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 claims 1-5, 11, 17, 22, 48, 51, 53, 54, 65, 66, and 79-83 in the reply filed on 02/06/2026 is acknowledged.
Applicant’s election without traverse of a small molecule as the first moiety, specifically GRL-617, a stapled peptide that binds to or recruits the protein degrader as the second moiety, papain-like protease as the first protein, human double minute 2 as the specific second protein, and a chimera comprising a compound having the structure of the molecule depicted in the law row of Fig. 7 in the reply filed on 02/06/2026 is acknowledged.
Claims 6-10, 12-16, 18-21, 23-47, 49, 50, 52, 55-56, 59-62, 64, and 67-71 were previously cancelled, and claims 57, 58, 63, and 72-78 are presently cancelled.
Claims 11 and 17 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 02/06/2026, and Applicant recited in the reply that claims 11 and 17 do not read on the elected species.
Claim Objections
Claim 65 is objected to because of the following informalities: Where possible, claims are to be complete in themselves. Incorporation by reference to a specific figure or table "is permitted only in exceptional circumstances where there is no practical way to define the invention in words and where it is more concise to incorporate by reference than duplicating a drawing or table into the claim. Incorporation by reference is a necessity doctrine, not for applicant’s convenience." Here, references to Fig. 7 and Fig. 14A are not necessary on account of the fact that there exists a practical way to define the invention in words or by duplicating the drawings in the claim. It is advised that Applicant define the invention in words or duplicate the drawings in the claim. Appropriate correction is required.
Claims 82 and 83 are objected to because of the following informalities: Claim 82 is an incomplete sentence, lacks substance, does not end with a period, and the figure in claim 83 is blurred and rendered unintelligible. It is advised that Applicant complete or remove the sentence of claim 82 and render clear or remove the figure of claim 83. Appropriate correction is required.
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.
Claim 54 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 65 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
As discussed above, claim 65 incorporates references to the specification, particularly Figures 7 and 14A, but this is permitted only in exceptional circumstances where there is no practical way to define the invention in words and where it is more concise to incorporate by reference than duplicating a drawing or table into the claim. The claim recites “[t]he chimera of claim 1, which comprises a compound having the structure of any one of the molecules depicted in Fig. 7 or Fig. 14A.” Seeing as the claim impermissibly references matter from the specification and does not define the invention in words or duplicate drawings or tables, the claim is rendered indefinite.
Claims 82 and 83 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
As discussed above, claim 82 recites the following incomplete sentence: “the chimera of claim 80, wherein the first moiety”. Given the fact that the sentence is incomplete, the claim fails to particularly point out and distinctly claim the subject matter which the inventors regard as the invention.
As discussed above, the figure in claim 83 is blurred and rendered unintelligible. Given the fact that the figure is unclear, the claim fails to particularly point out and distinctly claim the subject matter which the inventors regard as the invention.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 1, 4, 51, 53, and 54 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Liu et al. (Liu, Yuzhi et al. “The development of Coronavirus 3C-Like protease (3CLpro) inhibitors from 2010 to 2020.” European journal of medicinal chemistry vol. 206 (2020): 112711; made available online 6 August 2020).
With regard to claim 1, Liu et al. teach proteolytic targeting chimaera (PROTAC) technology that can be used in anti-coronaviral drugs that induce the intracellular degradation of functional non-structural proteins of exogenous viruses (see page 16, paragraph 1). They teach the use of a bifunctional small molecule that links a target protein and an E3 ligase in the cell such that the target protein is ubiquitinated, and the ubiquitinated protein is then recognized by the proteasome, which leads to degradation of the protein (see page 16, paragraph 1). They further teach that only the NS3/4A protease degrader DGY-08-097 of hepatitis virus has been reported in use against degradation of foreign proteins, and its antiviral activity and resistance characteristics are significantly superior to those of the traditional drugs, which they use as a motivation to apply this technology to coronaviral proteases (see page 16, paragraph 1). Thus, they propose that existing 3CLpro (a coronaviral protease) inhibitors can be combined with PROTAC technology to develop coronavirus 3CLpro PROTACs, which can lead to multiple rounds of 3CLpro degradation and would avoid the intracellular accumulation of 3CLpro in infected cells, completely blocking the biological function of coronavirus 3CLpro and its downstream viral proteins and inhibiting the assembly and replication of the coronavirus in infected cells (see page 16, paragraph 1). Within the bifunctional chimeras, Liu et al. also teach the use of inhibitors of coronaviral proteases, specifically 3CLpro, with piperidine, 3-pyridyl, or triazole moieties on account of benefits like their ability in interact with numerous classes of proteins (see page 6, paragraph 4 and page 8, paragraph 4). As seen in Figure 20 of Liu et al., the PROTAC functional domains are directly attached, seeing as the single PROTAC connects both the ligase and the 3CLpro (see Figure 20, page 15).
