Prosecution Insights
Last updated: July 17, 2026
Application No. 17/772,940

AZAPODOPHYLLOTOXIN DERIVATIVES AND METHODS OF TREATING LYMPHOMA AND KIDNEY CANCER

Final Rejection §103
Filed
Apr 28, 2022
Priority
Nov 04, 2019 — provisional 62/930,346 +1 more
Examiner
BRANDSEN, BENJAMIN MICHAEL
Art Unit
1693
Tech Center
1600 — Biotechnology & Organic Chemistry
Assignee
The Board of Trustees of the Leland Stanford Junior University
OA Round
2 (Final)
61%
Grant Probability
Moderate
3-4
OA Rounds
0m
Est. Remaining
79%
With Interview

Examiner Intelligence

Grants 61% of resolved cases
61%
Career Allowance Rate
64 granted / 105 resolved
+1.0% vs TC avg
Strong +18% interview lift
Without
With
+17.6%
Interview Lift
resolved cases with interview
Typical timeline
3y 5m
Avg Prosecution
27 currently pending
Career history
147
Total Applications
across all art units

Statute-Specific Performance

§101
2.1%
-37.9% vs TC avg
§103
54.8%
+14.8% vs TC avg
§102
24.0%
-16.0% vs TC avg
§112
5.0%
-35.0% vs TC avg
Black line = Tech Center average estimate • Based on career data from 105 resolved cases

