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 . 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.
Continued Examination Under 37 CFR 1.114
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 01/21/2026 has been entered.
Priority
The instant application is a 371 of PCT/US2021/023189 filed on 03/19/2021, which claims domestic benefit to US provisional application no. 62/991,818 filed on 03/19/2020.
Status of the Claims
The claim amendments and remarks filed on 01/21/2026 are acknowledged. Claims 1-2 are amended. Claims 4 and 10 are cancelled.
Accordingly, claims 1-3, 5-9, and 11-20 are pending and being examined on the merits herein.
Withdrawn Rejections
The 35 USC 112(b) rejection over claims 4 and 10 are withdrawn in view of claims 4 and 10 being cancelled.
The 35 USC 103 rejection over Irigoyen for claims 1-3, 5, 9, and 11, over Irigoyen in view of Margulies and Gralinksi for claims 6 and 12, over Irigoyen in view of Morgenstern for claims 7-8 and 13-14 is withdrawn because the primary reference (Irigoyen) in these previous rejections relied upon administering the GSK-2606414 inhibitor for treating SARS-CoV-2 suggested in Irigoyen, however instant claims 1 and 2 have been narrowed to specific inhibitors which does not include the GSK-2606414 inhibitor of Irigoyen.
The 35 USC 103 rejection over Irigoyen in view of Chan and Boyce for claims 4, 10, 15, and 18 are withdrawn in view of claims 4 and 10 being cancelled. Furthermore, this rejection relied upon substituting the GSK-2606414 inhibitor of Irigoyen with the Salubrinal of Chan and Boyce, however instant claims 1 and 2 have been narrowed to specific inhibitors which does not include the Salubrinal of Chan and Boyce.
The following grounds of rejection are new or amended as necessitated by Applicant’s amendments.
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 1-3, 9, 15, 17-18, and 20 are rejected under 35 U.S.C. 103 as being unpatentable over Irigoyen et al. (bioRxiv, 2018 in IDS filed on 09/16/2022) in view of Johnston et al. (Plos Pathogens, 2019 in PTO-892 dated 10/27/2025) and Chan et al. (Journal of Virology, 2006 in PTO-892 dated 10/27/2025).
Irigoyen et al. discloses the activation of the Unfolded Protein Response (UPR) and inhibition of translation initiation during Coronavirus infection (see Abstract). Irigoyen et al. discloses that coronavirus causes a broad range of diseases in animal and humans, ranging from the common cold to severe acute respiratory syndrome (SARS) (see first paragraph in “Introduction” page 3).
Irigoyen et al. demonstrates that PERK inhibitor GSK-2606414 was effective in inhibiting replication of MHV (mouse hepatitis virus) in MHV-infected cells (see section titled “Effect of the PERK inhibitor GSK-2606414 on MHV replication” pages 12-13). Irigoyen et al. discloses that MHV is a model murine coronavirus in the same genus as severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) (see Abstract). Irigoyen discloses that in MHV-infected cells, GSK-2606414 prevented phosphorylation of the PERK substrate, eIF2α, in a dose-dependent manner (see Fig 8A), which lead to a modest increase in both viral and host protein synthesis (see Fig 8A and 8B). Furthermore, Irigoyen discloses that despite the increase viral protein synthesis, the presence of GSK-260614 remarkably showed delayed formation of syncytia in comparison to untreated cells (see Fig 8C) and also discloses that quantification of released virions through TCID50 assays revealed ~four-fold reduction (~75% reduction) in virus titre in cells incubated with GSK-2606414 compared to control cells (see Fig S4B). Irigoyen et al. discloses that relieving inhibition of protein synthesis, which affects both cellular and viral proteins, is detrimental to virus production and the development of syncytia in virus infected cells (see section titled “Effect of the PERK inhibitor GSK-2606414on MHV replication” page 13).
Furthermore, Irigoyen et al. discloses that during CoV replication, the massive production and modification of viral proteins, as well as virion budding-related endoplasmic reticulum (ER) membrane depletion, can lead to overloading of the folding capacity of the ER and, consequently, ER stress (see page 3 lines 75-77). Irigoyen also discloses that UPR-mediated eIF2α phosphorylation may be favorable to MHV replication – perhaps by preventing translation of various anti-viral factors – and the pharmacological manipulation of this UPR branch can be explored as a potential target for antiviral intervention (see page 15, lines 383-385).
