Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
DETAILED ACTION
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
This action is in response to the papers filed on June 27, 2025. Pursuant to amendment filed on June 27, 2025, claims 1 and 15 are amended. Claims 4, 9, 12, 13, 18, and 19 were previously withdrawn.
Therefore, claims 1-3, 5-7, 10-11, 14-15, 17, and 20 are under examination.
Priority
The present application is claiming the benefit under 35 U.S.C. 119(e) of prior-filed provisional application 63/176,009, filed April 16,2021. Applicant's claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged.
Thus, the earliest possible priority for the instant application is April 16, 2021.
Specification Objection
The disclosure is objected to because of the following informalities: The specification references color drawings, specifically referring to Fig. 2, 4, 6, 8; See [0018], [0131], [0138-0139], [0140-0141]. Necessary correction is required. Applicant may obviate the objection by filing the petition for color drawings.
Drawings
The drawings are objected to under 37 CFR 1.83(a) because they fail to show color designated and as described in the specification, see Fig. 2, 4, 6, 8. Additionally, multiple figures are poorly rendered. The patent or application file contains at least one drawing executed in color. Copies of this patent or patent application publication with color drawings will be provided by the Office upon request and payment of the necessary fee. Color photographs will be accepted if the conditions for accepting color drawings and black and white photographs have been satisfied. See 37 CFR 1.84(b)(2).
Color photographs and color drawings are not accepted in utility applications unless a petition filed under 37 CFR 1.84(a)(2) is granted. Any such petition must be accompanied by the appropriate fee set forth in 37 CFR 1.17(h), one set of color drawings or color photographs, as appropriate, if submitted via the USPTO patent electronic filing system or three sets of color drawings or color photographs, as appropriate, if not submitted via the USPTO patent electronic filing system, and, unless already present, an amendment to include the following language as the first paragraph of the brief description of the drawings section of the specification:
Additionally, any structural detail that is essential for a proper understanding of the disclosed invention should be shown in the drawing. MPEP § 608.02(d). Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered, and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Modified and Maintained Claim Rejections - 35 USC § 102
Claims 1-3 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Cukras et al. (Mol Ther. 2018 Sep 5;26(9):2282-2294. Epub 2018 Jul 7., see IDS). This is a new rejection necessitated by amendment of the claims in the response filed October 11, 2024.
Regarding claims 1-3, Cukras discloses a method for treating retinal degeneration comprising administering to a patient with one or more missense mutations (Table 1) of endogenous Retinoschisin 1 (RSI) producing dysfunctional retinoschisin (RS1) protein a vector including an exogenous gene encoding a functional RS1 protein, i.e., supplementing the eye with the functional RS1 protein (abstract and pg. 2290, column 1, last para.). Cukras discloses the utility of AAV8 (abstract). Cukras specifically teaches the applicability of subretinal injection for XLRS administration, stating “the retinal fragility in XLRS disease has implications for gene-based therapeutic approaches, as these currently involve sub-retinal vector administration requiring surgical manipulation of the retina” (pg. 2282, column 2, para. 1).
Regarding the amendment that the method of treatment be suitable for retinal degeneration due to XLRS, Cukras specifically states the “study evaluated the safety and tolerability of ocular RS1 adeno-associated virus (AAV8-RS1) gene augmentation therapy to
the retina of participants with X-linked retinoschisis (XLRS). XLRS is a monogenic trait affecting only males, caused by mutations in the RS1 gene.” (Abstract)
Response to Applicants’ arguments as they apply to the rejection of claims 1-3 under 35 U.S.C. 102(a)(1) as being anticipated by Cukras et al. (Mol Ther. 2018 Sep 5;26(9):2282-2294. Epub 2018 Jul 7., see IDS).
Applicant’s arguments filed June 27, 2025, have been fully considered but they are not
persuasive.
At pages 5 of the remarks filed June 25, 2025, Applicants essentially argue the
following: The disclosure of Cukras does not support subretinal administration, and instead teaches a preferred method of treatment of XLRS as intravitreal administration.
