an "altered function" as recited. Third, there is no baseline or reference point for comparison by which to determine whether CCNE1 function is "altered." For example, one could use healthy tissues from the same subject (which may or may not be in the same cell cycle phase), a comparable tissue from another subject, average values from some pool of other subjects, or some other reference point. For at least these reasons, one of skill in the art could not reasonably determine what constitutes "altered function of CCNE1" or how one would determine whether a given sample has such altered function. Claims 9, 11-12, and 14-24 are indefinite for depending from claim 2, 4, or 5 without curing this indefiniteness.
Claim 2 is further indefinite for reciting administering azenosertib to the subject based upon results of the assay, because one of ordinary skill in the art could not reasonably determine the metes and bounds of this limitation. In particular, there is not basis in the claim for distinguishing administrations of azenosertib that are “based upon the results of the assay [for altered CCNE1 function]” from those that are not based on the assay. Based on the current record, one can only assume that if the assay is performed, and if azenosertib is then administered, then the administration was performed “based upon the results of the assay.” For the purpose of examination against the prior art, it will be understood that this recitation of claim 2 includes all instances in which an assay capable of evaluating CCNE1 function is performed and azenosertib is subsequently administered.
Claim 5 is further indefinite for reciting a step of “determining whether the subject is sensitized to treatment with [azenosertib],” where the determination is performed by the sub-steps of (i) obtaining a biological sample and (ii) performing an assay to determine if the subject has “altered function of CCNE1.” In particular, it would be unclear what constitutes a determination whether the subject is sensitized to treatment with azenosertib. The phrasing of this recitation appears to suggest that an “altered function of CCNE1” is tantamount to “sensitiz[ation] to treatment with [azenosertib],” however the fact that different expressions are used for these two things, and they are not expressly equated in the claim, makes the connection between them ambiguous. Furthermore, if altered function of CCNE1 does not directly correlate to sensitivity to azenosertib treatment, then the claim gives no indication of how a determination of such sensitization is reached or, indeed, what constitutes azenosertib sensitization.
Claim 5 is also further indefinite for reciting, “selecting a treatment protocol for the subject on the basis of the determination of whether the subject is sensitized to treatment with [azenosertib],” because a person of ordinary skill in the art could not reasonably determine the metes and bounds of this limitation. The claim recites no decision tree or correlation that forms the basis for determining a treatment protocol selection in view of azenosertib sensitization, such as “if the subject is sensitized, then a treatment characterized by [X] is selected.” While the specification suggests a correlation between increased CCNE1 activity and utility of azenosertib treatment, there is no hint of this correlation in the claim. As such, in determining whether a treatment protocol selection was made “on the basis of” a determination on azenosertib sensitization, one would be left largely speculating on the subjective state of mind of the person performing the method. For these reasons, claim 5 is further indefinite.
Claims 7, 15, and 17 are indefinite for reciting, “wherein the altered function of CCNE1 is CCNE1 protein overexpression,” because a person of ordinary skill in the art could not reasonably determine the metes and bounds of this limitation. In particular, while the phrase “protein overexpression” is qualitatively comprehensible, it refers to an inherently quantitative comparison and, in the absence of relevant details, cannot be evaluated with necessary precision. For example, neither the claim nor the specification provides a reference baseline against which expression is compared (e.g. healthy tissue, adjacent tissue, population average, etc.), nor is there any recited threshold of increase that constitutes “overexpression” within the context of the claim (e.g. 1.5× baseline, 3×, any statistically significant increase, etc.). In the absence of a more detailed, quantitative description of what constitutes “overexpression” in this context, one cannot reasonably determine the metes and bounds of the claim limitation.
Claim 15 is further indefinite for reciting “the method of claim 4 wherein the altered function of CCNE1 is CCNE1 protein overexpression.” Claim 4, from which claim 15 depends, recites identifying a subject having…”overexpression or altered function of CCNE1.” As such, claim 15 effectively recites identifying a subject having…overexpression or CCNE1 protein overexpression. This appears to recite the same element two times, as apparent identical alternatives.