With regard to claim 4, as discussed above, Liu et al. teach the use of a bifunctional small molecule to links the target protein and the E3 ligase (see page 16, paragraph 1).
With regard to claim 51, Liu et al. teach that the chimera discussed above can inhibit assembly and replication of coronavirus infected cells, as well as blocking the biological function of coronaviral proteases (see page 16, paragraph 1).
With regard to claim 53, Liu et al. teach that the chimera discussed above can inhibit assembly and replication of coronavirus infected cells, as well as blocking the biological function of coronaviral proteases (see page 16, paragraph 1).
With regard to claim 54, Liu et al. teach that the chimera discussed above can inhibit assembly and replication of coronavirus (an RNA virus) infected cells, as well as blocking the biological function of coronaviral proteases (see page 16, paragraph 1).
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 (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
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.
Claims 1-5, 22, 48, 51, 53, 54, 65, 66, and 79-81 are rejected under 35 U.S.C. 103 as being unpatentable over Liu et al. (Liu, Yuzhi et al. “The development of Coronavirus 3C-Like protease (3CLpro) inhibitors from 2010 to 2020.” European journal of medicinal chemistry vol. 206 (2020): 112711; made available online 6 August 2020) in view of Ratia et al. (Ratia, Kiira et al. “A noncovalent class of papain-like protease/deubiquitinase inhibitors blocks SARS virus replication.” Proceedings of the National Academy of Sciences of the United States of America vol. 105,42 (2008): 16119-24) and US 20190300576 A1, hereinafter Pentelute et al. (filed 2018-11-30 and published 2019-10-03), and in further view of Hines et al. (Hines, John et al. “MDM2-Recruiting PROTAC Offers Superior, Synergistic Antiproliferative Activity via Simultaneous Degradation of BRD4 and Stabilization of p53.” Cancer research vol. 79,1 (2019): 251-262) and US 9250238 B2, hereinafter Low et al., as evidenced by Uldrijan et al. (Uldrijan, Stjepan et al. “An essential function of the extreme C-terminus of MDM2 can be provided by MDMX.” The EMBO journal vol. 26,1 (2007): 102-12).
With regard to claim 1, as discussed above, Liu et al. teach proteolytic targeting chimaera (PROTAC) technology that can be used in anti-coronaviral drugs that induce the intracellular degradation of functional non-structural proteins of exogenous viruses (see page 16, paragraph 1). They teach the use of a bifunctional small molecule that links a target protein and an E3 ligase in the cell such that the target protein is ubiquitinated, and the ubiquitinated protein is then recognized by the proteasome, which leads to degradation of the protein (see page 16, paragraph 1). They further teach that only the NS3/4A protease degrader DGY-08-097 of hepatitis virus has been reported in use against degradation of foreign proteins, and its antiviral activity and resistance characteristics are significantly superior to those of the traditional drugs, which they use as a motivation to apply this technology to coronaviral proteases (see page 16, paragraph 1). Thus, they propose that existing 3CLpro (a coronaviral protease) inhibitors can be combined with PROTAC technology to develop coronavirus 3CLpro PROTACs, which can lead to multiple rounds of 3CLpro degradation and would avoid the intracellular accumulation of 3CLpro in infected cells, completely blocking the biological function of coronavirus 3CLpro and its downstream viral proteins and inhibiting the assembly and replication of the coronavirus in infected cells (see page 16, paragraph 1). Within the bifunctional chimeras, Liu et al. also teach the use of inhibitors of coronaviral proteases, specifically 3CLpro, with piperidine, 3-pyridyl, or triazole moieties on account of benefits like their ability in interact with numerous classes of proteins (see page 6, paragraph 4 and page 8, paragraph 4). As seen in Figure 20 of Liu et al., the PROTAC functional domains are directly attached, seeing as the single PROTAC connects both the ligase and the 3CLpro (see Figure 20, page 15).