Office Action

§103
CTFR 17/772,940 CTFR 98516 DETAILED ACTION Notice of Pre-AIA or AIA Status 07-03-aia AIA 15-10-aia 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 April 28, 2022, is a national stage application of PCT/US2020/058666, filed November 3, 2020, and claims the benefit of U.S. provisional application 62/930346, filed November 4, 2019. Status of the Application Applicant’s communication, received February 20, 2026, wherein claims 1, 2, and 32 are amended, claims 3-7, 9-12, 18-19, 27-28, and 64-65 are canceled, and new claims 34-39 are added, is acknowledged. Claims 1, 2, 32, and 34-39 are pending and examined on the merits herein. Withdrawn Objections Applicant’s amendment, received February 20, 2026, with respect to the objection to the drawings, has been fully considered and found to be persuasive to remove the objection because replacement drawings for Figure 7A, 7B, 7C, and 7D have been received. Therefore the objection is withdrawn. Applicant’s amendment, received February 20, 2026, with respect to the objections to claims 3, 4, 6, 7, 9, 10, 12, 18, 19, 27, and 28 for minor informalities, has been fully considered and found to be persuasive to remove the objection because claims 3, 4, 6, 7, 9, 10, 12, 18, 19, 27, and 28 are canceled. Therefore the objection is withdrawn. Withdrawn Rejections Applicant’s amendment, received February 20, 2026, with respect to the rejection of claims 1-7, 9-12, 18-19, 27-28, and 32 under 35 USC § 112(a) as lacking enablement for solvates and prodrugs of the claimed compounds, has been fully considered and found to be persuasive to remove the rejection because claims 3-7, 9-12, 18-19, 27-28, and 64-65 are canceled and independent claim 1 is amended to recite specific azapodophyllotoxin derivatives. Therefore the rejection is withdrawn. Applicant’s amendment, received February 20, 2026, with respect to the rejection of claims 3-7, 9-11, and 32 under 35 USC § 112(b) as indefinite, has been fully considered and found to be persuasive to remove the rejection because claims 3-7 and 9-11 are canceled and claim 32 is amended to remove the limitations lacking antecedent basis. Therefore the rejection is withdrawn. Applicant’s amendment, received February 20, 2026, with respect to the rejection of claims 4-5, 9-11, and 27-28 under 35 USC § 112(d) for failing to include all the limitations of the claims upon which these claims depend, has been fully considered and found to be persuasive to remove the rejection because claims 4-5, 9-11, and 27-28 are canceled. Therefore the rejection is withdrawn. Applicant’s amendment, received February 20, 2026, with respect to the rejection of claims 1-7, 10-12, and 32 under 35 USC § 102 as anticipated by Andreoli, has been fully considered and found to be persuasive to remove the rejection because claims 3-7 and 10-12 are canceled and claim 1 is amended to require inhibition of a myc-driven cancer cell, which the embodiments of Andreoli cited in the previous rejection do not teach. Therefore the rejection is withdrawn. Applicant’s amendment, received February 20, 2026, with respect to the rejection of claims 1-7, 10-12, and 32 under 35 USC § 102 as anticipated by Kumar, has been fully considered and found to be persuasive to remove the rejection because claims 3-7 and 10-12 are canceled and claim 1 is amended to require inhibition of a myc-driven cancer cell, which the embodiments of Kumar cited in the previous rejection do not teach. Therefore the rejection is withdrawn. Applicant’s amendment, received February 20, 2026, with respect to the rejection of claims 1-7 and 18-19 under 35 USC § 103 as unpatentable over Kumar in view of Husson, has been fully considered and found to be persuasive to remove the rejection because claims 3-7 and 10-12 are canceled and claim 1 is amended to require inhibition of a myc-driven cancer cell, which the embodiments of Kumar and Husson cited in the previous rejection do not teach. Therefore the rejection is withdrawn. Applicant’s amendment, received February 20, 2026, with respect to the nonstatutory double patenting rejection of claims 1, 3-7, 10, 12, and 32 as unpatentable over claims 1, 3, and 4 of U.S. Patent No. 11,771,692, has been fully considered and found to be persuasive to remove the rejection because claims 3-7, 10, and 12 are canceled and claim 1 is amended to recite specific azapodophyllotoxins which are not claimed by ‘692. Therefore the rejection is withdrawn. Applicant’s amendment, received February 20, 2026, with respect to the nonstatutory double patenting rejection of claims 2 and 11 as unpatentable over claims 1, 3, and 4 of U.S. Patent No. 11,771,692 in view of Kumar, has been fully considered and found to be persuasive to remove the rejection because claim 11 is canceled and claim 1 is amended to recite specific azapodophyllotoxins, which are not claimed by ‘692. Therefore the rejection is withdrawn. The following are new and/or modified grounds of rejection, necessitated by Applicant’s amendments received February 20, 2026. Claim Rejections - 35 USC § 103 07-06 AIA 15-10-15 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. 07-20-aia AIA 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. 