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 .
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 June 27, 2025, has been entered.
Priority
This application was filed August 12, 2020, and is a 371 application of PCT/US19/17512 filed February 11, 2019, which claims benefit to the provisional application 62/637,460 filed on March 2, 2018, and the provisional application 62/629,435 filed on February 12, 2018.
Claim Status
In the reply filed on June 27, 2025, Applicant has cancelled claims 3, 5, 7, 9-25. Claims 1-2, 4, 6, 8, 53-59 are pending.
Applicant’s election without traverse of Group I (Claims 1-2, 4, 6, and 8) drawn to a method for inhibiting inflammasome activation in cells of an inflammation-affected eye in a subject, in the reply filed on January 17, 2023, is acknowledged.
Currently, claims 1-2, 4, 6, 8, and 53-59 are currently under examination.
Withdrawn Objections & Rejections
Rejections and/or objections not reiterated from the previous office action are hereby withdrawn due to amendment. The following rejections and/or objections are either reiterated or newly applied. They constitute the complete set presently being applied to the instant application.
The rejection of claims 1-2 under 35 U.S.C. 103 as being unpatentable over Copland et al. (Clinical & Experimental Immunology 159.3: 303-314, published 2010, prior art of record), in view of Adhi, Mehreen, et al (PLoS One 8.10: e79661, published 2013, cited IDS 03/05/2021; hereinafter “Adhi”, prior art of record), Cashman et al. (PLoS One 6/4:e19078; published 2011, prior art of record) and Turnberg et al. (Mol Immuno, 40:145-153; published 2003, prior art of record) is withdrawn.
The rejection of claims 4, 6, 8 and 53-59 under 35 U.S.C. 103 as being unpatentable over Copland et al. (Clinical & Experimental Immunology 159.3: 303-314, published 2010, prior art of record), in view of Adhi, Mehreen, et al (PLoS One 8.10: e79661, published 2013, cited IDS 03/05/2021; hereinafter “Adhi”, prior art of record), Cashman et al. (PLoS One 6/4:e19078,published 2011, prior art of record) and Turnberg et al. (Mol Immuno, 40:145-153, published 2003, prior art of record), and further in view of Triantafilou et al. (Journal of cell science 126.13: 2903-2913, cited IDS 1/17/2023 published 2013; hereinafter “Triantafilou,” prior art of record) and Bouchon et al. (US2018/0085391, filed 8/07/2015, prior art of record) is withdrawn.
Claim Objections
Claim 2 is objected to because of the following informalities: abbreviation of NALP is not spelled out in its first recitation (e.g. Nucleotide-binding oligomerization domain, Leucine rich Repeat and Pyrin domain (NALP)).
Claims 6, 8, and 53-59 are objected to because of the following informalities: the claims recite the disease “a sarcoidosis” twice in the claim limitation.
Appropriate correction is required.
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.
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, 2, 4, 6, 8, and 53-59 are rejected under 35 U.S.C. 103 as being unpatentable over Adhi, Mehreen, et al (PLoS One 8.10: e79661, published 2013, cited IDS 03/05/2021; hereinafter “Adhi”, prior art of record) in view of Copland et al. (Clinical & Experimental Immunology 159.3: 303-314, published 2010, prior art of record), Horiuchi, Takahiko, et al. (Modern rheumatology 10.4: 276-278, published 2000, hereinafter as “Horiuchi”), and Kim, En Hyung, et al. (Journal of inflammation 12.1: 41, published 2015, hereinafter as “Kim”), as evidence by Triantafilou, Kathy, et al. (Journal of cell science 126.13: 2903-2913, cited IDS 1/17/2023, published 2013; hereinafter “Triantafilou”, prior art of record).
This is a new rejection, however, since it is substantially similar to a rejection mailed August 5, 2024, any aspect of applicant's response considered relevant to the rejection as newly set forth is responded to following the statement of rejection.