Applicant’s arguments are not persuasive because Cukras teaches sub-retinal injection as an effective route of administration for XLRS (pg. 2282, column 2, para. 1; pg. 2287, column 2, last para.) While, Cukras does note the increases in encouraging data for intravitreal delivery, Cukras also teaches sub-retinal delivery. Applicant’s citation to page 2289, left column, second paragraph, states:
“Intravitreal delivery is desirable in affording an easy and safe route for administration and the opportunity to reach a larger expanse of retina compared to sub-retinal application. As with sub-retinal delivery for genetic ocular diseases, intravitreal delivery will require the consolidation of appropriate vector, transgene, promoter, delivery technique, patient population, and selected primary clinical outcomes to discern which entities are truly therapeutic.”
Hence, Cukras does not teach away from sub-retinal administration merely by identifying intravitreal delivery as desirable, in specific contexts. Rather, Cukras expressly recognizes sub-retinal injection or delivery as an effective route of administration for XLRS and discusses intravitreal delivery as an additional or alternative approach.
Withdrawn- Claim Rejections - 35 USC § 103
In view of additional identified prior art, the rejection under 35 U.S.C. 103 to claims 1-3, 5-8, 10-11, 14 over Cukras et al. (Mol Ther. 2018 Sep 5;26(9):2282-2294. Epub 2018 Jul 7., see IDS), in view of Boye et al. (Hum Gene Ther. 2012 Oct;23(10):1101-15. Epub 2012 Sep 20.), Brydges et al. (US11,064,685B2), as well as claims 1-3, 5-8, 10-11, 14-17, and 20 over Cukras, Boye, Brydges, and further in view of Hickey et al. (Gene Ther. 2017 Nov 16;24(12):787–800.) has been withdrawn. Applicants’ arguments are moot in view of the withdrawn rejection. A response to Applicant’s arguments pertinent to a new or remaining rejection can be found below.
New Claim Rejections - 35 USC § 103
Claims 1-3, 5-8, 10-11, and 14 are rejected under 35 U.S.C. 103 as being unpatentable over Cukras et al. (Mol Ther. 2018 Sep 5;26(9):2282-2294. Epub 2018 Jul 7., see IDS), in view of Boye et al. (Hum Gene Ther. 2012 Oct;23(10):1101-15. Epub 2012 Sep 20.), Brydges et al. (US11,064,685B2), and further in view of Min et al. (Mol Ther. 2005 Oct;12(4):644-51.), Janssen et al. (Mol Ther. 2008 Jun;16(6):1010-7. Epub 2008 Mar 25.), and TeamedOn/AGTC (TeamedOn and AGTC Announce a Licensing Agreement Advancing X-Linked Retinoschisis Gene Therapy Program, BioSpace, Published April 12, 2021.; hereinafter “TeamedOn”).
Regarding claims 1-3, Cukras discloses a method for treating retinal degeneration comprising administering to a patient with one or more missense mutations (Table 1) of endogenous Retinoschisin 1 (RSI) producing dysfunctional retinoschisin (RS1) protein a vector including an exogenous gene encoding a functional RS1 protein, i.e., supplementing the eye with the functional RS1 protein (abstract and pg. 2290, column 1, last para.). Cukras discloses the utility of AAV8 (abstract). Cukras specifically teaches the applicability of subretinal injection for XLRS administration, stating
“The retinal fragility in XLRS disease has implications for gene-based therapeutic approaches, as these currently involve sub-retinal vector administration requiring surgical manipulation of the retina” (pg. 2282, column 2, para. 1).
Regarding the amendment that the method of treatment be suitable for retinal degeneration due to XLRS, Cukras specifically states the “study evaluated the safety and tolerability of ocular RS1 adeno-associated virus (AAV8-RS1) gene augmentation therapy to the retina of participants with X-linked retinoschisis (XLRS). XLRS is a monogenic trait affecting only males, caused by mutations in the RS1 gene.” (Abstract)
Furthermore, the ordinary artisan would have recognized administering an AAV treatment of retinal degeneration, due to X-linked Juvenile Retinoschisis (XLRS) resulting from one or more missense mutations of endogenous Retinoschisin 1 (RS1) producing dysfunctional retinoschisin (RS1) protein, by the subretinal injection route was an established approach in the prior art, further in view of Min, Janssen, and TeamedOn.