With regard to claim 2, although Liu et al. teach the chimera discussed above wherein a first and second moiety can be joined together to target and ubiquitinate coronaviral proteases, they do not teach that the second moiety can be the HDM2-targeting moiety SEQ ID NO: 1 of the instant application. Here, Pentelute et al. claim that the peptide of SEQ ID NO: 40 of the reference application, which is identical to SEQ ID NO: 1 of the instant application (see claims 1, 12, and 40). They motivate its use by teaching that it can be used to disrupt p53-MDM2 interaction when used in a pharmaceutical composition (see claims 1, 12, and 40). This is a motivation for the use of the peptide in disease treatment because p53 is an essential regulator of disease response (see [0442]). Specifically, as stresses are imposed on a cell, p53 is believed to orchestrate a response that leads to either cell-cycle arrest and DNA repair or programmed cell death (see [0442]). Here, it is worth noting that, according to Uldrijan et al., MDM2 and HDM2 are different names for the name ubiquitin ligase that targets p53 (see Abstract and page 102, paragraph 2). Seeing as p53 can be altered by MDM2, if MDM2 is intercepted by MDM2-targeting moieties like those taught in Pentelute et al., suppression of p53 can be prevented, maintaining normal cell responses to stressors (see [0442-0443]). This provides a clear motivation for the use of MDM2-targeting moieties in disease treatment given the broad role of p53 as an important regulator of cell death in response to disease. Pentelute et al. do not, however, incorporate this MDM2 moiety into a PROTAC chimera like that of Liu et al.
Although Pentelute et al. do not explicitly claim that the aforementioned sequence is used in a PROTAC like that of Liu et al., Hines et al. teach that the use of MDM2-binding moieties in PROTACs is well-known in the art (see page 3, paragraph 3). Specifically, they teach that the first all-small molecule PROTAC included recruitment of MDM2 (see page 3, paragraph 3), and that MDM2 can be used for nanomolar-potency PROTAC mediated target degradation, as it retains the p53-stabilizing activity of the parent molecule, allowing a MDM2-recruiting PROTAC to be more active against disease (see page 3, paragraph 4). Here, Hines et al. provide a clear motivation for targeting MDM2 in PROTACs because of their interaction with p53, and Pentelute et al. teach MDM2-p53-targeting peptides that modulate MDM2-p53 activity. As discussed above, given the clear motivations to use SEQ ID NO: 40 of Pentelute et al. (SEQ ID NO: 1 of the instant application) to target MDM2-p53 interaction because of the role of p53 in disease-related cell death, as well as the clear motivation to use MDM2-targeting moieties in PROTACs recited by Hines et al., it would have been obvious to one having ordinary skill in the art prior to the effective filing date of the instant application to combine the references to use SEQ ID NO: 1 of the instant application in a PROTAC chimera like that of Liu et al.
With regard to claim 3, Liu et al. teach the chimera discussed above, but they do not teach the use of a linker between the moieties of the chimera. Here, Low et al. teach a linker comprising the linker structure of Fig. 7 of the instant application (see columns 103 and 104, Scheme 11). Low et al. motivate the use of linkers such as this on account of the fact that their linker is a bishydrazide, and bishydrazides can be useful as chelating agents or as supramolecular recognition motifs (see column 22, lines 17-18). Moreover, they are often used to link polymers or biopolymers, and they found benefits like an ability to be selectively monofunctionalized (see column 22, lines 20-27). They further teach that their linkers can be useful in pathogen detection within the context of their invention (see column 29, lines 21-23). These benefits provide clear motivations to combine the references and use the linkers of the invention of Low et al. in anti-pathogen treatments. As such it would have been obvious to one having ordinary skill prior to the effective filing date of the instant application to combine the references and use the linkers of the invention of Low et al. in anti-pathogen treatments like the chimera of Liu et al.