Regarding claim 1-2, Adhi discloses a method comprising: administering to an eye of the subject an effective amount of a composition comprising a nucleic acid encoding a membrane independent CD59 protein (i.e. inhibitor of MAC)(see e.g. page 2) operably linked to a promoter and signal sequence (see e.g. abstract, Fig. 2); wherein the membrane independent CD59 protein is expressed and secreted in cells of the eye of the subject (see e.g. abstract, fig. 5), and wherein the composition is administered to the eye of the subject by intravitreal injection. (see e.g. page 2-3, fig. 2).
Adhi is silent regarding the treatment of uveitis in a subject afflicted with autoimmune uveitis, and Adhi does not explicitly state wherein the composition inhibits inflammasome activation and wherein the subject has displayed positive results for expression or activity of at least one inflammasome activity marker in the eye of the subject.
However, the prior art of Copland teaches that local administration by intravitreal injection (i.e. administering to the eye of the subject) an effective amount of a composition comprising a MAC complex inhibitor (i.e. anti-C5 antibody)(see e.g. abstract, page 305, 310, and 312), which effected the inhibition of C5 cleavage (i.e. MAC complex) on the disease progression and severity in experimental autoimmune uveoretinitis (EAU)(i.e. autoimmune uveitis), which was characterized by structural retinal damage mediated by infiltrating macrophages (see e.g. abstract, Fig. 5).
Regarding claim 1, as discussed above, Copland discloses a method of treating uveitis in a subject afflicted with autoimmune uveitis (see e.g. abstract, page 304 and 312).
Accordingly, it would have been obvious for one of ordinary skill in the art to modify the method as taught by Adhi and incorporate the treatment of a subject afflicted with autoimmune uveitis as taught Copland because both Adhi and Copland disclose using the complement system to regulate the membrane attack complex (MAC) for treating disease of the eye (see e.g. respective abstracts). Further, Copland discloses that the overexpression of complement regulatory proteins, such as CD55, have been demonstrated to prevent the generation of pathogenic effector T cells in experimental autoimmune uveitis (EAU)(see page 304). Moreover, Copland suggests that the complement pathway may be a target for therapy in uveitis (page 304). Additionally, Adhi discloses that the regulation of complement activation is essential and tightly maintained by a large family of membrane-associated and soluble regulators, such as CD59 and CD55 (see e.g. page 1). Therefore, it would have been obvious for a person of ordinary skill in the art to modify the method of Adhi for treating autoimmune uveitis as suggested by Copland because it would have been obvious for a person of ordinary skill in the art to substitute one MAC inhibitor for another. Moreover, a person of ordinary skill in the art would have had a reasonable expectation of success because both Adhi and Copland demonstrate treating pathologies of the eye due to MAC deposition. Furthermore, an artisan of ordinary skill in the art of (i.e. gene therapy) has good reason to pursue the known options within his or her technical grasp (KSR International Co. v. Teleflex Inc., 82 USPQ2d 1385 (US 2007).
Regarding claim 1-2, and 4, Adhi does not explicitly teach a positive results for expression or activity of at least one inflammasome activity marker, such as caspase 1, IL-1 β, or NALP3 (i.e. NLRP3) in the eye of the subject.
Nevertheless, the expression or activity of at least one inflammasome activity marker such as, caspase-1, NLRP3, or IL-β would naturally occur from a MAC attack as evidence by Triantafilou, which discloses that there is a novel link between inhibition of MAC and inflammasome activation (e.g. IFN-γ, caspase-1, NLRP3, and IL-1β) (see e.g. abstract, page 2903-2904, and 2911, and Fig. 2-3).
Providing guidance on instances where the method steps of the prior art and instant claims are the same, Ex parte Marhold, 231 USPQ 904, 905 (Bd. Pat. App. & Int. 1986) relying on In re Sussman, 141 F.2d 267, 269-70, 60 USPQ 538, 540-41 (CCPA 1944) states “[T]hat since the steps are the same, the results must inherently be the same unless they are due to conditions not recited in the claims.”
In the instant case, since claims 1, 2, and 4 indicate that that method steps of claim 1 are sufficient to active the inflammasome, and since the method of Adhi, as modified by Copland, carries out these steps, the referenced method naturally produce the activity of the inflammasome activity markers IL-β, caspase-1, and NLRP3 as evidence by Triantafilou. Thus, a person of ordinary skill in the art would have had a reasonable expectation of having a positive results (i.e. elevated expression) or activity of at least one inflammasome activity markers, such as IL-β, caspase-1, or NLRP3, because an artisan would know that there is a novel link between MAC and inflammasome activation as evidence by Triantafilou (see e.g. abstract, page 2903-2904, and 2911, and Fig. 2-3).
