Prosecution Insights
Last updated: April 19, 2026
Application No. 16/669,191

COMPOSITIONS AND METHODS FOR TREATING CANCER

Non-Final OA §103§112
Filed
Oct 30, 2019
Examiner
RAHMAN, MASUDUR
Art Unit
1633
Tech Center
1600 — Biotechnology & Organic Chemistry
Assignee
UNIVERSITY OF VIRGINIA PATENT FOUNDATION
OA Round
5 (Non-Final)
70%
Grant Probability
Favorable
5-6
OA Rounds
4y 1m
To Grant
99%
With Interview

Examiner Intelligence

Grants 70% — above average
70%
Career Allow Rate
69 granted / 99 resolved
+9.7% vs TC avg
Strong +37% interview lift
Without
With
+37.4%
Interview Lift
resolved cases with interview
Typical timeline
4y 1m
Avg Prosecution
34 currently pending
Career history
133
Total Applications
across all art units

Statute-Specific Performance

§101
4.0%
-36.0% vs TC avg
§103
44.5%
+4.5% vs TC avg
§102
20.4%
-19.6% vs TC avg
§112
20.3%
-19.7% vs TC avg
Black line = Tech Center average estimate • Based on career data from 99 resolved cases

Office Action

§103 §112
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 . DETAILED ACTION A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 03 November 2025 has been entered. Claim status In the amendment filed 03 November 2025, Applicant has amended claims 1. Claims 18-38 are withdrawn and added new claim 40. Therefore, claims 1-2, 5-9, and 12-40 are herein pending. Election/Restrictions Applicant elected of group I, claims 1-2, 5-9, 12-17 drawn to a vector comprising a first nucleic acid encoding a promoter operably linked to each of a second nucleic acid encoding a therapeutic polypeptide and a third nucleic acid encoding a peptide domain, and a kit comprising said vector, in the reply filed on 8-2-22. The new claim 40 is within the scope of the elected invention. The Applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01 (a)). Claims 18-38 are withdrawn without traverse from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected subject matter, there being no allowable generic or linking claim. Claims 1-2, 5-9, 12-17 and 39-40 are herein under consideration. Priority This application was filed 10/30/2019 and claims benefit to the Priority from Provisional Application 62752631 filed on 10/30/2018. Thus, the earliest possible priority for the instant application is 10/30/2018. Withdrawn Objections to Drawing applicant has amended the specification to delete reference "Figure 6C" in line 17 of page 90 of the specification filed on 03 November 2025. Therefore, the prior objection to drawing is withdrawn. Withdrawn 35 USC § 103 Applicant has amended the claim 1 and executively recites that the promoter directs expression of the fusion protein in the target tissue to provide selective cell killing in the target tissue. In the cited in PTO892 prior art Albeck used an Erk regulation strategy with a reporter plasmid to measure Erk activity, therefore, Albeck did not to teach or reasonably suggest that the vector with a therapeutic polypeptide, such as a therapeutic polypeptide that can provide for selective killing of cells in the target tissue, such as cancer cells as claimed in amended claim 1. Therefore, the prior rejection of Claim(s) 1-2, and 15 are rejected under 35 U.S.C. 103 as being unpatentable over Albeck et al., (Molecular Cell, Vol. 49, p. 249-261, 2013) and Claims 1 and 12-13 under 35 U.S.C. 103 as being unpatentable over Albeck et al, in view of Luo et al., (WO2005035777) and Claims 1, 14 and 16-17 under 35 U.S.C. 103 as being unpatentable over Albeck et al., in view of Goodearl et al., (US5882893A) and Debinski et al., (US20080188438A1) are withdrawn. Claim Rejections - 35 USC § 112(a) (Written description) The following is a quotation of the first paragraph of 35 U.S.C.112(a): (a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention. The following is a quotation of the first paragraph of pre-AIA 35 U.S.C.112: The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention. Claims 1-2, 12-17 and 40 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim contains subject matter that was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for pre-AIA the inventor, at the time the application was filed, had possession of the claimed invention. Under the written description guidelines (see MPEP 2163), the Examiner is directed to determine whether one skilled in the art would recognize that the Applicant was in possession of the claimed invention as a whole at the time of filing. The following considerations are critical to this determination. To satisfy the written description requirement, a patent specification must describe the claimed invention in sufficient detail so that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. See, e.g., Moba, B.V. v. Diamond Automation, Inc., 325 F.3d 1306, 1319, 66 USPQ2d 1429, 1438 (Fed. Cir. 2003); Vas-Cath, Inc. v. Mahurkar, 935 F.2d at 1563, 19 USPQ2d at 1116. An original claim may lack written description support when (1) the claim defines the invention in functional language specifying a desired result but the disclosure fails to sufficiently identify how the function is performed or the result is achieved or (2) a broad genus claim is presented but the disclosure only describes a narrow species with no evidence that the genus