Min taught subretinal AAV-mediated delivery of human RS1 cDNA in an XLRS animal model and reports restoration or improvement of retinal structure and function following RS1 gene therapy (Abstract; pg. 645, column 1-column 2, bridging para.; pg. 647, column 2, para 3). Min therefore confirms that subretinal delivery of an AAV vector encoding functional RS1 was a known and successful approach for treating XLRS-associated retinal pathology before the effective filing date of the instant application (pg. 650, column 1, para. 4).
Janssen similarly taught subretinal AAV-mediated RS1 delivery in a retinoschisin-deficient model and reports sustained retinoschisin expression and beneficial effects on retinal function, retinal structure, and photoreceptor survival (Abstract; pg. 1011, Section: Results; Fig. 1; pg. 1013-1014, bridging para.). Thus, Janssen further confirms that the ordinary artisan would have understood subretinal AAV-RS1 delivery to be viable and predictable approach for treating XLRS-related retinal degeneration.
TeamedOn further taught that XLRS gene therapy program involving an hRS1 gene therapy candidate and that subretinal administration was established as a reasonable route of administration producing detectable biological activity of rAAV2tYF-CB-hRS1 (pg. 2, para. 1-3). The teachings of TeamedOn confirm that subretinal administration of RS1 gene therapy for XLRS was a practical and biologically motivated route for XLRS gene therapy, particularly as an alternative to intravitreal administration.
Thus, before the effective filing date of the instant application, the ordinary artisan would have found it obvious to administer an AAV vector encoding a functional RS1 protein to treat degeneration due to X-linked juvenile retinoschisis (XLRS) in an patient having one or more RS1 missense mutations producing dysfunctional retinoschisin protein, as taught by Cukras, using the subretinal administration route for AAV-mediated RS1 gene delivery as further taught and supported by Min, Janssen and TeamedOn, thereby yielding the claimed method of treating XLRS-associated retinal degeneration by supplementing dysfunctional endogenous RS1 protein with functional RS1 protein via subretinal injection. The ordinary artisan would have had a reasonable expectation of success because Cukras teaches AAV-mediated RS1 gene augmentation for XLRS patients via subretinal injection, while Min and Janssen teach that subretinal AAV-mediated RS1 delivery restored or improved retinal structure and function in XLRS/retinoschisin-deficient models, and TeamedOn confirms that subretinal administration of an hRS1 XLRS gene therapy candidate was recognized in the art as a route expected to produce detectable biological activity.
Regarding claims 5-7, the teachings of Cukras, Min, Janssen and Teamed on render claim 1 obvious. Cukras teaches that the AAV-RS1 vector includes regulatory elements for driving expression of the RS1 coding sequence in ocular/retinal cells, including a tissue-selective human retinoschisin promoter and an interphotoreceptor retinoid-binding protein enhancer element to promote expression in relevant retinal cells. Cukras further teaches AAV8-RS1 is a replication-deficient, nonpathogenic AAV vector serotype 8 that delivers a human retinoschisin-coding sequence. Gene expression is driven from a modified tissue-selective human retinoschisin promoter, thus limiting expression to ocular cells normally expressing this gene. Promoter activity is augmented by an interphotoreceptor retinoid-binding protein (IRBP) enhancer element (pg. 2290, column 1, last para.).