Even though Irigoyen suggests the use of a PERK inhibitor for treating SARS-CoV or MERS-CoV, Irigoyen et al. does not teach one of the recited compounds in instant claims 1 and 2 as well as an inhibitor of UPR and/or ISR that is not a PERK inhibitor as recited in instant claims 15 and 18.
Johnston discloses that Herpesviruses usurp host cell protein synthesis machinery to convert viral mRNAs into proteins, and the endoplasmic reticulum (ER) to ensure proper folding, post-translation modification and trafficking of secreted and transmembrane viral proteins (see Abstract). Johnston discloses that overloading ER folding capacity activates the UPR, whereby sensor proteins ATF6, PERK, and IRE1 initiate a stress-mitigating transcription program that accelerates catabolism of misfolded proteins while increasing ER folding capacity (see Abstract). Johnston discloses that Kaposi’s sarcoma-associated herpesvirus (KSHV) can be reactivated from latency by chemical induction of ER stress and demonstrates that ATF6, PERK, and IRE1 were activated upon reactivation from latency and were required for KSHV lytic replication (see Abstract and Fig. 1). Johnston discloses that in order to determine whether activation of PERK or downstream engagement of the ISR are important for viral replication, TREx BCBL1-RTA cells were treated with selective PERK inhibitor GSK2606414 or the ISR inhibitor ISRIB, a small molecule that blocks eIF2 alpha phosphorylation. Johnston demonstrates in Fig 6G that GSK2606414 and ISRIB each inhibited viral particle release by 50% (see second paragraph on page 12 and Figure 6G on page 13).
Chan et al. discloses the modulation of the Unfolded Protein Response by the Severe Acute Respiratory Syndrome Coronavirus Spike Protein (see Abstract). Chan et al. demonstrate that SARS-CoV infection induces ER stress and UPR through S protein (see Fig. 2 on page 9282 and bottom right column on page 9282). Chan et al. discloses that S protein modulated ER stress differentially by stimulating PERK and eIF2 alpha phosphorylation (see bottom right column on page 9282 and Fig.4 on page 9284). Chan et al. discloses that this UPR modulation by the S protein likely represents a viral strategy to combat cellular response and to facilitate viral replication (see left column page 9283). Chan et al. discloses that modulation of ER stress and UPR by SARS-CoV reveals a novel opportunity for pharmaceutical intervention of SARS, and due to the importance of ER stress in various human diseases, including viral infection, small molecules that specifically counteract ER stress have been under intense investigation (see bottom right column page 9285). Chan et al. concludes that because antivirals highly effective for the treatment of SARS have not been identified, further investigations on the use of various ER stress-modulating pharmaceutical agents for anti-SARS-CoV therapy are warranted (see bottom right column page 9285 through left column page 9286).
It would have been prima facie obvious before the effective filing date of the claimed invention to have substituted the GSK-2606414 PERK inhibitor of Irigoyen with the ISRIB of Johnston with further guidance from Chan and to administer this ISRIB to a subject for treating a coronavirus or diseases/disorders caused by coronavirus infection as suggested in Irigoyen and Chan to arrive at the claimed invention.
One of ordinary skill in the art would have made this substitution with a reasonable expectation of success because both Irigoyen et al. and Johnston et al. disclose viruses that induce ER stress and modulate UPR for viral replication, and both references also demonstrate the use of compounds, GSK-2606414 PERK (Irigoyen and Johnston) and ISRIB (Johnston), that inhibit viral replication by counteracting the ER stress via UPR pathway modulation such as PERK or ISR inhibition. Furthermore, Chan also provides guidance that coronaviruses induce ER stress and modulate UPR for viral replication, and further suggests the use of small molecules that specifically counteract ER stress to provide therapeutic effects against coronavirus. Therefore, an ordinary skilled artisan could have predictably considered trying alternative UPR modulating compounds such as the ISRIB of Johnston for the UPR modulation and subsequent reduced viral titre demonstrated in Irigoyen et al. with a reasonable expectation of success.
