DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Priority
The instant application claims priority to 371 National Stage Application PCT/EP2023/051296, filed January 19th, 2023, and foreign application, EP22305072.5 filed January 24th, 2022, under 35 U.S.C. 119(a)-(d. Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55. The priority date of January 24th, 2022 is acknowledged.
Information Disclosure Statement
The information disclosure statement (IDS) filed on July 22nd, 2024 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Claim Status
The claims listing filed on July 22nd, 2024 is pending. Claims 1-12 are being examined on the merits in this office action.
Claim Objections
Claim 6 is objected to because of the following informalities: anesthetic is misspelled. Appropriate correction is required.
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.
Claims 1 –6 and 9-12 are rejected under 35 U.S.C. 103 as being unpatentable over Estaquier et al (US20100298209A1) in view of Plassmeyer et al (Plassmeyer, M. et al. Caspases in COVID-19 Disease and Sequela and the Therapeutic Potential of Caspase Inhibitors. medRxiv; 2020.11.02.2022363).
Estaquier et al. claim structure I
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in which: B is the sequence Valine-Aspartic acid (VD), R1 and R2 are hydrogen, R3 and R4 are a fluoro, and the aspartic acid is O-methylated [claims 2, 6, 8, and 10-11]. The compound is caspase inhibitor claimed for the prophylaxis and/or treatment of a SARS coronavirus [claims 12 and 16]. Specifically, Estaquier et al. teach the exact structure of instant formula (I) [0075].
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Estaquier et al. do not teach that caspase inhibition is efficacious against the species SARS-CoV-2, specifically.
Plassmeyer et al. teach that the gene expression levels of select caspases were increased in in vitro SARS-CoV-2 infection models, and single cell RNA-Seq data of blood from COVID-19 patients showed a distinct caspase expression in T cells, neutrophils, and dendritic cells [Abstract line 5]. Pan-caspase inhibition could emerge as a therapeutic strategy to ameliorate or prevent severe COVID-19 outcomes.
Therefore, prior to the effective filing date, one of ordinary skill in the art would find it obvious to use caspase inhibitor instant formula (I) for the treatment of a SARS virus- as taught by Estaquier et al.-like SARS-CoV-2 because Plassmeyer et al. teach that caspase inhibition also could be effective in the later developed SARS-CoV-2.
Regarding claim 2, Estaquier et al.’s active substance is its structure I, which is preferably instant formula I [Abstract and 0122].
Regarding claim 3, Estaquier et al. state that its structure I may be administered in dry form, in solid form (in particular tablet, powder, gelatin capsule, pill, granules, suppository, polymer capsule or compressed tablet, and more precisely accelerated release tablet, enteric-coated tablet or sustained release tablet), in gel form or in the form of a solution or liquid suspension (in particular syrup, injectable, infusible or drinkable solution, microvesicles, liposomes). The compounds can also be in the form of doses in dry form (powder, lyophilisate, etc.) for reconstitution at the time of use using a suitable diluent. Thus, Estaquier et al. also teach pharmaceutically acceptable vehicles
Regarding claim 4, Estaquier et al. claim a composition comprising its structure I and at least one other antiviral agent [claim 35].
Regarding claim 5, Estaquier et al. teach a kit comprising (i) at least one compound of structure I and; (ii) at least one other antiviral agent, in particular at least one other antiretroviral agent, in which compounds (i) and (ii) are separate from one another [0177].
Regarding claim 6, Estaquier et al. claim a composition comprising its structure I and at least one other antiviral agent [claim 35].
Regarding claim 9, Estaquier et al. do not teach the antiviral agent being a monoclonal antibody. Plassmeyer et al. state that the use of specific anti-IL-6 monoclonal antibody has marginal clinical benefit in moderate-severe COVID-19, but it attenuates the cytokine storm [pg 3 pgh 1 line 5].
It is prima facie obvious to combine two compositions, each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose. In re Kerkhoven, 205 U.S.P.Q. 1069 (CCPA 1980). The idea for combining said compositions flows logically from their having been individually taught in the prior art. In re Crockett, 126 U.S.P.Q. 186, 188 (CCPA 1960) [MPEP 2144.06 (I)].
The natural presumption that two or more individually known antiviral agents would, when combined, provide a third composition also useful for treating viral infection caused by SARS-CoV-2, flows logically from each having been individually taught in the prior art. Thus, one of ordinary skill in the art would find it prima facie obvious to combine a monoclonal antibody with instant formula I in a method for treating SARS-CoV-2 to attenuate the effects of a cytokine storm.