With regard to claims 5 and 79, Liu et al. teach the chimera discussed above. Although Liu et al. do not explicitly teach inhibiting PLpro, they do teach inhibiting 3CLpro, another coronaviral protease, and they also teach the observation that key 3CLpro inhibitors, specifically tanshinone-type diterpenes, are selective inhibitors of SARS-CoV 3CLpro and PLpro (see page 13, paragraph 2). Given that tanshinone-type diterpenes are identified as having advantages in selectively inhibiting SARS-CoV 3CLpro, there is a clear motivation to choose tanshinone-type diterpenes compounds as the 3CLpro inhibitor in PROTACs (see page 13, paragraph 2). Seeing as there is a clear motivation to use said inhibitors, and since these tanshinone-type diterpenes are also known selectively inhibit PLpro, it would have been obvious to one having ordinary skill in the art prior to the effective filing date of the instant application to use PLpro inhibitors like tanshinone-type diterpenes in PROTACs, thereby targeting PLpro (see page 13, paragraph 2). This does not, however, provide a motivation for the use of GRL-0617 to target PLpro in particular, nor does it necessarily motivate inhibiting PLpro in the absence of 3CLpro inhibitors.
Although Liu et al. teach the broad motivation to use a PLpro inhibitor in the chimera of Liu et al. discussed above, they do not teach the use of GRL-0617 as the Plpro inhibitor. Here, Ratia et al. teach that GRL-0617 is a potent inhibitor of PLpro, and Ratia et al. motivate its use on account of the fact that it has no associated cytotoxicity and has a unique mode of inhibition that shuts down catalysis at the PLpro active site (see Abstract). Moreover, Ratia et al. argue that the aforementioned benefits of using GRL-0617 make PLpro a viable target for the development of antivirals directed against SARS-CoV because potent noncovalent cysteine protease inhibitors can be developed with specificity directed toward pathogenic deubiquitinating enzymes without inhibiting host deubiquitinating enzymes (see Abstract), further motivating the use of PLpro inhibitors in antivirals targeting SARS-CoV replication. Beyond this, they also motivate the use of PLpro inhibitors on account of the fact that PLpro and 3CLpro function in the same way, specifically catalyzing their own release and that of the other nsps from the polyprotein, thereby initiating virus-mediated RNA replication (see page 16119, paragraph 6). They particularly motivate PLpro inhibitors in the place of 3CLpro inhibitors because, despite numerous studies, potent antivirals that directly target 3CLpro have yet to be developed, whereas the study of Ratia et al. clearly establishes potent inhibitors of PLpro, including GRL-0617 (see 16120, paragraph 4). Given this clear motivation to use GLR-0617 as the targeting moiety for PLpro in SARS-CoV antivirals, it would have been obvious to one having ordinary skill prior to the effective filing date of the instant application to combine the references and choose a GRL-0617 PLpro inhibitor when choosing a SARS-CoV protease target in a chimera like that taught in Liu et al. because of its potent inhibitory properties and lack of cytotoxicity.
Liu et al. and Ratia et al. provide clear motivations for targeting PLpro with the first moiety (see Liu et al. page 13, paragraph 2 and Ratia et al. page 16119, paragraph 6 and 16120, paragraph 4). Further, as discussed above, Ratia et al. provide a clear motivation for using GRL-0617 (see Abstract). Given the reasoning discussed above, it would have been obvious to one having ordinary skill in the art prior to the effective filing date of the instant application to combine the references to target PLpro with the chimera of Liu et al.
With regard to claim 22, as discussed above, Pentelute et al. provide a clear motivation for using the MDM2 (HDM2)-targeting sequence of SEQ ID NO: 1 of the instant application (see claims 1, 12, and 40 and SEQ ID NO: 40 of the reference). Given the reasoning provided above, it would have been obvious to one having ordinary skill in the art prior to the effective filing date of the instant application to combine the aforementioned references and use this HDM2-targeting moiety in an anti-pathogen chimera like that of Liu et al.