One of ordinary skill in the art could have administered ISRIB to a subject for treating a coronavirus or diseases/disorders caused by coronavirus infection with a reasonable expectation of success because Irigoyen et al. demonstrates that GSK-2606414, an UPR modulating compound that inhibits PERK, is effective at inhibiting cells infected by MHV, which is a model murine coronavirus in the same genus as SARS-CoV and MERS-CoV, and also provides guidance that coronavirus causes a broad range of diseases in animals and humans, ranging from the common cold to SARS. Furthermore, Chan suggests the use of small molecules that specifically counteract ER stress to provide therapeutic effects against coronavirus and further suggests inhibitors that were effective in herpesvirus that have similar viral replication mechanisms, and Johnston demonstrates inhibiting viral replication of Herpesviruses by blocking pathways of the UPR using PERK inhibitor GSK2606414 or the ISR inhibitor ISRIB.
Claims 1-3, 9, 16, and 19 are rejected under 35 U.S.C. 103 as being unpatentable over Irigoyen et al. (bioRxiv, 2018 in IDS filed on 09/16/2022) in view of Smith et al. (Journal of Medicinal Chemistry, 2015 in PTO-892 dated 10/27/2025) and as evidenced by Torcis (AMG PERK 44 compound information in PTO-892 dated 10/27/2025).
The teachings of Irigoyen et al. are as described above.
Even though Irigoyen suggests the use of a PERK inhibitor for treating SARS-CoV or MERS-CoV, Irigoyen et al. does not teach one of the recited compounds in claims 1 and 2 such as AMG PERK 44.
Smith teaches the structure-based design and optimization of a novel series of selective PERK inhibitors, resulting in the identification of compound 44 as a potent, highly selective, and orally active tool compound suitable for PERK pathway biology exploration both in vitro and in vivo (see Abstract). Here, the compound 44 of Smith is the recited AMG PERK 44 compound as evidenced by Torcis.
Smith teaches that the first potent and selective PERK inhibitors, seen in Fig.1 on page 1427, include GSK-2606414, its fluorinated analog compound 1, and GSK-2656157, which was optimized for preclinical evaluation (see left column page 1427). Smith discloses that there were no known selective PERK inhibitors studies exploring the UPR, and prompted them to initiate a search for tool compounds to validate PERK as an oncology target (see left column, page 1427). Smith teaches their study involved a structure – activity relationship (SAR) and optimization by identifying potent PERK inhibitors as well as modulating certain functional groups / moiety features on these compounds (see section “Lead Optimization and SAR” starting on page 1427 through page 1432). Smith teaches that the final piece of SAR around the kinase hinge-binding moiety involved changing the 2-methylbenzothizaole of compound 38 for the analogous 2-methylquinoline of compound 44 (see right column page 1432).
Smith teaches that compound 44 was an equally potent PERK inhibitor in vitro, with 1000-fold selectivity over GCN2 and with no measurable effects due to GCN2 inhibition in the cellular assays (second paragraph right column page 1432). It had exquisite selectivity over a large panel of kinases, and while the rat pharmacokinetic properties were only moderate, the mouse pharmacokinetic properties were significantly better (Table 2). Oral bioavailability of compound 44 in rat (and mouse) was significantly improved compared with that of compound 38, making it a superior in vivo tool compound. A cocrystal structure of 44 with PERK (Figure 5a) revealed that the quinoline methyl group projects toward the hinge Cys891 carbonyl and the distance (3.4 Å) is suggestive of a hydrogen bond between a methyl C−H and the carbonyl oxygen. The source of the selectivity imparted by the quinoline methyl group of 44 over GCN2 is suggested by comparing the apo structures26 of mouse PERK27 and yeast GCN228 (Figure 5b), where it is evident that the hinge Cys residues of the two proteins adopt different conformations in the apo state. If this difference translates to the protein structure with inhibitor bound, it would place the hinge Cys carbonyl of GCN2 closer to the quinoline methyl group of 44, leading to an unfavorable interaction (see right column page 1432). Smith also demonstrates that compound 44 robustly inhibited PERK autophosphorylation in a pharmacodynamic model for measuring in vivo PERK inhibition (see left column page 1433 and Figure 7 on page 1433).