For the same reasoning applied to claims 7, 15, and 17, claim 4 is also further indefinite for reciting “overexpression…of CCNE1,” within the recitation of identifying a subject having…(b) overexpression…of CCNE1. As above, one of skill in the art could not reasonably determine what constitutes overexpression of CCNE1 within this context.
A note on claim interpretation: With respect to claims 6, 14, and 16, one can find different definitions of what constitutes gene “amplification,” (i.e. some references distinguish (i) low-level copy number gain, where a wild type 2 copies of a gene is increased by a relatively small amount such as to 4 or fewer copies; from (ii) gene amplification which requires a larger increase in copy number). In the present context, “gene amplification” as used in the present claims will be understood as referring to any (non-aneuploid) gain in CCNE1 copy number.
Claims 9 and 11-12 are indefinite for depending from claim 2 without curing its reason for indefiniteness. Claims 14, 18-19, and 23 are indefinite (and claim 15 is further indefinite) for depending from claim 4 without fully curing its reasons for indefiniteness. Claims 16, 20-21 and 24 are indefinite (and claim 17 is further indefinite) for depending from claim 5 without curing all its reasons for indefiniteness.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. § 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. § 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 2, 4-7, 9, 11-12, and 14-21 are obvious over Huang in view of Gorski:
Claims 2, 4-7, 9, 11-12, and 14-21 are rejected under 35 U.S.C. § 103 as being unpatentable over International Patent Application Publication No. WO 2019/173082 to Huang et al. (hereinafter “Huang”), in view of the non-patent publication, CCNE1 Amplification as a Predictive Biomarker of Chemotherapy Resistance in Epithelial Ovarian Cancer, Diagnostics, 10, art. 279, pgs. 1–14 (2020) by Gorski et al. (hereinafter “Gorski”).
Claim 2 recites a method of treating a cancer, comprising steps of (i) obtaining a biological sample from a subject; (ii) performing at least one assay on the biological sample to determine if the subject has altered function of CCNE1; and (iii) administering an effective amount of azenosertib to the subject based upon results of the assay.
Huang discloses substituted 1,2-dihydro-3H-pyrazolo[3,4-d]pyrimidin-3-ones as WEE1 inhibitors for treating cancer. Huang teaches that the compound azenosertib (ZN-c3), whose structure is expressly depicted on page 141 of Huang (middle column of line drawings, third from the bottom), is a compound of Formula (I) that inhibits WEE1 kinase activity. Huang teaches that compounds of Formula (I), including azenosertib, may be used to treat cancer (paragraph [0006]; claims 125–127), such as ovarian cancer, gallbladder/bile duct cancer, and a variety of hematological malignancies, among other cancers (paragraph [0138]; claim 125). Huang thus teaches a method of treating cancer comprising administering to a subject an effective amount of azenosertib. Huang does not expressly teach obtaining a biological sample from the subject and performing an assay to determine if the subject has altered function of CCNE1, however it would have been obvious, to include a step of obtaining a biological sample from the subject and performing an assay to determine CCNE1 amplification status prior to administering azenosertib, because CCNE1 amplification was well-known in the art as a predictive biomarker for selecting cancer patients likely to benefit from WEE1 inhibitor treatment. See, for example, Gorski.