07-23-aia AIA 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. 07-20-02-aia AIA 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. 07-21-aia AIA Claim s 1-2 are rejected under 35 U.S.C. 103 as being unpatentable over Kumar (Kumar, A.; et al. European Journal of Pharmaceutical Sciences 2011, vol. 44, pp. 21-26; cited in previous office action) in view of Yamada (Yamada, Y.; et al. Cancer Science 2013, vol. 104, pp. 304-312; cited in PTO-892) . Kumar teaches N-hydroxyethyl-4-aza-didehydropodophyllotoxin derivatives as potential antitumor agents (p. 21, Title). Kumar teaches compounds 7a-f, 8a-f, and 9a-f, with variable groups R 1 , R 2 , and R 3 as shown in Figure 2 (p. 23, Figure 2; structures shown below). PNG media_image1.png 290 385 media_image1.png Greyscale Compound 7a has the same structure as compound NSC750212 shown in claim 1, compound 7c has the same structure as NSC750719 shown in claim 1, compound 7d has the same structure as compound AR-02 shown in claim 1, compound 9c has the same structure as compound NSC750722 shown in claim 1, and compound 9d has the same structure as compound AR-03 shown in claim 1. Kumar teaches testing several of these compounds, including compounds 7a, 7c, and 9c, against a panel of cancer cell lines (p. 24, Table 3) at concentrations of 100, 10, 1.0, 0.1, and 0.01 μM (p. 23, right column, first paragraph, lines 16-20). Kumar teaches that compound 7a has a GI 50 value of 0.47 μM against the CCRF-CEM cell line and 0.26 μM against the A498 renal cancer cell line. Kumar teaches that compound 7c has a GI 50 value of 0.28 μM against CCRF-CEM cell line and 0.20 μM against the A498 renal cancer cell line. Kumar teaches that compound 9c has a GI 50 value of 0.12 μM against CCRF-CEM cell line and 0.13 μM against the A498 renal cancer cell line (p. 24, Table 3). Accordingly, one of ordinary skill in the art would have recognized these compounds as having antiproliferative activity against cancer cell lines. Kumar does not teach the cancer cell lines, such as the A498 renal cancer cell line, as being a myc-driven cancer cell, as recited in claim 1. In addition, Kumar does not teach wherein the contacting inhibits tubulin polymerization by at least 20% relative to a control and monoglycerol metabolism by at least 20% relative to a control as recited in claim 1. Yamada teaches that expression of MYC mRNA relative to normal kidney cells is significantly increased in A498 cells (p. 309, Figure 3a). Yamada teaches that MYC mRNA expression, protein expression, cell viability, and invasion cell ratio are all decreased by knockdown of MYC by siRNA in A498 cells (p. 310, Figure 4a-d). Therefore, because MYC is upregulated in A498 cells, and the viability and invasion cell ratio of A498 cells are reduced by knockdown of MYC, A498 is reasonably considered as a myc-driven cancer cell line. It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the present application to inhibit the proliferation of a myc-driven cancer cell using an azapodophyllotoxin disclosed by Kumar. One of ordinary skill in the art would have been motivated to inhibit the proliferation of a myc-driven cancer cell using an azapodophyllotoxin disclosed by Kumar because Kumar teaches presently claimed compounds as having an antiproliferative activity against cancer cell lines, including the renal cancer cell line A498. Accordingly, one of ordinary skill in the art would have recognized the utility of these compounds for inhibiting proliferation of cell lines such as A498. Moreover, because Yamada teaches A498 is a myc-driven cancer cell line, one of ordinary skill in the art, when considering a compound taught by Kumar for inhibiting proliferation of the A498 cell line, would have thus contemplated inhibiting proliferation of a myc-driven cancer cell using a claimed compound. Kumar does not teach wherein contacting inhibits tubulin polymerization by at least 20% relative to a control and monoglycerol metabolism by at least 20% relative to a control. However, as evidence, the instant specification provides that compound NSC750212 can work through the inhibition of tubulin polymerization, such that it is more efficacious than Nocodazole in preventing depolymerization in vitro (FIG. 7, panel A) (p. 60, lines 30-32). In addition, the specification provides that proteomic analysis of tumors excised from mice derived from the human ALL cell line CCRF and treated with NSC750212 showed a decrease in tubulin up to termination of treatment, and that NSC750212 treated tumors showed lowered levels of tubulin expression in both the fine needle aspirates and the core biopsy (p. 61, lines 1-8). In addition, the instant specification discloses that RCC treated with NSC750212 shows elevated levels of monoglycerols compared to untreated RCC (FIG. 8) (p. 61, lines 11-15). Therefore, contacting A498 cells with NSC750212 (taught as compound 7a by Kumar) would be expected to have the effect of inhibiting tubulin polymerization and monoglycerol metabolism. The specification further provides that tubulin polymerization may be inhibited by, for example, 20% or more (p. 17, lines 7-8), and monoglycerol metabolism may be inhibited