It would have been prima facie obvious before the effective filing date of the claimed invention to have substituted the GSK-2606414 PERK inhibitor of Irigoyen with the compound 44 (AMG PERK 44) of Smith to arrive at the claimed invention. One of ordinary skill would have been motivated to make this substitution because Smith discloses their study focused on optimizing PERK inhibitors, leading to the discovery of compound 44, which offered several advantages such as exquisite selectivity over a large panel of kinases, improved oral bioavailability, and robust PERK autophosphorylation inhibition. One of ordinary skill in the art would have a reasonable expectation of success because both Irigoyen and Smith disclose that GSK-2606414 and AMG PERK44 are potent PERK inhibitors, and Irigoyen demonstrates that PERK inhibition led to reduced viral titre in MHV, which is a model murine coronavirus in the same genus as SARS-CoV and MERS-CoV.
Claims 5-6 and 11-12 are rejected under 35 U.S.C. 103 as being unpatentable over Irigoyen et al. (bioRxiv, 2018 in IDS filed on 09/16/2022) in view of Smith et al. (Journal of Medicinal Chemistry, 2015 in PTO-892 dated 10/27/2025), as applied to claims 1-2 above, and further in view of Margulies et al. (US20200054638A1 in IDS filed on 09/16/2022), Gralinski et al. (Journal of Pathology, 2015 in PTO-892 dated 05/05/2025), and Stansfield et al. (US20160039798A1 in PTO-892).
The combined teachings of Irigoyen and Smith are as described above and teach the method recited in claims 1-2 as discussed above. Furthermore, Smith demonstrates that compound 44 robustly inhibited PERK autophosphorylation in a pharmacodynamic model for measuring in vivo PERK inhibition (see left column page 1433 and Figure 7 on page 1433). Here, compound 44 had an ED50 of around 3 mg/kg and ED90 of around 60 mg/kg at the 4 hour time point.
The combined references, however, do not teach administering the AMF PERK 44 inhibitor inhibits viral activity by at least 50% or administering in a range of about 0.1 mg/kg to about 500 mg/kg per day for treating coronavirus.
Margulies et al. discloses methods of preventing and/or treating lung injury and/or lung inflammation in a subject comprising administering to the subject a therapeutically effective dose of a PERK pathway inhibitor (see Abstract). Margulies et al. discloses in Embodiment 2 (see paragraph 0168) that the lung injury comprises of acute respiratory distress syndrome (ARDS), and discloses that the PERK inhibitor can be GSK-2606414 (see paragraph 0055). Furthermore, Margulies discloses in FIG.6 and paragraph 0014 that 30 mg/kg oral administration of GSK2606414 was effective in a rat model of ventilator-induced lung injury.
Gralinski et al. (Journal of Pathology, 2015) discloses that acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS), can arise after many types of injury to the lung, including sepsis, mechanical and chemical injury, and bacterial and viral infections. Furthermore, Gralinski et al. discloses that SARS-CoV can cause the development of severe lung disease, including ARDS (see page 191 left column second paragraph).
Stansfield discloses PERK inhibitor compounds (Abstract). Stansfield discloses that aberrant activation of the UPR has been implicated in a wide variety of pathologies and inhibition of the PERK-branch of the UPR can relieve PERK-mediated protein translation inhibition and hence repress protein synthesis under ER stress (paragraph 0003). Therefore, Stansfield discloses that their PERK inhibitor compounds may be therapeutically useful for a variety of diseases that are associated with UPR activation such as viral and inflammatory diseases and others (paragraph 0003 and 0010). Stansfield discloses that an effective therapeutic daily amount of their PERK inhibitor compounds ranges from 0.005 mg/kg to 50 mg/kg (paragraph 0310)
It would have been prima facie obvious before the effective filing date of the claimed invention to have administered the AMG PERK 44 as taught in the combined teachings of Irigoyen and Smith described above in a dosage of 30 mg/kg per day as disclosed in Margulies et al. with further guidance from Gralinski et al., Smith et al., and Stansfield to arrive at the claimed invention. One of ordinary skill in the art would have made these modifications with a reasonable expectation of success because Margulies et al. provides guidance that a 30 mg/kg dosage of GSK2606414 is effective for inhibiting PERK activation and treating a related respiratory syndrome, Gralinski et al. provides guidance that acute lung injury and ARDS can be induced by viral infections such as coronavirus, and Smith demonstrates that AMG PERK 44 was an effective in vivo PERK inhibitor with an ED50 of around 3 mg/kg and ED90 of around 60 mg/kg. Furthermore, Stansfield discloses an effective dosage amount between 0.005 mg/kg to 50 mg/kg per day to treat UPR associated diseases such as viral or inflammatory diseases using a PERK inhibitor.