Regarding claim 10, Estaquier et al. claim using a compound of structure I in a method for inhibiting viral replication and viral protein synthesis in an animal or human [claims 23-24].
Regarding claims 11 and 12, Plassmeyer et al. teach that inflammatory microvascular thrombi are present in the lung, kidney, and heart, containing neutrophil extracellular traps associated with platelets and fibrin along with changes in red blood cell morphology in COVID-19 patients [pg 17 pgh 2 line 3]. Also, both the metabolic inflammation and apoptosis play a central role in the pathogenesis of metabolic disease such as obesity, diabetes and the progression of nonalcoholic steatohepatisis (NASH) to more severe liver disease [pg 17 pgh 3 line 1]. Their findings support a novel alternate therapeutic approach against COVID-19 using a caspase inhibitor early on in the course of infection to alleviate or prevent disease progression [pg 18 pgh 2 line 1]. Thus, one of ordinary skill in the art can deduce that cardiac injury due to inflammatory microvascular thrombi is part of the diagnosis of COVID-19 and COVID-19 plays a role in the pathogenesis of liver injury. Therefore, prior to the effective filing date, it was obvious to use a caspase inhibitor, such as instant formula I, to prevent a complication of COVID-19, such as liver and heart injury, as Plassmeyer et al. teach that caspase inhibition may prevent disease progression.
Claim 7 is rejected under 35 U.S.C. 103 as being unpatentable over Estaquier et al and Plassmeyer et al., as applied to claims 1-6 and 9-12, in further view of Southerland et al (Southerland B, Kulkarni-Datar K, Keoni C, et al. Q-VE-OPh, a Negative Control for O-Phenoxy-Conjugated Caspase Inhibitors. Journal of Cell Death. 2010;3).
Estaquier and Plassmeyer et al. teach using a caspase inhibitor like instant formula I for the treatment of SARS-CoV-2. Estaquier et al. also teach structure I
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, where B is dipeptide sequence, R1 and R2 are a hydrogen, R3 and R4 are fluoro, preferably being Q-VD-OPh (N-(2(quinolyl)valyl-aspartyl-(2,6-difluorophenoxy)methyl ketone), optionally in an O-methylated form [claims 2, 6, 8, and 10-11 and abstract]. Estaquier and Plassmeyer et al do not teach a compound of formula (I) where B is particularly Val-Glu, instead of Val-Asp, to read on instant N-(2(quinolyl)-valyl-glutamyl-(2,6- difluorophenoxy)methyl ketone.
Southerland et al. teach compounds:
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(Q-VD-OPh) and
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(Q-VE-OPh) [pg 36, Fig. 1], where Q-VE-OPh substitutes a single amino acid, glutamic acid (E) for the aspartic acid (D) in Q-VD-OPh, thereby retaining the identical charge and molecular properties with only the addition of an extra –CH2 group [pg 35, pgh 7 line 5]. Southerland et al. teach that Q-VE-OPh exhibit similar properties as Q-VD-OPh on inhibiting the activation of caspases and cell apoptosis but require 20x greater concentration to have inhibitory effect [pg 36 pgh 1 line 15]. Southerland studied inhibitory effect of Q-VE-OPh and Q-VD-OPh on Jurkat human T leukemia cells [pg 37 Fig 2].
Thus, Southerland et al. teach N-(2(quinolyl)-valyl-glutamyl-(2,6- difluorophenoxy) methyl ketone’s two closest homologues-Q-VE-OPh and Q-VD-OPh-having similar properties on inhibiting the activation of caspases and cell apoptosis, but requiring vastly different concentrations. Estaquier et al teach a method of prophylaxis and/or treatment of viral infection with pharmaceutical composition comprising compound of formula (I), such as Q-VD-OPh in aspartate O-methylated form.
Compounds which are position isomers (compounds having the same radicals in physically different positions on the same nucleus) or homologs (compounds differing regularly by the successive addition of the same chemical group, e.g., by -CH2- groups) are generally of sufficiently close structural similarity that there is a presumed expectation that such compounds possess similar properties. In re Wilder, 563 F.2d 457, 195 USPQ 426 (CCPA 1977). See also In re May, 574 F.2d 1082, 197 USPQ 601 (CCPA 1978) [MPEP 2144.09 (II)]
Southerland et al.’s Q-VE-OPh differs from N-(2(quinolyl)-valyl-glutamyl-(2,6- difluorophenoxy) methyl ketone by the addition of a CH3 group at the oxygen and Estaquier et al.’s aspartate O-methylated Q-VD-OPh differs from N-(2(quinolyl)-valyl-glutamyl-(2,6- difluorophenoxy) methyl ketone by the addition of a CH2 group within aspartate’s chain.