With regard to claim 48, Pentelute et al. teach the use of pharmaceutically acceptable carriers in conjunction with the peptides of their invention, including HDM2-targeting moieties (see Pentetule et al. [0422], [0424], and [0426-0427]). As discussed above, there is a clear motivation to combine the aforementioned references to teach the chimera, and given this motivation, it would have been obvious to use the chimera of Liu et al. in combination with the peptide sequence SEQ ID NO 40 of Pentelute et al. and a pharmaceutically acceptable carrier (see Pentetule et al. [0422], [0424], and [0426-0427]).
With regard to claim 65, Liu et al. teach the PROTAC discussed above. Although the references of Liu et al., Ratia et al., Pentelute et al., and Hines et al. provide clear motivations for linking GRL-0617 and the sequence of SEQ ID NO: 1 of the instant application in a chimera like that of Liu et al., they do not explicitly teach the linker depicted in Fig. 7 of the instant application. As discussed above, Low et al. teach a linker comprising the linker structure of Fig. 7 of the instant application (see columns 103 and 104, Scheme 11). Low et al. motivate the use of linkers such as this on account of the fact that their linker is a bishydrazide, and bishydrazides can be useful as chelating agents or as supramolecular recognition motifs (see column 22, lines 17-18). Moreover, they are often used to link polymers or biopolymers, and they found benefits like an ability to be selectively monofunctionalized (see column 22, lines 20-27). They further teach that their linkers can be useful in pathogen detection within the context of their invention (see column 29, lines 21-23). These benefits provide clear motivations to combine the references and use the linkers of the invention of Low et al. in anti-pathogen treatments. As such it would have been obvious to one having ordinary skill prior to the effective filing date of the instant application to combine the references and use the linkers of the invention of Low et al. in anti-pathogen treatments like the chimera of Liu et al.
With regard to claim 66, Pentelute et al. teach the use of pharmaceutically acceptable carriers in conjunction with the peptides of their invention, including HDM2-targeting moieties (see Pentetule et al. [0422], [0424], and [0426-0427]). As discussed above, there is a clear motivation to combine the references, and given this motivation, it would have been obvious to use the chimera of Liu et al. in combination with the peptide sequence SEQ ID NO 40 of Pentelute et al. and a pharmaceutically acceptable carrier (see Pentetule et al. [0422], [0424], and [0426-0427]).
With regard to claims 80 and 81, as discussed above, Pentelute et al. claim that the peptide of SEQ ID NO: 40 of the reference application, which is identical to SEQ ID NO: 1 of the instant application (see claims 1, 12, and 40). They motivate its use by teaching that it can be used to disrupt p53-MDM2 interaction when used in a pharmaceutical composition (see claims 1, 12, and 40). This is a motivation for the use of this HDM2-targeting peptide in disease treatment because p53 is an essential regulator of disease response because, as stresses are imposed on a cell, it is believed to orchestrate a response that leads to either cell-cycle arrest and DNA repair or programmed cell death (see [0442]). Seeing as p53 can be altered by MDM2, if MDM2 is intercepted by MDM2-targeting moieties like those taught in Pentelute et al., suppression of p53 can be prevented, maintaining normal cell responses to stressors (see [0442-0443]). This provides a clear motivation for the use of MDM2-targeting moieties in disease treatment given the broad role of p53 as a regulator of cell death in response to disease. Again, as discussed above, Hines et al. teach that the use of MDM2-binding moieties in PROTACs is well-known in the art (see page 3, paragraph 3). Given the reasoning to combine the references provided above, it would have been obvious to one having ordinary skill in the art prior to the effective filing date of the instant application to combine the references and use the sequence of Pentelute et al. in a chimera like that of Liu et al.
Summary
Claims 1, 3, 4, 51, 53, and 54 are rejected under 35 U.S.C. 102(a)(1) on the grounds of anticipation. Claims 1-5, 22, 48, 51, 53-54, 65-66, 79-81 are rejected under 35 U.S.C. 103 on the grounds of obviousness. Claims 54, 65, 82, and 83 are rejected under 35 U.S.C. 112(b). Claims 65 and 82-83 are objected to on the grounds of informalities.
Conclusion
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/BRENDAN P. OLISS/Examiner, Art Unit 1658
/LIANKO G GARYU/Supervisory Patent Examiner, Art Unit 1654