While Cukras does not expressly teach the rhodopsin promoter, Min teaches where the promoter was substituted with the rhodopsin promoter (Abstract and pg. 647, column 1, para. 3), and Janssen teaches where the activity is driven under the control of an opsin promoter (pg. 1016, column 1, last para.). Additionally, Boye teaches that use of a human rhodopsin kinase promoter in an AAV vector results in rod-and cone-specific expression in the retina following subretinal delivery. Thus, before the effective filing date of the instant application, the ordinary artisan would have found it obvious to use the rhodopsin kinase promoter taught by Boye in the AAV-RS1 gene therapy method taught by Cukras as further supported by Min, Janssen, and Teamed On, thereby yielding a vector including a promoter that drives expression of the exogenous RS1 gene in the retina, including a rhodopsin kinase promoter. The ordinary artisan would have had a reasonable expectation of success because Cukras teaches retinal expression of functional RS1 for XLRS gene augmentation, Min and Janssen teach subretinal AAV-RS1 delivery for XLRS-related disease, and Boye teaches the rhodopsin kinase promoter predicated drives photoreceptor-specific expression in retinal tissue after subretinal AAV delivery.
Regarding claim 10-11, the teachings of Cukras, Min, Janssen and Teamed on render claim 1 obvious. Cukras additionally teaches the effective treatment with the AAV vector in human patients carrying point mutations (patient 1: R102W, patient 3: R141H, patient 5: 179D, patient 6: P192S, patient 9: G70S).
While Cukras does not specifically teach the missense mutation C59S, there is no evidence of record indicating that the treatment of this point mutation would be different from the others described, or the function of the dysfunctional protein would not be restored. As per MPEP § 716.02, [a]ny differences between the claimed invention and the prior art may be expected to result in some differences in properties. The issue is whether the properties differ to such an extent that the difference is really unexpected. In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). Furthermore, the ordinary artisan would have found obvious to use the method taught by Cukras to treat patients exhibiting any point mutation resulting in dysfunctional RS1 protein. Especially in view of the prior art teaching dysfunctional RS1 exhibiting C95S point mutation (see Brydges; column 4, lines 43-44, Fig. 6, 11, and claims 1, 8, 19, 25).
Regarding claim 14, the teachings of Cukras, Min, Janssen and Teamed on render claim 1 obvious. Additionally, Cukras teaches the use of electroretinography or ERG (pg. 2291, column 2, para. 2) to assess retinal function, providing reports of ERG measurements of the treated patients eyes, with patient 9 showing at least a transitory structural and functional improvement (pg. 2285, column 1, last para.)
***
Claims 15, 17, and 20, are rejected under 35 U.S.C. 103 as being unpatentable over Cukras, in view of Min, Janssen, TeamedOn, Boye, Brydges, and further in view of Hickey et al. (Gene Ther. 2017 Nov 16;24(12):787–800.).
Regarding claim 15, Cukras discloses a method for treating retinal degeneration comprising administering to a patient with one or more missense mutations (Table 1) of endogenous Retinoschisin 1 (RSI) producing dysfunctional retinoschisin (RS1) protein a vector including an exogenous gene encoding a functional RS1 protein, i.e., supplementing the eye with the functional RS1 protein (abstract and pg. 2290, column 1, last para.). Cukras discloses the utility of AAV8 (abstract). Cukras specifically teaches the applicability of subretinal injection for XLRS administration, stating
“The retinal fragility in XLRS disease has implications for gene-based therapeutic approaches, as these currently involve sub-retinal vector administration requiring surgical manipulation of the retina” (pg. 2282, column 2, para. 1).
Regarding the amendment that the method of treatment be suitable for retinal degeneration due to XLRS, Cukras specifically states the “study evaluated the safety and tolerability of ocular RS1 adeno-associated virus (AAV8-RS1) gene augmentation therapy to the retina of participants with X-linked retinoschisis (XLRS). XLRS is a monogenic trait affecting only males, caused by mutations in the RS1 gene.” (Abstract)
Furthermore, the ordinary artisan would have recognized administering an AAV treatment of retinal degeneration, due to X-linked Juvenile Retinoschisis (XLRS) resulting from one or more missense mutations of endogenous Retinoschisin 1 (RS1) producing dysfunctional retinoschisin (RS1) protein, by the subretinal injection route was an established approach in the prior art, further in view of Min, Janssen, and TeamedOn.