Hence, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the present invention to combine Estaquier’s structure I with N-(2(quinolyl)-valyl-glutamyl-(2,6- difluorophenoxy)methyl ketone to a method of treatment of SARS-CoV-2 since its known analogs-Southerland et al.’s Q-VE-OPh and Estaquier et al.’s aspartate O-methylated Q-VD-OPh-are effective caspase inhibitors and Plassmayer et al. teach caspase inhibition to be efficacious against SARS-CoV-2. Thus, arriving at the claimed method and composition with the reasonable expectation of success.
Claim 8 is rejected under 35 U.S.C. 103 as being unpatentable over Estaquier et al and Plassmeyer et al., as applied to claims 1-6 and 9-12, in further view of Yin et al (Wanchao Yin et al. Structural basis for inhibition of the RNA-dependent RNA polymerase from SARS-CoV-2 by remdesivir. Science 368,1499-1504(2020)).
Estaquier and Plassmeyer et al. teach using a caspase inhibitor like instant formula I for the treatment of SARS-CoV-2. Estaquier et al. teach a composition comprising structure I and at least one other antiviral agent [0005]. Estaquier et al do not teach the antiviral agent to be a viral RNA-dependent RNA polymerase modulators.
Yin et al. teach that replication of SARS-CoV-2 requires the viral RNA-dependent RNA polymerase (RdRp) enzyme, a target of the antiviral drug remdesivir. They report the structures of the SARS-CoV-2 RdRp complex in the apo form as well as in complex with a template-primer RNA and the active form of remdesivir. The structures reveal how chain elongation is inhibited by remdesivir [pg 5 pgh 2 line 8]. Thus, viral RNA-dependent RNA polymerase modulator remdesivir is individually known as antiviral drug, effective against SARS virus.
It is prima facie obvious to combine two compositions, each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose. In re Kerkhoven, 205 U.S.P.Q. 1069 (CCPA 1980). The idea for combining said compositions flows logically from their having been individually taught in the prior art. In re Crockett, 126 U.S.P.Q. 186, 188 (CCPA 1960) [MPEP 2144.06 (I)].
The natural presumption that two or more individually known antiviral agents would, when combined, provide a third composition also useful for treating viral infection caused by SARS-CoV-2, flows logically from each having been individually taught in the prior art.
Therefore, since prior art teaches an antiviral composition suitable to treat viral infection caused by SARS virus, where various known antiviral agents, discussed above, are used individually or in combination, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the present invention to combine known in the art antiviral agents to arrive to the composition of claim 8 with the reasonable expectation of success.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1-10 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-12 and 15-20 of copending Application No. 17998512 in view of Estaquier et al (US 2010/0298209 A1).
Regarding claim 1, ‘512 claim a method of preventing or treating a viral infection caused by SARS-CoV-2 comprising administering therapeutically effective amount of antiviral composition comprising compound of formula (I):
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[claims 1-5 and 16-17]. ‘512’s formula differs from instant formula (I) by one CH2 in the R group of glutamate, changing it to an aspartate in instant formula (I).
Compounds which are position isomers (compounds having the same radicals in physically different positions on the same nucleus) or homologs (compounds differing regularly by the successive addition of the same chemical group, e.g., by -CH2- groups) are generally of sufficiently close structural similarity that there is a presumed expectation that such compounds possess similar properties. In re Wilder, 563 F.2d 457, 195 USPQ 426 (CCPA 1977). See also In re May, 574 F.2d 1082, 197 USPQ 601 (CCPA 1978) [MPEP 2144.09 (II)]
Hence, it is prima facie obvious that one of ordinary skill in the art would expect instant formula (I) to also treat an infection caused by SARS-CoV-2 because it only differs from ‘512’s formula by one CH2. Furthermore, Estaquier et al. also teach instant formula (I).
Estaquier et al. claim structure I
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in which: B is a single amino acid is the sequence Valine-Aspartic acid (VD), R1 and R2 are hydrogen, and R3 and R4 are a fluoro, in which one of aspartic acids is O-methylated [claims 2, 6, 8, and 10-11]. The compound is caspase inhibitor claimed for the prophylaxis and/or treatment of a SARS coronavirus [claims 12 and 16]. Specifically, Estaquier et al. teach the exact structure of instant formula (I) [0075]
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.