Lastly, even though the combined teachings described above do not teach that AMG PERK 44 inhibited viral activity by at least 50% by, one of ordinary skill in the art could have reasonably expected that the AMG PERK 44 as described above would result in inhibiting at least 50% viral activity because Irigoyen demonstrates a ~four-fold reduction (~75% reduction) in virus titre in cells incubated with GSK-2606414 compared to control cells, and Smith discloses that AMG PERK 44 is an equivalent PERK inhibitor with additional advantages such as improved oral bioavailability as described above.
Furthermore, this 50% viral activity inhibition would flow naturally from the combined teachings described above because the combined teachings provide guidance of administering the same AMG PERK 44 in the same effective dosages for treating MERS-CoV, and as demonstrated in FIG. 6A and 6B of the instant disclosure, AMG PERK 44 effectively inhibited viral titer for in vitro MERS-CoV infected fibroblast (FB) in a dose-dependent manner (also see page 30 of instant specification).
MPEP 2145 II recites “The fact that appellant has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious." Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter.m 1985) (The prior art taught combustion fluid analyzers which used labyrinth heaters to maintain the samples at a uniform temperature. Although appellant showed that an unexpectedly shorter response time was obtained when a labyrinth heater was employed, the Board held this advantage would flow naturally from following the suggestion of the prior art.). See also Lantech Inc. v. Kaufman Co. of Ohio Inc., 878 F.2d 1446, 12 USPQ2d 1076, 1077 (Fed. Cir. 1989), cert. denied, 493 U.S. 1058 (1990) (unpublished — not citable as precedent) ("The recitation of an additional advantage associated with doing what the prior art suggests does not lend patentability to an otherwise unpatentable invention.").”
Claims 7-8 and 13-14 are rejected under 35 U.S.C. 103 as being unpatentable over Irigoyen et al. (bioRxiv, 2018 in IDS filed on 09/16/2022) in view of Smith et al. (Journal of Medicinal Chemistry, 2015 in PTO-892 dated 10/27/2025), as applied to claims 1-2 above, and further in view of Morgenstern et al. (Biochemical and Biophysical Research Communications, 2005 in PTO-892 dated 05/05/2025).
The combined teachings of Irigoyen and Smith are as described above and teach the method recited in claims 1-2 as discussed above.
The combined references, however, do not teach further administering an antiviral drug such as interferon or ribavirin.
Morgenstern et al. discloses that ribavirin can inhibit SARS-CoV replication in five different cell types of animal or human origin at therapeutically achievable concentrations (see Abstract). Furthermore, Morgenstern et al. discloses that the combination of ribavirin and interferon-β was highly synergistic for anti-SARS-CoV action (see Abstract).
It would have been prima facie obvious before the effective filing date of the claimed invention to have combined the AMG PERK 44 as taught in the combined teachings of Irigoyen and Smith described above with the ribavirin and interferon-β of Morgenstern to treat coronavirus or diseases/disorders caused by coronavirus. One of ordinary skill in the art would have made this modification with a reasonable expectation of success because both Irigoyen et al. and Morgenstern et al. teach that their respective compounds are useful for the same purpose of treating SARS-CoV. See In re Kerkhoven, MPEP 2144.06 section I.
Response to Arguments
Applicant’s arguments filed on 1/21/2026 have been fully considered in so far as they apply to the rejections of the instant office action, but were not persuasive.