by, for example, 20% or more (p. 17, lines 14-15). Kumar teaches treats cells with a range of concentrations of compound (i.e., 100, 10, 1.0, 0.1 , and 0.01 μM). In view of this range of concentrations, one of ordinary skill in the art would have further contemplated additional concentrations of compound, for the purposes of optimizing the concentration of azapodophyllotoxin used for inhibiting cell proliferation, because even higher concentrations of compound may provide superior inhibition of a cancer cell proliferation. As stated, during such optimization, one of ordinary skill in the art would have contemplated a concentration of azapodophyllotoxin sufficient to achieve the required 20% inhibition of tubulin polymerization and monoglycerol metabolism, absent evidence to the contrary. MPEP 2112 at I states: “[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. IRECO Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999).” In this instance, because the prior art renders obvious contacting a myc-drive cancer cell with a claimed compound for the purposes of inhibiting its growth, specific limitations describing the mechanism of said compounds for inhibiting the growth of this cancer are also necessarily present when practicing this method obvious over the prior art. Therefore the invention taken as a whole is prima facie obvious . 07-21-aia AIA Claim s 34-35 are rejected under 35 U.S.C. 103 as being unpatentable over Kumar (Kumar, A.; et al. European Journal of Pharmaceutical Sciences 2011, vol. 44, pp. 21-26; cited in previous office action) in view of Yamada (Yamada, Y.; et al. Cancer Science 2013, vol. 104, pp. 304-312; cited in PTO-892) and Shroff (Shroff, E. H.; et al. Proceedings of the National Academy of Sciences 2015, vol. 112, pp. 6539-6544; cited in PTO-892) . Kumar teaches as described in the above rejections under 35 U.S.C. § 103. Kumar does not teach a method of treating an individual with a myc-driven cancer, the method comprising: determining the presence of a myc-driven cancer in the individual; administering to the individual with an azapodophyllotoxin derivative selected from those shown in the claim, and wherein the administering inhibits tubulin polymerization and monoglycerol metabolism to inhibit proliferation of the myc-driven cancer, as recited in claim 34. Yamada teaches as described in the above rejections under 35 U.S.C. § 103. Shroff teaches that the MYC oncogene is frequently mutated and overexpressed in human renal cell carcinoma (RCC) (p. 6539, Abstract, lines 1-2). Shroff teaches that their study shows, through a conditional transgenic mouse model, that the MYC oncogene, but not the RAS oncogene, initiates and maintains RCC (p. 6539, Abstract, lines 4-6). Shroff further teaches the MYC pathway is activated in most cases of human RCC , genomically amplified in 5–10% of patients, overexpressed in 20% of patients, and associated with a hereditary RCC syndrome, suggesting a causal role in the pathogenesis (p. 6539, left column, second paragraph, lines 1-4) (emphasis added). Accordingly, one of ordinary skill in the art would have reasonably considered human RCC as a myc-driven cancer. In addition, one of ordinary skill in the art would have recognized that most cases of human RCC are driven by myc, as taught by Shroff. It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the present application to administer an azapodophyllotoxin recited in claim 34, such as NSC750212 (taught as compound 7a by Kumar), to a patient suffering from renal cell carcinoma. One of ordinary skill in the art would have been motivated to administer a compound recited in claim 34 to a patient suffering from renal cell carcinoma because Kumar teaches their compounds are effective for inhibiting the growth of renal cancer cell lines, including the renal cancer cell line A498, and thus one of ordinary skill in the art would have recognized these compounds may be administered to patients with renal cancer as a potential treatment for said cancer. Moreover, in view of Yamada and Shroff, one of ordinary skill in the art would have recognized renal cancer cells, having increased expression of myc, as myc-driven cancers, and thus would have contemplated administering a compound taught by Kumar for treating a myc-driven cancer. Regarding the step of determining the presence of a myc-driven cancer in an individual, because Shroff teaches the MYC pathway is activated in most cases of human RCC , during the step of identifying a cohort of patients with renal cell carcinoma that may be treated with an azapodophyllotoxin compound taught by Kumar, one of ordinary skill in the art would have identified patients with a myc-driven cancer, because most cases of human RCC are driven by myc, absent evidence to the contrary. Regarding the requirement that administering inhibits tubulin polymerization and monoglycerol metabolism to inhibit proliferation of the myc-driven cancer, as stated above, this limitation is interpreted herein as necessarily present when practicing the method obvious over Kumar in view of Yamada and Shroff. MPEP 2112 at I states: “[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. IRECO Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999).” In this instance, because the prior art renders obvious administration of the claimed compounds to an individual for the purposes of treating a myc-driven cancer, limitations describing the mechanism of said compounds for treating cancer are also necessarily present when practicing the method obvious over the prior art. Therefore, the invention taken as a whole is prima facie obvious . 