is contemplated. See Ariad Pharms., Inc. v. Eli Lilly & Co., 598 F.3d 1336, 1349-50 (Fed. Cir. 2010) (en banc). The written description requirement is not necessarily met when the claim language appears in ipsis verbis in the specification. "Even if a claim is supported by the specification, the language of the specification, to the extent possible, must describe the claimed invention so that one skilled in the art can recognize what is claimed. The appearance of mere indistinct words in a specification or a claim, even an original claim, does not necessarily satisfy that requirement." Enzo Biochem, Inc. v. Gen-Probe, Inc., 323 F.3d 956, 968, 63 USPQ2d 1609, 1616 (Fed. Cir. 2002). Accordingly, to satisfy the written description requirement, the specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. Vas-Cath, Inc. v. Mahurkar, 935 F.2d 1555, 1562-63, 19 USPQ2d 1111 (Fed. Cir. 1991). See also MPEP 2163. Claim 1 is broadly drawn to a vector comprising a first nucleic acid sequence comprising a promoter operably linked to a second nucleic acid sequence encoding the genus of any therapeutic polypeptide. Claim 40 broadly drawn to activation of the genus of any prodrug as the effect of any therapeutic protein. However, the disclosure as originally filed does not provide adequate written description support for the full breadth of the invention as presently claimed. The specification discloses that the therapeutic polypeptide comprises a Herpes simplex virus thymidine kinase (HSVtk) polypeptide or a yeast cytosine deaminase (yCD) polypeptide ([0309]-[0310] of US20240115727A1) and the prodrug is selected from the group consisting of ganciclovir, acyclovir and 5-fluorocytosine [0020], [0320]. SEPC discloses in Figs. 5A and 5B that the HSVtk kinase was used with a nuclear localization sequence (NLS), and an FRA-1 integrated reporter element (FRA-1 PEST domain) (FIRE). The construct is used with ganciclovir (GCV), a prodrug converted to a toxic product by HSVtk. Therefore, phosphorylation of the FIRE domain by ERK stabilizes HSVtk-FIRE fusion protein expression, creating an alternative ERK-selective suicide gene product ([0414] of US20240115727A1). In an alternative embodiment SEPC discloses in Figs. 12A and 12B, that yCD was used with a nuclear localization sequence (NLS), and an FRA-1 integrated reporter element (FRA-1 PEST domain) (FIRE). The construct is used with 5-fluorocytosine (5-FC), a prodrug converted to a toxic product by yCD. Therefore, phosphorylation of the FIRE domain by ERK stabilizes yCD-FIRE fusion protein expression, creating an alternative ERK-selective suicide gene product ([0421] of US20240115727A1). Furthermore, Fig. 3 discloses the HSVtk expression in dividing cells results in cell death when combined with exposure to the herpes medications acyclovir or ganciclovir, through phosphorylation of these nucleoside analogs into aberrant nucleotides that are incorporated into DNA ([0397] of US20240115727A1). Therefore, SPEC has specific adequate support for specific prodrug converted to a toxic product by specific therapeutic polypeptide. Accordingly, the specification fails to adequately describe the full scope of claim 1 and 40. The specification supports only a narrow scope of the inventive concept as described in above, but does not provide support for the full scope of the product of any prodrug converted or activated to a toxic product by any therapeutic polypeptide. In the prior art Beltinger et al. (PNAS Vol. 96, pp. 8699–8704, July 1999; cited in PTO892; hereinafter “Beltinger”) discloses that Herpes Simplex Virus thymidine kinase (HSV-TK) can activate the prodrug ganciclovir by phosphorylating it into an active, toxic form (GCV-P). This activated ganciclovir triphosphate can then be incorporated into DNA, causing chain termination and leading to cell death. This mechanism is the basis for the HSV-TK/GCV system used in suicide gene therapy, where it's designed to kill cells that express the HSV-TK gene (abstract and p. 8699 left col. 2nd ¶). Furthermore, Pierrefite-Carle et al. (J Natl Cancer Inst. 1999 Dec 1;91(23):2014-9; cited in PTO892; hereinafter “Pierrefite-Carle”) cytosine deaminase can activate 5-fluorocytosine by converting it into the toxic anticancer prodrug 5-fluorouracil (5-FU). This process is used in targeted cancer therapy, where the cytosine deaminase gene is introduced into cancer cells. When a patient is treated with 5-fluorocytosine, the enzyme converts it to 5-FU inside the tumor, killing the cancer cells. This enzyme-prodrug system is a form of cancer gene therapy. By introducing the CD gene into tumor cells, they become a "suicide gene" system. Therefore, it is obvious that prior art does not support to identify the genus of any prodrug converted or activated to a toxic product by any therapeutic polypeptide. The prior art does not support to any prodrug converted or activated to a toxic product by any therapeutic polypeptide. Accordingly at the time of filling any prodrug converted or activated to a toxic product by any therapeutic polypeptide is not well established and POSITA cannot predictably identify any prodrug converted or activated to a toxic product by any therapeutic polypeptide that exercise