Accordingly, it would have been obvious to a person of ordinary skill in the art to employ the methods as taught by Adhi for positive result for elevated expression or activity of at least one inflammasome activity marker such as IFN-γ (as taught by Copland), or IL-1β, caspase-1, or NLRP3 (as evidence by Triantafilou) of in the inflammation-affected eye of a subject because Adhi discloses a method of administering to an eye of the subject an effective amount of a composition comprising a nucleic acid encoding a membrane independent CD59 protein which is an inhibitor of MAC (see e.g. page 2). Thus, a person of ordinary skill in the art would have a reasonable expectation of success because the inhibition of MAC as taught by Adhi with Copland would naturally lead to expression or activity of the inflammasome activity markers as evidence by Triantafilou.
Regarding claims 6, 53 and 54, as discussed above, Adhi discloses administering to an eye of the subject an effective amount of a composition comprising a nucleic acid encoding a membrane independent CD59 protein (i.e. inhibitor of MAC)(see e.g. page 2) to a diabetic subject (see e.g. abstract).
Adhi is silent regarding a subject that has been diagnosed with or is supposed of being afflicted with Behcet’s disease (BD).
However, the prior art of Horiuchi discloses that the deficiency of the complement system is associated with Behcet’s disease (BD)(see e.g. page 278). Further, the prior art of Kim which teaches that there is an increased expression of NLRP3 (i.e. NALP) inflammasome components in patient with BD (see e.g. title and abstract).
Accordingly, it would have been obvious for one of ordinary skill in the art to practice the method of Adhi with treating a subject afflicted with Bechet’s disease (BD) as taught by Horiuchi and Kim because both Adhi and Horiuchi discloses methods of targeting the complement system (see e.g. respective abstracts). Further, it would have been obvious for a person of ordinary skill in the art to use the method of Adhi and Copland for another eye related disease such as BD because Horiuchi discloses that typical symptoms of BD include oral and genital uveitis (see e.g. page 276 and 278), and Kim discloses that BD patients naturally have increased expression of NLRP3 (i.e. NALP) inflammasome components (see e.g. page 5). Thus, it would have been done with a reasonable expectation of success. Furthermore, an artisan of ordinary skill in the art of (i.e. gene therapy) has good reason to pursue the known options within his or her technical grasp (KSR International Co. v. Teleflex Inc., 82 USPQ2d 1385 (US 2007).
Regarding claims 8, and 55-59, as discussed above, Adhi discloses an individual not diagnosed or afflicted with a allergic conjunctivitis, a blepharitis, a chronic conjunctivitis, an episcleritis, a keratitis, a retinitis, an ocular cicatricial pemphigoid, a mucous membrane pemphigoid, a pterygium scleritis, a Stevens-Johnson syndrome, an Eales Disease, a Behcet's disease, a polyarteritis nodosa, a Wegener's granulomatosis a Vogt-Koyanagi-Harada Disease, a sympathetic ophthalmia, or a sarcoidosis (see e.g. abstract, whole document).
Hence the claimed invention as a whole was prima facia obvious in the absence of evidence to the contrary.
Response to Traversal:
Applicant argues that the Examiners obviousness rejection of record uses hindsight reasoning that is scientifically and medically improper (Remarks, page 9). Applicant asserts that the method of Copland would not be simply substituted by the gene therapy of Adhi because Copland is silent with respect to the complement regulatory protein CD59 (Remarks, page 9).
Applicant’s arguments with respect to the previous rejection has been fully considered and are partially persuasive. Therefore, the rejection has been withdrawn. However, upon further consideration, a new ground of rejection is made in view of Adhi, Copland, Horiuchi, and Kim, as evidence by Triantafilou, as discussed above. It is noted that Copland is not cited for teaching the complement regulatory protein CD59, and Copland is cited for teaching autoimmune uveitis (see e.g. abstract).