Applicant states that Chan merely suggests that small molecules which counteract ER stress may treat SARS, and that Chan does not provide any guidance on what these molecules may be. Applicant states that an ordinary skilled artisan would recognize that an effective treatment for one virus will not necessarily be effective for a different virus. Applicant further states that Johnston also does not provide any reasonable expectation of success in using ISRIB for treating coronavirus. Applicant states that Johnston teaches that ISRIB may be an effective treatment for KSHV and not coronavirus.
In response to Applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). Furthermore, MPEP 2141 II C states that "A person of ordinary skill in the art is also a person of ordinary creativity, not an automaton." KSR, 550 U.S. at 421, 82 USPQ2d at 1397. "[I]n many cases a person of ordinary skill will be able to fit the teachings of multiple patents together like pieces of a puzzle." Id. at 420, 82 USPQ2d at 1397. Office personnel may also take into account "the inferences and creative steps that a person of ordinary skill in the art would employ." Id. at 418, 82 USPQ2d at 1396.”
Here, the new rejection above relies on the combined teachings of Irigoyen, Johnston, and Chan to arrive at the claimed invention. While neither Chan nor Johnston teaches using ISRIB for the treatment of a coronavirus, Irigoyen and Chan disclose or suggest the use of small molecules that specifically counteract ER stress to provide therapeutic effects against coronavirus, Chan further suggests the use of inhibitors that were effective in herpesvirus that have similar viral replication mechanisms via UPR modulation, and Johnston demonstrates inhibiting viral replication of Herpesviruses by blocking pathways of the UPR using PERK inhibitor GSK2606414 or the ISR inhibitor ISRIB. Therefore, when viewing the combination of these references, an ordinary skilled artisan could have predictably considered trying alternative UPR modulating compounds such as the ISRIB of Johnston for the UPR modulation and subsequent reduced viral titre demonstrated by the GSK2606414 of Irigoyen et al. with a reasonable expectation of success.
Applicant states that Smith does not provide any reasonable expectation of success in using the AMG PERK 44 against coronavirus. Applicant states that an ordinary skilled artisan would recognize that an inhibitor will not necessarily serve as an effective treatment for a specific virus merely because it demonstrates certain pharmacokinetic properties. Applicant states that Smith provides no teaching or suggestion that AMG PERK 44 will have any therapeutic use for any disease or condition, and that Smith’s “discovery” of AMG PERK 44 as a PERK inhibitor does not provide any disclosure or suggestion to treat coronavirus.
In response to Applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). Furthermore, MPEP 2141 II C states that "A person of ordinary skill in the art is also a person of ordinary creativity, not an automaton." KSR, 550 U.S. at 421, 82 USPQ2d at 1397. "[I]n many cases a person of ordinary skill will be able to fit the teachings of multiple patents together like pieces of a puzzle." Id. at 420, 82 USPQ2d at 1397. Office personnel may also take into account "the inferences and creative steps that a person of ordinary skill in the art would employ." Id. at 418, 82 USPQ2d at 1396.”
Here, the amended rejection above relies on the combined teachings of Irigoyen and Smith. While Smith does not teach or suggest the use of AMG PERK 44 against a coronavirus, an ordinary skilled artisan would have been motivated to substitute the GSK2606414 PERK of Irigoyen with the AMG PERK 44 of Smith because Smith discloses their study focused on optimizing PERK inhibitors, leading to the discovery of compound 44, which offered several advantages such as exquisite selectivity over a large panel of kinases, improved oral bioavailability, and robust PERK autophosphorylation inhibition. One of ordinary skill in the art would have a reasonable expectation of success because both Irigoyen and Smith disclose that GSK-2606414 and AMG PERK 44 are potent PERK inhibitors, and Irigoyen demonstrates that PERK inhibition led to reduced viral titre in MHV, which is a model murine coronavirus in the same genus as SARS-CoV and MERS-CoV.
Conclusion
No claim is found allowable.
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/D.H.C./Examiner, Art Unit 1693
/SCARLETT Y GOON/Supervisory Patent Examiner
Art Unit 1693