Gorski teaches that overexpression of cyclin E1 (CCNE1) increases the speed that cells progress through the G1/S phase restriction point, leading to genomic instability (section 3.2, first paragraph), that CCNE1 amplification is one of the most common genetic alterations in epithelial ovarian cancer (Abstract; section 3.1), and that CCNE1 amplification is a potential predictive marker of cytotoxic chemotherapy resistance (Abstract; section 5.2.1). Gorski further teaches that WEE1 kinase activation prevents cell division at the G2/M phase checkpoint until DNA damage is repaired, so that WEE1 kinase inhibition, in conjunction with cyclin E1 amplification, may cause massive DNA damage in CCNE1 amplified cells, leading to preferential cell death in these cells, such as CCNE1 amplified ovarian cancer cells (section 6.2, paragraph spanning the bottom of pg. 8 to the top of pg. 9). On this basis, Gorski teaches that specific targeting (i.e. inhibition) of Wee1 kinase holds promise as a therapeutic option in cancers having amplified CCNE1 (section 6.2). Based on these teachings of Gorski, it would have been obvious to try, and one would have had a reasonable expectation of success, in particularly targeting the method of Huang to CCNE1-amplified cancers, by testing cancer tissues for CCNE1 amplification as an adjunct to administering the WEE1 inhibitor of Huang (i.e. obtaining or having obtained a sample of the cancerous tissue, and performing or having performed a test to determine if CCNE1 is amplified (has altered CCNE1 function)).
Claim 4 recites a method of treating a cancer comprising identifying a subject having (a) the cancer and (b) overexpression or altered function of CCNE1, and administering an effective amount of azenosertib or a pharmaceutically acceptable salt thereof to the subject. Huang is applied to claim 4 as to claim 2 with respect to the administering step. The step of identifying a subject having overexpression or altered function of CCNE1 is not expressly taught by Huang. However, as discussed above in connection with claim 2, Gorski teaches that it was well-known in the art to identify cancer subjects having CCNE1 amplification — a form of altered CCNE1 function — as a criterion for selecting subjects for WEE1 inhibitor therapy. Gorski further teaches that CCNE1 protein overexpression accompanies CCNE1 gene amplification in chemoresistant ovarian cancer subjects, and that these CCNE1-altered subjects represent the population most likely to benefit from WEE1 inhibition (Abstract; sections 3.2, 5.2, 6.2). The motivation to combine is the same as stated for claim 2. Claim 4 is therefore obvious over Huang in view of Gorski.
Claim 5 recites a method of treating cancer comprising determining whether the subject is sensitized to azenosertib treatment by obtaining a biological sample, performing an assay to determine if the subject has altered function of CCNE1, and selecting a treatment protocol on the basis of that determination. Huang is applied to claim 5 as to claims 2 and 4. Gorski is applied to claim 5 as to claim 2: Gorski teaches the practice of assaying a biological sample for CCNE1 amplification to identify the subset of cancer patients who are likely to be sensitive to WEE1 inhibitor therapy (sections 6.2, 7.1), which corresponds to determining whether a subject is sensitized to treatment and selecting a treatment protocol accordingly. Claim 5 is therefore obvious over Huang in view of Gorski.
With respect to claims 6, 14, and 16, Gorski expressly teaches that CCNE1 gene amplification is the operative biomarker for identifying candidates for WEE1 inhibitor therapy (sections 5.2.1, 6.2). With respect to claims 7, 15, and 17, Gorski teaches that, while CCNE1 amplification is a more reliable predictive biomarker of chemotherapy resistance than is cyclin E1 overexpression, it is nonetheless a well-accepted notion that gene amplification contributes to increased protein expression (section 5.2.1). As such, one would have had a reasonable expectation of success in using protein overexpression as an indicator of WEE1 sensitization, even if it may be less reliable that CCNE1 amplification.
With respect to claims 9, 18, and 20 both Huang (paragraph [0138]) and Gorski (abstract) expressly teach treatment of ovarian cancer, and with respect to claims 11, 19, and 21 Gorski teaches that CCNE1 is frequently amplified in epithelial ovarian cancer (abstract). With respect to claim 12, Gorski teaches that CCNE1 amplification has been identified as a primary oncogenic driver in a subset of high grade serous ovarian cancer (abstract, and pg. 5, first two paragraphs). On this basis, and in view of the above-referenced teachings of Gorski, it would have been obvious to try, and one would have had a reasonable expectation of success, in applying the method of Huang and Gorski to subjects having high grade serous ovarian cancer.