in this invention to prepare the vector directs expression of the fusion protein in the target tissue to provide selective cell killing in the target tissue. Therefore, it concludes that the claimed genus of any prodrug converted or activated to a toxic product by any therapeutic polypeptide doesn't have an adequate written description. It concludes that a skilled artisan would find the specification inadequately described. Therefore, the Applicant did not sufficiently possess the broader invention as claimed in claim 1 and dependent claims 2, 12-17 and 40. Subject matter free of art. Current application in claim 5 applicant claimed a vector comprising a first nucleic acid sequence comprising a promoter operably linked to a second nucleic acid sequence encoding a therapeutic polypeptide and a third nucleic acid sequence encoding a Fra1-based integrative reporter (FIRE) domain that is stabilized against degradation when phosphorylated by extracellular regulated kinase (ERK) activity in a target tissue, wherein the second nucleic acid sequence and the third nucleic acid sequence are in frame with each other such that the vector encodes a fusion protein comprising the therapeutic polypeptide and the FIRE domain and further wherein the promoter directs expression of the fusion protein in the target tissue, wherein the therapeutic polypeptide comprises a Herpes simplex virus thymidine kinase (HSVtk) polypeptide or a yeast cytosine deaminase (yCD) polypeptide. In the closest prior art, Albeck teaches a vector comprising NLS-mVenus-Fra-1 (163-271), which rapidly is degraded but is stabilized by ERK/RSK after phosphorylation of Fra-1 domain (e.g., Figure 1C, p. 250). FIRE is designed as amino acids 163-271 of Fra-1 were fused to the C terminus of mVenus, with a nuclear localization sequence (NLS) at the N terminus (e.g., Figure 1(C), p. 251). Figure 1(D) shows induction of FIRE fluorescence. Cells treated with EGF shows expression of FIRE fluorescence (green line) (e.g., Figure 1(D), p. 251, Figure 1D, p. 250). However, Albeck didn’t fuse mVenus in the C-terminus to inducting FIRE fluorescence. Albeck only used an ERK regulation strategy with a reporter plasmid to measure ERK activity, not with a therapeutic polypeptide, such as a therapeutic polypeptide that can provide for selective killing of cells in the target tissue, such as cancer cells. Particularly, Albeck only showed that the fusion protein approach could be used to stabilize the expression of a fluorescent protein, which lacked an effect in the target tissue, such as enzymatic activity. Albeck does not teach or fairly suggest a vector comprising a first nucleic acid sequence comprising a promoter operably linked to a second nucleic acid sequence encoding a therapeutic polypeptide, wherein the therapeutic polypeptide comprises a Herpes simplex virus thymidine kinase (HSVtk) polypeptide or a yeast cytosine deaminase polypeptide. Accordingly, instant claims 5-9 and 39 are representing a novel, non-obvious product and distinct from the prior art. RESPONSE TO ARGUMENTS Applicant's arguments filed on 03 November 2025 are acknowledged. Applicant' s arguments with respect to Claims 1-2, and 12-17 rejected under 35 U.S.C. § 103 upon the contention that the claims are unpatentable over Albeck in view of Luo, Albeck in view of Goodearl and Debinski have been considered but are moot because the rejection under 103 has been withdrawn and discusses in “Withdrawn 35 USC § 103” ¶. Conclusion Claims 1-2,12-17 and 40 are rejected. Claims 5-9 and 39 are allowed. Examiner Contact Information Any inquiry concerning this communication or earlier communications from the examiner should be directed to MASUDUR RAHMAN whose telephone number is (571)272-0196. The examiner can normally be reached M-F 8-5 (EST). 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, Christopher Babic can be reached on (571) 272-8507. 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. /MASUDUR RAHMAN/ Patent Examiner, Art Unit 1633 /JEREMY C FLINDERS/ Primary Examiner, Art Unit 1684
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Prosecution Timeline

Oct 30, 2019
Application Filed
Sep 23, 2022
Non-Final Rejection — §103, §112
Mar 28, 2023
Response Filed
May 23, 2023
Final Rejection — §103, §112
Nov 30, 2023
Notice of Allowance
Jul 01, 2024
Request for Continued Examination
Jul 09, 2024
Response after Non-Final Action
Aug 15, 2024
Non-Final Rejection — §103, §112
Jan 21, 2025
Response Filed
Apr 21, 2025
Final Rejection — §103, §112
Oct 10, 2025
Examiner Interview Summary
Oct 10, 2025
Examiner Interview (Telephonic)
Nov 03, 2025
Request for Continued Examination
Nov 04, 2025
Response after Non-Final Action
Dec 04, 2025
Non-Final Rejection — §103, §112 (current)

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Study what changed to get past this examiner. Based on 5 most recent grants.

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Prosecution Projections

5-6
Expected OA Rounds
70%
Grant Probability
99%
With Interview (+37.4%)
4y 1m
Median Time to Grant
High
PTA Risk
Based on 99 resolved cases by this examiner. Grant probability derived from career allow rate.

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