In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971). In the instant case, the obviousness rejection is based on the prior art and is not from applicant disclosure. As discussed above, the inhibition of the MAC by CD59 to treat eye disease is taught by Adhi and inhibiting MAC through other means to treat autoimmune uveitis is taught by Copland, hence all of the claimed elements are taught by the prior art. Therefore, the inhibition of MAC for treating eye diseases has been made obvious by the prior art so no knowledge is gleamed from applicant disclosure as asserted above.
Applicant asserts that the techniques of Copland and Adhi are wholly different and would not necessarily translate to the same effect (Remarks, page 9). Further Applicant asserts that “one of skill in the relevant art would not substitute antibody blockage for ectopic protein expression with a reasonable expectation of success in the immune privileged space of the eye” (Remarks, page 10).
Applicant arguments are acknowledged, have been fully considered, and have been deemed unpersuasive.
In response to applicant argument the teachings of the techniques of Copland and Adhi are wholly different, Applicants response is reminded that the standard for obviousness is a reasonable expectation of success. Further, it is noted that Applicant asserts that Copland is wholly focused on C5 and its cleavage to C5a and C5b. However, Applicants analysis of Copland does not say how it pertains to the instant scenario, so the Examiner is unsure of the response.
In response to Applicants assertion that “one of skill in the relevant art would not substitute antibody blockage for ectopic protein expression with a reasonable expectation of success in the immune privileged space of the eye” (Remarks, page 10). It is noted that this assertion is unsupported, and the Applicant has not provided details on how this pertains to the instant scenario. As discussed above, a person of ordinary skill in the art would employ a MAC inhibitor as taught by Adhi in order to treat autoimmune uveitis as taught by Copland.
Applicant argues that Copland is silent with respect to complement regulatory protein CD59 (Remarks, page 9). Applicant asserts that Copland uses ectopic IFN-y as an activator of macrophages that has synergistic effect with the cleavage product C5a, and not as a marker (Remarks, page 9). Applicant argues that Copland is wholly focused on C5 and its cleavage to C5a and C5b (Remarks, page 10).
Applicant arguments are acknowledged, have been fully considered, and have been deemed unpersuasive.
In response to applicant’s piece meal analysis and argument, the prior art of Copland is strictly relied upon for inhibiting MAC to treat autoimmune uveitis. As discussed above, the inhibition of the MAC by CD59 to treat eye disease is taught by Adhi. Therefore, it would have been obvious for a person of ordinary skill in the art to inhibit MAC for treating an eye disease. It is noted that Copland discloses IFN-y having a synergistic effect with the cleavage product C5a (see e.g. page 308-312, Fig. 4). Thus, this further suggests that the expression or activity of at least one inflammasome activity marker (e.g. IFN-y, caspase-1, NLRP3, and/or IL-β) would naturally occur from inhibiting MAC. Providing guidance on instances where the method steps of the prior art and instant claims are the same, Ex parte Marhold, 231 USPQ 904, 905 (Bd. Pat. App. & Int. 1986) relying on In re Sussman, 141 F.2d 267, 269-70, 60 USPQ 538, 540-41 (CCPA 1944) states “[T]hat since the steps are the same, the results must inherently be the same unless they are due to conditions not recited in the claims.” As discussed above, the expression or activity of at least one inflammasome activity marker (e.g. caspase-1, NLRP3, and/or IL-β) would naturally occur from inhibiting MAC as evidence by Triantafilou, which discloses that there is a novel link between inhibiting MAC and inflammasome activation (e.g. caspase-1, NLRP3, and IL-1β) (see e.g. abstract, page 2903-2904, and 2911, and Fig. 2-3). Thus, at least one inflammasome activity marker (e.g. IFN-γ, caspase-1, NLRP3, and IL-1β) would naturally be elevated by expression or activity since the method of Adhi, as modified by Copland, carries out the steps of administering CD59 to the eye of a subject with autoimmune uveitis.
Applicant argues that Adhi does not teaches a direct role of CD59 in inflammation and is limited retina in diabetic retinopathy and age-related macular degeneration (Remarks, page 10). Applicant asserts that the Examiner has not provided a reasonable expectation of success or motivation to combine Copland and Adhi (Remarks, page 10).