Thus, prior to the effective filing date, it was prima facie obvious to one of ordinary skill in the art to add a CH2 to
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, and therefore claim a method for preventing and/or treating a viral infection caused by SARS-CoV-2 in a patient in need thereof, wherein said method comprises a step of administering, to said patient, a compound of instant formula (I).
Regarding claim 2, ‘512 claim a method of preventing or treating an infection using the compound of claim 1 as the active ingredient [claim 10]. Thus, it was obvious to claim a method for preventing and/or treating a viral infection caused by SARS-CoV-2 in a patient in need thereof, wherein said method comprises a step of administering, to said patient in need thereof, a pharmaceutical composition comprising, as active ingredient, the compound of formula (I) or a pharmaceutically acceptable salt or solvate as defined in claim 1.
Regarding claim 3, ‘512 claim a method of preventing or treating a viral infection caused by coronavirus comprising administering therapeutically effective amount of antiviral composition comprising compound of formula (I) further comprising one or more carrier(s), diluent(s) or adjuvant(s) [claim 10]. The viral infection can be SARS-CoV-2 [claim 17]. Thus, it was obvious to claim a method according to claim 2, wherein said pharmaceutical composition further comprises at least one pharmaceutically acceptable vehicle.
Regarding claim 4, ‘512 claim a method of preventing or treating a viral infection caused by coronavirus comprising administering therapeutically effective amount of antiviral composition comprising compound of formula (I) and at least one additional antiviral and/or anti-inflammatory agent [claim 12]. The viral infection can be SARS-CoV-2 [claim 17]. Thus, it was obvious to claim a method according to claim 2, wherein said pharmaceutical composition further comprises at least one additional therapeutic agent.
Regarding claim 5, ‘512 claim a method of preventing or treating a viral infection caused by coronavirus comprising administering therapeutically effective amount of antiviral composition comprising compound of formula (I) and at least one antiviral and/or anti-inflammatory agent different from formula (I) [claim 12]. The viral infection can be SARS-CoV-2 [claim 17]. Thus, it was obvious to claim a method for preventing and/or treating a viral infection caused by SARS-CoV-2 in a patient in need thereof, wherein said method comprises a step of administering, to said patient, a kit of parts comprising or consisting of: a) a compound of formula (I) or a salt or solvate thereof as defined in claim 1 or a pharmaceutical composition comprising, as active ingredient, the compound of formula (I) or a pharmaceutically acceptable salt or solvate, and b) at least one additional therapeutic agent or a pharmaceutical composition comprising at least one additional therapeutic agent.
Regarding claim 6, ‘512 claim a method of preventing or treating a viral infection caused by coronavirus comprising administering therapeutically effective amount of antiviral composition comprising compound of formula (I) and at least one antiviral and/or anti-inflammatory agent different from formula (I) [claim 12]. The viral infection can be SARS-CoV-2 [claim 17]. Thus, it was obvious to claim a method according to claim 4, wherein said at least one additional therapeutic agent is selected from the group consisting of anti-viral agents, anti-inflammatory agents, analgesic agents, muscle- relaxant agents, anesthetic agents, diuretic agents and antibiotic agents.
Regarding claim 7, the compound originally claimed by ‘512 in a method of preventing or treating a viral infection caused by SARS-CoV-2 is N-(2(quinolyl)-valyl-glutamyl-(2,6- difluorophenoxy)methyl ketone
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[claims 1-5 and 16-17].
It is prima facie obvious to combine two compositions, each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose. In re Kerkhoven, 205 U.S.P.Q. 1069 (CCPA 1980). The idea for combining said compositions flows logically from there having been individually taught in the prior art. In re Crockett, 126 U.S.P.Q. 186, 188 (CCPA 1960) [MPEP 2144.06 (I)].
The natural presumption that two or more individually known antiviral agents would, when combined, provide a third composition also useful for treating viral infection caused by SARS-CoV-2, flows logically from each having been individually taught by ‘512 and Estaquier et al. Thus, it was obvious to claim a method according to claim 5, wherein said at least one additional therapeutic agent is the N-(2(quinolyl)-valyl-glutamyl-(2,6- difluoro phenoxy) methyl ketone or a pharmaceutically acceptable salt or solvate thereof.