07-21-aia AIA Claim s 37-38 are rejected under 35 U.S.C. 103 as being unpatentable over Kumar (Kumar, A.; et al. European Journal of Pharmaceutical Sciences 2011, vol. 44, pp. 21-26; cited in previous office action) in view of Andreoli (Andreoli, M.; et al. Journal of Medicinal Chemistry 2014, vol. 57, pp. 7916-7932; cited in previous office action), Yamada (Yamada, Y.; et al. Cancer Science 2013, vol. 104, pp. 304-312; cited in PTO-892) and Shroff (Shroff, E. H.; et al. Proceedings of the National Academy of Sciences 2015, vol. 112, pp. 6539-6544; cited in PTO-892) . Andreoli is cited in IDS received April 28, 2022. However, the document included with the IDS does not include the supporting information, which is cited in the rejection below. A copy of Andreoli with its supporting information as a single document was included with the previous office action. Kumar teaches as described in the above rejections under 35 U.S.C. § 103. Kumar does not teach any of the specific compounds recited in claim 37. Andreoli teaches 4-azapodophyllotoxins of the general formula shown in Table 1, with variable groups R 1 , R 2 , R 3 , and R 4 as shown (p. 7918, Table 1; general structure shown below). Andreoli teaches these compounds as inhibitors of the GBP1:PIM1 interaction (p. 7916, Title). PNG media_image2.png 159 121 media_image2.png Greyscale As one example compound, Andreoli teaches compound NSC750210, which has R 1 as 6,7-OCH 2 O, and R 2 , R 3 , and R 4 as OCH 3 (p. 7918, Table 1), which is the same compound as compound 7a taught by Kumar. In addition, Andreoli teaches compounds that are recited in claim 37, including the compounds NSC756089, AR-051 (referred to as NSC756087 by Andreoli), and AR-038 (referred to as NSC756085 by Andreoli) (all compounds shown on. p. 7918, Table 1). Andreoli further teaches testing their compounds against the NCI-60 cancer cell line, which includes, for example, several renal cancer cell lines, including the A498 cell line (see NCI-60 cell lines listed in Figures 2SI-5SI, document pp. 21-24). Andreoli teaches that their screening was a two-stage process, beginning with the evaluation of all compounds against the 60 cell lines at a single dose of 10 μM. Andreoli teaches 31 compounds that exhibited significant growth inhibition were evaluated against the NCI-60 at five concentration levels to a final concentration of 0.1 nM (p. 7917, right column, first full paragraph, lines 8-14). Andreoli teaches these 31 compounds are shown in Table 1 (p. 7918), and include, for example, NSC756089 and AR-051 (referred to as NSC756087 by Andreoli). Therefore, based on Andreoli, one of ordinary skill in the art would have recognized compounds of claim 37 as showing significant growth inhibition of cancer cell lines. Yamada and Shroff teach as described in the above rejections under 35 U.S.C. § 103. It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the present application to administer an azapodophyllotoxin recited in claim 37 to a patient suffering from renal cell carcinoma. One of ordinary skill in the art would have been motivated to administer a compound recited in claim 37 to a patient suffering from renal cell carcinoma because Kumar teaches their compounds, which are structurally related to the compounds of claim 37, differing only in their substitution of the phenyl group, are effective for inhibiting the growth of renal cancer cells lines, including the renal cancer cell line A498, and Andreoli teaches compounds of claim 37, including NSC756089 and AR-051, show significant growth inhibition against cancer cell lines in the NCI-60 panel of cell lines. Accordingly, one of ordinary skill in the art would have recognized the compounds taught by Andreoli as effective for treating cancer, and in view of the activity of the structurally related azapodophyllotoxin compounds of Kumar for treating renal cancer cell lines, would have contemplated administering the compounds of Andreoli to patients to treat the full scope of cancers, including to patients with renal cell carcinoma. Moreover, in view of Yamada and Shroff, one of ordinary skill in the art would have recognized renal cancer cells, which exhibit increased expression of myc, as myc-driven cancers, and thus would have reasonably for administering a compound of claim 37 for treating a myc-driven cancer. Regarding the step of determining the presence of a myc-driven cancer in an individual, because Shroff teaches the MYC pathway is activated in most cases of human RCC , during the step of identifying a cohort of patients with renal cell carcinoma that may be treated with an azapodophyllotoxin compound taught by Andreoli, one of ordinary skill in the art would have reasonably identified individuals with a myc-driven cancer, because