Applicant arguments are acknowledged, have been fully considered, and have been deemed unpersuasive.
In response to applicant’s piece meal analysis and argument, the prior art Adhi discloses administering CD59 to the eye of the subject and the prior art of Copland discloses inhibiting MAC to treat autoimmune uveitis, as discussed above. Accordingly, it would have been obvious for one of ordinary skill in the art to modify the method as taught by Adhi and incorporate the treatment of a subject afflicted with autoimmune uveitis as taught Copland because both Adhi and Copland disclose using the complement system to regulate the membrane attack complex (MAC) for treating disease of the eye (see e.g. respective abstracts). Moreover, Copland suggests that the complement pathway may be a target for therapy in autoimmune uveitis (see e.g. page 304). Thus, a person of ordinary skill the art would have had a reasonable expectation of success of using an inhibitor of MAC for treating an eye disease.
Applicant argues that the inhibitors such as CD55 are not analogous to CD59 (Remarks, page 11). Applicant asserts that a person of skill in the art, seeking to minimize complement-induced inflammation, would not have been motivated to exploit the narrow and separate effect of CD59, allowing the generation of inflammatory mediators upstream (Remarks, page 11).
Applicant arguments are acknowledged, have been fully considered, and have been deemed unpersuasive.
In response to Applicants arguments that CD55 and CD59 are not analogous, it is noted that Applicant “does not dispute that there are several members of the MAC complex that lead to autoimmune uveitis” (Remarks, page 11). Furthermore, Adhi discloses that the regulation of complement activation is essential and tightly maintained by a large family of membrane-associated and soluble regulators such as CD55 and CD59 (see e.g. page 1). Moreover, there is no obviousness requirement for CD55 and CD59 to be analogous but they both need to inhibit MAC. Furthermore, there is no claim limitation to a person of ordinary skill in the art for seeking to minimize complement induced inflammation. Thus, applicant argument is not commensurate in scope with the claims. As discussed above, a person of ordinary skill in the art could have easily administer CD59 as taught by Adhi as a treatment of a subject afflicted with autoimmune uveitis as taught by Copland with a reasonable expectation of success because both teach inhibiting the MAC complex for treatment of ocular related diseases.
Applicant asserts that Copland teaches IFN-γ as an inflammasome activity marker is unsupported (Remarks, page 11).
Applicant arguments are acknowledged, have been fully considered, and have been deemed partially persuasive. As stated supra, the rejection has been withdrawn. However, upon further consideration, a new ground of rejection is made in view of Adhi, Copland, Horiuchi, and Kim, as evidence by Triantafilou. Applicant assertion regarding Copland teaching IFN-γ as an inflammasome activity marker is addressed above. Furthermore, it is noted that Copland is no longer cited for teaching IFN-γ.
Applicant argues that the additional reference of Triantafilou does not remedy the deficiency of Triantafilou or any of the other cited reference (Remarks, page 13). Applicant asserts that the prior art of Triantafilou is not directed to the eye of the subject (Remarks, page 13-14). Further, Applicant asserts that Sohn et al., (i.e. Exhibit A in Remarks, from 5/16/2023) supports Applicants assertion that MAC activation is attenuated by delivery of an expression vector encoding CD59 (Remarks, page 13).
Applicant arguments are acknowledged, have been fully considered, and have been deemed unpersuasive.
In the instant case, Triantafilou is not cited for administering CD59 to the eye of the subject. In response to applicant’s piece meal analysis and argument, 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). The prior art of Triantafilou is cited as an evidentiary reference for inflammasome markers being expressed due to MAC inhibition. As discussed above, the prior art Adhi is cited for administering CD59 to the eye of the subject, and the prior art of Copland is cited inhibiting MAC to treat autoimmune uveitis.