Min taught subretinal AAV-mediated delivery of human RS1 cDNA in an XLRS animal model and reports restoration or improvement of retinal structure and function following RS1 gene therapy (Abstract; pg. 645, column 1-column 2, bridging para.; pg. 647, column 2, para 3). Min therefore confirms that subretinal delivery of an AAV vector encoding functional RS1 was a known and successful approach for treating XLRS-associated retinal pathology before the effective filing date of the instant application (pg. 650, column 1, para. 4).
Janssen similarly taught subretinal AAV-mediated RS1 delivery in a retinoschisin-deficient model and reports sustained retinoschisin expression and beneficial effects on retinal function, retinal structure, and photoreceptor survival (Abstract; pg. 1011, Section: Results; Fig. 1; pg. 1013-1014, bridging para.). Thus, Janssen further confirms that the ordinary artisan would have understood subretinal AAV-RS1 delivery to be viable and predictable approach for treating XLRS-related retinal degeneration.
TeamedOn further taught that XLRS gene therapy program involving an hRS1 gene therapy candidate and that subretinal administration was established as a reasonable route of administration producing detectable biological activity of rAAV2tYF-CB-hRS1 (pg. 2, para. 1-3). The teachings of TeamedOn confirm that subretinal administration of RS1 gene therapy for XLRS was a practical and biologically motivated route for XLRS gene therapy, particularly as an alternative to intravitreal administration.
Thus, before the effective filing date of the instant application, the ordinary artisan would have found it obvious to administer an AAV vector encoding a functional RS1 protein to treat degeneration due to X-linked juvenile retinoschisis (XLRS) in an patient having one or more RS1 missense mutations producing dysfunctional retinoschisin protein, as taught by Cukras, using the subretinal administration route for AAV-mediated RS1 gene delivery as further supported by Min, Janssen and TeamedOn, thereby yielding the claimed method of treating XLRS-associated retinal degeneration by supplementing dysfunctional endogenous RS1 protein with functional RS1 protein via subretinal injection. The ordinary artisan would have had a reasonable expectation of success because Cukras teaches AAV-mediated RS1 gene augmentation for XLRS patients via subretinal injection, while Min and Janssen teach that subretinal AAV-mediated RS1 delivery restored or improved retinal structure and function in XLRS/retinoschisin-deficient models, and TeamedOn confirms that subretinal administration of an hRS1 XLRS gene therapy candidate was recognized in the art as a route expected to produce detectable biological activity.
However, the combined teachings of Cukras, Min, Janssen, and TeamedOn do not teach the administration of AAV2.7m8 vector for treating retinal degradation, including a rhodopsin kinase promoter.
However, the ordinary artisan would have recognized the AAV2 variant AAV2.7m8 serotype as an effective delivery vector for administration of the gene therapy to the retina, further in view of Hickey. Hickey teaches an analysis of the adeno-associated virus (AAV) serotype that best targets specific retinal cell types and the route of surgical delivery—intravitreal or subretinal, concluding that AAV2/2(7m8) was the most effective at transducing a
range of cell types in degenerate mouse retina and macaque and human retinal explants (Abstract; pg. 788, column 2, para. 3; and pg. 793, column 1, para. 2).
Before the effective filing date of the instant application, the ordinary artisan would have found it obvious to have delivered the gene therapy including a rhodopsin kinase promoter and exogenous gene encoding a functional RS1 protein to a patient, as taught by the combined teaching of Cukras, Min, Janssen, and TeamedOn, by simply substituting the AAV2.7m8 vector, as taught by Hickey, for the delivery of the gene therapy to the retina to obtain predictable results. The ordinary artisan would have expected a reasonable expectation of success, since Hickey teaches the great efficacy of degenerate retinal cell transduction using the AAV2.7m8 vector.
Regarding claim 17, the combined teachings of Cukras, Min, Hanssen, TeamedOn, and Hickey render claim 15 obvious. Cukras teaches the effective treatment with the AAV vector in human patients carrying point mutations (patient 1: R102W, patient 3: R141H, patient 5: 179D, patient 6: P192S, patient 9: G70S).