most cases of human RCC are driven by myc, absent evidence to the contrary. Regarding the requirement wherein administering the compound inhibits tubulin polymerization and monoglycerol metabolism to inhibit proliferation of the myc-driven cancer, as stated above, this limitation is interpreted herein as necessarily present when practicing the method obvious over Kumar in view of Andreoli, Yamada, and Shroff. MPEP 2112 at I states: “[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. IRECO Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999).” In this instance, because the prior art renders obvious administration of the claimed compounds for the purposes of treating a myc-driven cancer, limitations describing the mechanism of said compounds for treating cancer are also necessarily present when practicing the method obvious over the prior art. Therefore, the invention taken as a whole is prima facie obvious . Allowable Subject Matter 12-151-08 AIA 07-43 12-51-08 Claim s 32, 36, and 39 are objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims. Claims 32, 36, and 39 depend from claims 1, 34, and 37, respectively, and require further comprising a step of determining that the administering is effective to inhibit tubulin polymerization and monoglycerol metabolism. This additional step of determining that the administering is effective to inhibit tubulin polymerization and monoglycerol metabolism is novel and nonobvious over the prior art of record. The closest prior art references to the method of claims 32, 36, and 39 are Andreoli and Kumar, who teach azapodophyllotoxins, including the specific claimed compounds, as effective for inhibiting the proliferation of various cancer cell lines, as described in the above rejections under 35 U.S.C. § 103. Andreoli teaches these compounds as inhibitors of the GBP1:PIM1 interaction, which is required for initiation of a signaling pathway that induces resistance to paclitaxel (p. 7916, Abstract). However, neither Andreoli nor Kumar teach the effect of these compounds for inhibiting tubulin polymerization. In addition, neither Andreoli nor Kumar teach the effect of these compounds on monoglycerol metabolism. Although these effects are necessarily present when using these azapodophyllotoxins for the purposes of inhibiting cell proliferation or for treating cancer, neither Andreoli nor Kumar recognize these compounds as inhibiting tubulin polymerization and monoglycerol metabolism, and accordingly, one of ordinary skill in the art would not have been motivated to perform the additional method step of further determining that contacting the cell or administering to an individual the azapodophyllotoxin derivative was effective to inhibit tubulin polymerization and monoglycerol metabolism, as required by claims 32, 36, and 39. Conclusion Claims 1-2, 34-35, and 37-38 are rejected. 12-151-08 AIA 07-43 12-51-08 Claim s 32, 36, and 39 are objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims. 07-40 AIA Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL . See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a). A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action. Any inquiry concerning this communication or earlier communications from the examiner should be directed to BENJAMIN BRANDSEN whose telephone number is (703)756-4780. The examiner can normally be reached Monday - Friday from 9:00 am to 5:00 pm. Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Scarlett Goon can be reached at (571)270-5241. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300. Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000. /B.M.B./ Examiner, Art Unit 1693 /ANDREA OLSON/ Primary Examiner, Art Unit 1693 Application/Control Number: 17/772,940 Page 2 Art Unit: 1693 Application/Control Number: 17/772,940 Page 3 Art Unit: 1693 Application/Control Number: 17/772,940 Page 4 Art Unit: 1693 Application/Control Number: 17/772,940 Page 5 Art Unit: 1693 Application/Control Number: 17/772,940 Page 6 Art Unit: 1693 Application/Control Number: 17/772,940 Page 7 Art Unit: 1693 Application/Control Number: 17/772,940 Page 8 Art Unit: 1693 Application/Control Number: 17/772,940 Page 9 Art Unit: 1693 Application/Control Number: 17/772,940 Page 10 Art Unit: 1693 Application/Control Number: 17/772,940 Page 11 Art Unit: 1693 Application/Control Number: 17/772,940 Page 12 Art Unit: 1693 Application/Control Number: 17/772,940 Page 13 Art Unit: 1693 Application/Control Number: 17/772,940 Page 14 Art Unit: 1693 Application/Control Number: 17/772,940 Page 15 Art Unit: 1693 Application/Control Number: 17/772,940 Page 16 Art Unit: 1693
Read full office action

Prosecution Timeline

Apr 28, 2022
Application Filed
Sep 05, 2025
Non-Final Rejection mailed — §103
Feb 20, 2026
Response Filed
Jun 16, 2026
Final Rejection mailed — §103 (current)

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Prosecution Projections

3-4
Expected OA Rounds
61%
Grant Probability
79%
With Interview (+17.6%)
3y 5m (~0m remaining)
Median Time to Grant
Moderate
PTA Risk
Based on 105 resolved cases by this examiner. Grant probability derived from career allowance rate.

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