Claims 22-24 are obvious over Huang, Gorski, and Etemadmoghadam:
Claims 22-24 are rejected under 35 U.S.C. § 103 as being unpatentable over Huang, in view of Gorski, further in view of the non-patent publication, Integrated Genome-Wide DNA Copy Number and Expression Analysis Identifies Distinct Mechanisms of Primary Chemoresistance in Ovarian Carcinomas, Clin. Cancer Res., 15, pgs. 1417–1427 (2009) by Etemadmoghadam et al. (hereinafter “Etemadmoghadam”).
Claims 22-24 depend from claims 6, 14, and 16 respectively, and further recite that the CCNE1 copy number of the amplified CCNE1 is at least 6. Huang and Gorski are applied to claims 22-24 as to claims 6, 14, and 16, respectively, but neither Huang nor Gorski expressly recites a CCNE1 copy number threshold of “at least 6.” It would have arguably been obvious on its face to apply the method of Huang and Gorski to subjects having amplified CCNE1 with copy number of at least 6, as the amplified CCNE1 cancers of Gorski naturally include cancers in which the CCNE1 copy number is 6 or more. To this point, the specific copy number threshold of “at least 6” recited in claims 22-24 represents no more than a routine selection from within the group of amplified CCNE1 cancers disclosed by Gorski, and there is no showing of criticality for the “at least 6” threshold relative to other thresholds of CCNE1 amplification. Notwithstanding this, it further would have been obvious, to apply the method of Huang and Gorski to cancers having CCNE1 copy number of at least 6 because this copy number range was well-established in the art as indicative of clinically significant CCNE1 amplification in ovarian cancer. See, for example, Etemadmoghadam.
Etemadmoghadam teaches a genome-wide analysis of DNA copy number variation in 118 ovarian tumors, demonstrating that amplification of 19q12 — the chromosomal region containing CCNE1 — is significantly associated with primary chemoresistance in advanced-stage serous ovarian cancer (Abstract; Results). Etemadmoghadam characterizes CCNE1 copy number using quantitative-PCR and oligonucleotide microarray analysis, and teaches that tumors with high CCNE1 copy number and protein expression are the subpopulation associated with chemoresistance and the subpopulation for which CCNE1-targeted therapeutic strategies are relevant (Abstract; Conclusions), and further shows that cancers having CCNE1 copy number of 6 or greater are enriched in cases showing poor responsiveness to primary treatment (pg. 1424, left column, second and third paragraphs; and Fig. 3A), an attribute discussed by Gorski as being a characteristic of CCNE1-amplified ovarian cancers generally. It would have been obvious to apply the method of Huang and Gorski to CCNE1-amplified ovarian cancers having copy number of at least 6, in order to take advantage of the synergistic cancer cell destruction mechanism taught by Gorski, against cancers tending to be the most resistant to alternate state-of-the-art treatments as taught by Etemadmoghadam.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 2, 4–7, 9, 11–12, and 14–24 are provisionally rejected on the ground of nonstatutory double patenting over the ’446 application, in view of Gorski, Etemadmoghadam:
Claims 2, 4–7, 9, 11–12, and 14–24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-50 of copending Application No. 19/201,446 (hereinafter “the ’446 application”), in view of Gorski, and Etemadmoghadam.
Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the ’446 application recite methods of treating cancer that broadly overlap with those of the present claims, particularly in view of the secondary references. Claim 1 of the ’446 application recites a method of treating cancer comprising administering to a subject selected to have a predetermined Cyclin E1 status an effective dose of azenosertib. Claim 7 specifies that the Cyclin E1 status is measured by Cyclin E1 protein expression level. Claim 21 specifies that the predetermined Cyclin E1 status is accompanied by CCNE1 gene-amplified status. Claim 22 specifies that the CCNE1 gene-amplified status is measured by CCNE1 gene copy number. Claim 23 specifies that the CCNE1 gene-amplified status is a copy number of at least 3, 4, 5, 6, 7, or more. The claims of the ’446 application thus recite the features that Huang is cited for in the rejections for obviousness under 35 U.S.C. § 103, above, plus additional features of the instant claims. Gorski and Etemadmoghadam are cited as above, such that all instant claims are obvious variations of the claimed methods of the ’446 application.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 2, 4–7, 9, 11–12, and 14–24 are provisionally rejected on the ground of nonstatutory double patenting over the ’378 application, in view of Gorski and Etemadmoghadam:
Claims 2, 4–7, 9, 11–12, and 14–24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-60 of copending Application No. 19/201,378 (hereinafter “the ’378 application”), in view of Gorski and Etemadmoghadam.
Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the ’378 application recite methods of treating cancer that broadly overlap with those of the present claims, particularly in view of the secondary references. Claim 1 of the ’378 application recites a method of treating cancer comprising administering to a subject a daily dose of azenosertib according to a specified dosing regimen, and claim 34 recites wherein the cancer is a solid tumor such as ovarian cancer (e.g. HGSOC). The claims of the ’378 application thus teaches the features for which Huang is cited in the rejections for obviousness under 35 U.S.C. § 103, above. Gorski and Etemadmoghadam are cited as above, such that all instant claims are obvious variations of the claimed methods of the ’378 application.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 2, 4–7, 9, 11–12, and 14–24 are provisionally rejected on the ground of nonstatutory double patenting over the ’321 application, in view of Gorski and Etemadmoghadam:
Claims 2, 4–7, 9, 11–12, and 14–24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 5 of copending Application No. 19/404,321 (hereinafter “the ’321 application”), in view of Gorski and Etemadmoghadam.
Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the ’321 application recite methods of treating cancer that broadly overlap with those of the present claims, particularly in view of the secondary references. Claim 1 of the ’321 application recites a method of treating cancer comprising administering an effective dose of azenosertib to a subject selected to have a cancer with a homologous recombination repair deficiency (HRD). Claims 36 through 38 of the ’321 application specify that the cancer includes ovarian cancer, and specifically high grade serous ovarian cancer. The claims of the ’321 application thus teaches the features for which Huang is cited in the rejections for obviousness under 35 U.S.C. § 103, above. While, as mentioned, the claims of the ’321 application recite that the cancer has a HRD, that does not preclude the CNNE1 function analysis of Gorski. Gorski and Etemadmoghadam are cited as above, such that all instant claims are obvious variations of the claimed methods of the ’321 application.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 2, 4–7, 9, 11–12, and 14–24 are provisionally rejected on the ground of nonstatutory double patenting over the ’951 application, in view of Berton-Rigaud, Gorski, and Etemadmoghadam:
Claims 2, 4–7, 9, 11–12, and 14–24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of copending Application No. 18/554,951 (hereinafter “the ’951 application”), in view of the non-patent publication, Gynecologic Cancer InterGroup (GCIG) Consensus Review for Uterine and Ovarian Carcinosarcoma, Int. J. Gyn. Cancer, 24, pgs. S55-S60 (2014) by Berton-Rigaud et al. (hereinafter, “Berton-Rigaud”), further in view of Gorski and Etemadmoghadam.
Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the ’951 application recite a method of treating a cancer highly similar to ovarian cancer. Claim 1 of the ’951 application recites a method of treating a subject having uterine serous carcinoma (USC) comprising administering a therapeutically effective amount of ZN-c3, or a pharmaceutically acceptable salt thereof, to the subject in accordance with a dosing regimen. ZN-c3 is azenosertib. The claims of the ’951 application thus recite the features for which Huang is cited in the rejections for obviousness under 35 U.S.C. § 103, above, except that the former are directed to treatment of USC, rather than the ovarian cancer of Gorski. However, Berton-Rigaud discloses that USC shares molecular characteristics with ovarian serous carcinoma (abstract) and is histologically similar to ovarian serous carcinoma (pg. S84, left column, second paragraph), and that the two generally have similar treatment protocols (pg. S87, right column, final paragraph). As such, it would have been obvious to apply the method of the claims of the ’951 application, directed to USC, to the ovarian cancers of Gorski. Gorski and Etemadmoghadam are cited as above, such that all instant claims are obvious variations of the claimed methods of the ’951 application.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 2, 4–7, 9, 11–12, and 14–24 are provisionally rejected on the ground of nonstatutory double patenting over the ’055 application, in view of Gorski and Etemadmoghadam:
Claims 2, 4–7, 9, 11–12, and 14–24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 of copending Application No. 18/634,055 (hereinafter “the ’055 application”), in view of Gorski and Etemadmoghadam.
Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the ’055 application recite methods of treating cancer that broadly overlap with those of the present claims, particularly in view of the secondary references. Claim 1 of the ’055 application recites a use of a combination comprising an effective amount of a WEE1 inhibitor (Compound A) and an effective amount of an anti-CD47 antibody (Compound B) for treating a disease or condition. Claim 4 identifies Compound A as having the structure of azenosertib (ZN-c3), and claim 11 specifies that the disease or condition includes ovarian cancer. The claims of the ’055 application thus recite the features for which Huang is cited in the rejections for obviousness under 35 U.S.C. § 103, above. While the reference claims further require a second therapeutic agent, this does not exclude the method of Huang or of the instant claims. Gorski and Etemadmoghadam are cited as above, such that all instant claims are obvious variations of the claimed methods of the ’055 application.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 2, 4–7, 9, 11–12, and 14–24 are provisionally rejected on the ground of nonstatutory double patenting over the ’164 application, in view of Gorski and Etemadmoghadam:
Claims 2, 4–7, 9, 11–12, and 14–24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 of copending Application No. 18/648,164 (hereinafter “the ’164 application”), in view of Gorski and Etemadmoghadam.
Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the ’164 application recite methods of treating cancer that broadly overlap with those of the present claims, particularly in view of the secondary references. The ’164 application recites in claim 1 a use of a combination comprising an effective amount of a WEE1 inhibitor (Compound A) and an effective amount of a DNA damage response (DDR) inhibitor (Compound B). Claim 4 identifies Compound A as having the structure of azenosertib (ZN-c3), and claim 14 specifies that the disease or condition includes ovarian cancer. The claims of the ’164 application thus recite the features for which Huang is cited in the rejections for obviousness under 35 U.S.C. § 103, above. While the reference claims further require a second therapeutic agent, this does not exclude the method of Huang or of the instant claims. Gorski and Etemadmoghadam are cited as above, such that all instant claims are obvious variations of the claimed methods of the ’164 application.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 2, 4–7, 9, 11–12, and 14–24 are provisionally rejected on the ground of nonstatutory double patenting over claims 12 and 13 of the ’327 application, in view of Gorski and Etemadmoghadam:
Claims 2, 4–7, 9, 11–12, and 14–24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 12 and 13 of copending Application No. 19/045,327 (hereinafter “the ’327 application”), in view of Gorski and Etemadmoghadam.
Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the ’327 application recite methods of treating cancer that broadly overlap with those of the present claims, particularly in view of the secondary references. The ’327 application recites in claim 12 a method of inhibiting, ameliorating, or treating a cancer in a subject, the method comprising identifying a modulation in the PPP2R1A protein or encoding gene that confers sensitivity to ZN-c3 (azenosertib) in a biological sample obtained from the subject, and administering ZN-c3 to the subject when the polymorphism is identified. Claim 13 of the ’327 application specifies that the cancer comprises non-small cell lung cancer, breast cancer, colorectal cancer, ovarian cancer, uterine serous carcinoma, or endometrial cancer. Claims 12 and 13 of the ’327 application thus recite the features for which Huang is cited in the rejections for obviousness under 35 U.S.C. § 103, above. Gorski and Etemadmoghadam are cited as above. While the claims of the ’327 application are directed to identifying alterations in PPP2R1A to select suitable treatment candidates, this does not preclude also identifying the CCNE1 alterations as rendered obvious by Gorski. As such, all instant claims are obvious variations of the claimed methods of the ’327 application.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
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/ALEXANDER K. SHOWALTER/Examiner, Art Unit 1629
/JEFFREY S LUNDGREN/Supervisory Patent Examiner, Art Unit 1629
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