Regarding claim 8, ‘512 claim a method of preventing or treating a viral infection caused by coronavirus comprising administering therapeutically effective amount of antiviral composition comprising compound of formula (I) and a viral RNA-dependent RNA polymerase modulator [claim 12, 15, and 19]. The viral infection can be SARS-CoV-2 [claim 17]. Thus, it was obvious to claim a method according to claim 6 wherein said anti-viral agents are viral RNA- dependent RNA polymerase modulators or fusion inhibitors.
Regarding claim 9, ‘512 claim a method of preventing or treating a viral infection caused by coronavirus comprising administering therapeutically effective amount of antiviral composition comprising compound of formula (I) and monoclonal antibodies [claim 12, and 15]. The viral infection can be SARS-CoV-2 [claim 17]. Thus, it was obvious to claim a method according to claim 6 wherein said anti-inflammatory agents are monoclonal antibodies.
Regarding claim 10, ‘512 claim a method of prevention or treating a viral infection caused by coronavirus comprising instant formula (I), wherein the method reduces and/or inhibits viral replication or viral protein synthesis [claims 6-7]. The infection can be SARS-CoV-2 [claim 17]. Thus, it was obvious to claim a method according to claim 1, wherein the method is implemented to prevent, inhibit and/or reduce viral replication and/or viral protein synthesis in a subject infected by SARS-CoV-2.
This is a provisional nonstatutory double patenting rejection.
Claims 11-12 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-12 and 15-20 of copending Application No. 17998512 in view of Estaquier et al (US 2010/0298209 A1), as applied to claims 1-10, in further view of Plassmeyer et al (Caspases in COVID-19 Disease and Sequela and the Therapeutic Potential of Caspase Inhibitors Matthew Plassmeyer et al. medRxiv 2020.11.02.20223636).
Regarding claim 11, ‘512 claim a method of prevention or treating a viral infection caused by SARS-Cov-2 comprising instant formula (I) [claims 1 and 17]. ‘512 does not claim the method preventing a complication of COVID-19.
Plassmeyer et al. teach that inflammatory microvascular thrombi are present in the lung, kidney, and heart, containing neutrophil extracellular traps associated with platelets and fibrin along with changes in red blood cell morphology in COVID-19 patients [pg 17 pgh 2 line 3]. Also, both the metabolic inflammation and apoptosis play a central role in the pathogenesis of metabolic disease such as obesity, diabetes and the progression of nonalcoholic steatohepatisis (NASH) to more severe liver disease [pg 17 pgh 3 line 1]. Their findings support a novel alternate therapeutic approach against COVID-19 using a caspase inhibitor early in the course of infection to alleviate or prevent disease progression [pg 18 pgh 2 line 1]. Thus, one of ordinary skill in the art can deduce that cardiac injury due to inflammatory microvascular thrombi is part of the diagnosis of COVID-19 and COVID-19 plays a role in the pathogenesis of liver injury.
Therefore, prior to the effective filing date, it was obvious to claim a method according to claim 1, wherein this method is implemented to prevent a complication of COVID-19 because instant formula (I) is a caspase inhibitor, as taught by Estaquier et al, and Plassmeyer et al. teach that caspase inhibition may prevent disease progression of liver and heart injuries due to COVID-19.
Regarding claim 12, ‘512 claim a method of prevention or treating a viral infection caused by SARS-Cov-2 comprising instant formula (I) [claims 1 and 17]. ‘512 does not claim the method preventing a complication of COVID-19.
Estaquier et al teach that instant formula (I) is a caspase inhibitor and Plassmeyer et al. teach that caspase inhibition may prevent disease progression of liver and heart injuries due to COVID-19. Thus, it was obvious to claim a method according to claim 11, wherein the complication of COVID-19 is pneumonia, acute respiratory distress syndrome (ARDS), acute respiratory failure, liver injury or cardiac injury.
This is a provisional nonstatutory double patenting rejection.
Conclusion
Claim 6 is objected to. Claims 1-12 are rejected under 35 U.S.C. 103. Claims 1-12 are provisionally rejected on the ground of nonstatutory double patenting.
Correspondence
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SACHI JAUHARI whose telephone number is (571)272-3769. The examiner can normally be reached Mon-Fri 9-4.
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/SACHI JAUHARI/Examiner, Art Unit 1654
/LIANKO G GARYU/Supervisory Patent Examiner, Art Unit 1654
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