While combined teachings do not specifically teach the missense mutation C59S, there is no evidence of record indicating that the treatment of this point mutation would be different from the others described, or the function of the dysfunctional protein would not be restored. As per MPEP § 716.02, [a]ny differences between the claimed invention and the prior art may be expected to result in some differences in properties. The issue is whether the properties differ to such an extent that the difference is really unexpected. In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). Furthermore, the ordinary artisan would have found obvious to use the method taught by Cukras to treat patients exhibiting any point mutation resulting in dysfunctional RS1 protein. Especially in view of the prior art teaching dysfunctional RS1 exhibiting C95S point mutation (see Brydges; column 4, lines 43-44, Fig. 6, 11, and claims 1, 8, 19, 25).
Regarding claim 20, the combined teachings of Cukras, Min, Hanssen, TeamedOn, and Hickey render claim 15 obvious. Cukras teaches the use of electroretinography or ERG (pg. 2291, column 2, para. 2) to assess retinal function, providing reports of ERG measurements of the treated patients eyes, with patient 9 showing at least a transitory structural and functional improvement (pg. 2285, column 1, last para.)
Response to Applicants’ arguments as they apply to the rejection of claims 1-3, 5-7, 10-11, 14-15, 17, and 20 under 35 USC § 103
Applicant’s arguments filed June 27, 2025, have been fully considered but they are not
persuasive.
At pages 4-6 of the remarks filed June 25, 2025, Applicants essentially argue the
following:
Applicant argues that Cukras does not support subretinal administration and instead teaches intravitreal administration as a preferred route for treating XLRS.
This argument is not persuasive because Cukras teaches AAV-mediated RS1 gene augmentation for XLRS patients having RS1 mutations and recognized subretinal vector administration in the retinal gene-therapy context.
Applicant argues that the references teach away from subretinal administration because Cukras does not suggest use of subretinal administration for the treatment of subjects with XLRS RSI missense mutations and Boye describes localized bleb transduction.
This argument is not persuasive because a reference does not teach away merely by identifying a preferred or alternative route. Cukras does contraindicate subretinal administration. Likewise, Boye’s disclosure of localized subretinal transduction reflects a known feature of subretinal delivery, not a teaching that the route is unsuitable. The following references are cited as evidence without relying on the rejection. As evidenced by Boye et al. (Hum Gene Ther. 2016 Aug;27(8):580-97.; hereinafter “Boye 2016”) prior art clearly established that
“Subretinal injection is the current standard method for delivering AAV to the retinal pigment epithelium (RPE) of patients with inherited retinal disease.” (pg. 580, column 1, para. 1)
While applicants argue that this diminishes the practicality of the method, no evidence is cited. Moreover, subretinal injection has been established to transduce photoreceptors, and clinical ocular gene therapy programs are known to utilize subretinal administration to achieve delivery to photoreceptors and RPE. The cited art, including newly cited Min, Janssen, and TeamedOn, provide compelling disclosures that the method of administration via the subretinal route was a well-known, conventional, and established procedure in such methods.
Applicant argues that the claimed method produces unexpected results.
This argument is not persuasive because the arguments of counsel cannot take the place of evidence in the record. In re Schulze, 346 F.2d 600, 602, 145 USPQ 716, 718 (CCPA 1965). Examples of attorney statements which are not evidence, and which must be supported by an appropriate affidavit or declaration include statements regarding unexpected results, commercial success, solution of a long-felt need, inoperability of the prior art, invention before the date of the reference, and allegations that the author(s) of the prior art derived the disclosed subject matter from the inventor or at least one joint inventor. Additionally, this argument is not commensurate in scope with the pending claims. Claim 1 broadly cover subretinal administration of vectors encoding functional RS1 for XLRS due to missense mutations, without being limited to the specific constructs, promoter, dose, model, treatment conditions, or experimental parameters relied upon by applicants.
Conclusion
Claims 1-3, 5-7, 10-11, 14-15, 17, and 20 are rejected. No claims are allowed.
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/J.D.L./Examiner, Art Unit 1633
/FEREYDOUN G SAJJADI/Supervisory Patent Examiner, Art Unit 1699
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