In response to Applicant assertion that Shon et al., provides evidence that a person of ordinary skill in the art would not expect inflammasome activity markers. It is noted that Shon et al., discloses that a “blockade of the MAC-inhibitor CD59 by intracameral injection of a blocking antibody (i.e., injection of the blocking antibody into a chamber of the eye, thereby releasing inhibition of MAC formation and deposition) did not induce intraocular inflammation”(page 10). Contrary to Applicants assertion the prior art of Shon et al., is directed to suppressing CD59 and uses a blocking antibody rather than the gene therapy of AAV2/8-soluble CD59 as taught by Adhi. Further, the prior art of Shon et al., discloses that the reason that suppression of Crry, and not CD59, induced severe anterior uveitis may be that these two molecules restrict different steps in the complement cascade (page 10). Thus, the evidence of Shon et al., is not commensurate in scope with the claims that administration of a membrane independent CD59 is expressed and secreted in the cells of the eye of the subject afflicted with autoimmune uveitis. Providing guidance on instances where the method steps of the prior art and instant claims are the same, Ex parte Marhold, 231 USPQ 904, 905 (Bd. Pat. App. & Int. 1986) relying on In re Sussman, 141 F.2d 267, 269-70, 60 USPQ 538, 540-41 (CCPA 1944) states “[T]hat since the steps are the same, the results must inherently be the same unless they are due to conditions not recited in the claims.” As stated supra, Triantafilou discloses that there is a novel link between MAC and inflammasome activation of markers caspase-1, NLRP3, and IL-1β (see e.g. abstract, page 2903-2904, and 2911, and Fig. 2-3). Thus, a person of ordinary skill in the art would inherently expect the expression or activity of at least one inflammasome activity marker (e.g. IFN-y caspase-1, NLRP3, and/or IL-β) because the inflammasome activity markers would naturally occur from inhibiting MAC. Thus, through the scientific nexus of the MAC complex, it would have been obvious for a person of ordinary skill in the art to choose to administer a MAC inhibitor (e.g. CD59) in order to cause the attenuation of the MAC complex, which would naturally display inflammasome activity markers in the affected eye of the autoimmune uveitis subject.
In view of the foregoing, when all of the evidence is considered, the totality of the rebuttal evidence of nonobviousness fails to outweigh the evidence of obviousness.
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 1-2, 4, 6, 8 and 53-59 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-52 of co-pending Application No. 19/253,268 (reference application).
This rejection is a new rejection necessitated by the filing of Application 19/253,269.
The subject matter claimed in the instant application is fully disclosed in the referenced application as follows: A method for treating uveitis in a subject afflicted with autoimmune uveitis, the method comprising: administering to an eye of the subject an effective amount of a composition comprising a nucleic acid encoding a membrane independent CD59 protein operably linked to a promoter and signal sequence; wherein the membrane independent CD59 protein is expressed and secreted in cells of the eye of the subject, wherein the composition inhibits inflammasome activation, wherein the subject has displayed positive results for expression or activity of at least one inflammasome activity marker in the eye of the subject, and wherein the composition is administered by intravitreal injection. Thus, the cited application anticipates and/or makes obvious a method for treating uveitis in a subject afflicted with autoimmune uveitis the method comprising: administering to an eye of the subject an effective amount of a composition comprising a nucleic acid encoding a membrane independent CD59 protein operably linked to a promoter and signal sequence of the instant application. It is clear that all the elements of the cited application claim 1-51 are to be found in instant claims 1-2, 4, 6, 7, and 53-59.
Thus, these claims 1-52 would anticipate the instant claimed invention, which is drawn A method for treating uveitis in a subject afflicted with autoimmune uveitis, the method comprising: administering to an eye of the subject an effective amount of a composition comprising a nucleic acid encoding a membrane independent CD59 protein operably linked to a promoter and signal sequence; wherein the membrane independent CD59 protein is expressed and secreted in cells of the eye of the subject, wherein the composition inhibits inflammasome activation, wherein the subject has displayed positive results for expression or activity of at least one inflammasome activity marker in the eye of the subject, and wherein the composition is administered by intravitreal injection. The presently claimed invention thus embraces the competing claims.
This is a provisional nonstatutory double patenting rejection.
Conclusion
No claim is allowed.
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JOSEPHINE GONZALES
Examiner
Art Unit 1631
/JOSEPHINE GONZALES/Examiner, Art Unit 1631
/JAMES D SCHULTZ/Supervisory Patent Examiner, Art Unit 1631