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 .
Applicant’s amendment and response filed on 1/7/2026 has been received and entered into the case.
Claims 17-25 have been canceled, claims 1-16 have been withdrawn from consideration as being drawn to non-elected subject matter, and claims 26-32 have been considered on the merits. All arguments have been considered.
Response to Amendment
The claim rejections under 35 USC 112 have been withdrawn due to the instant amendment. However, new claim rejections under 35 U.S.C. 112 are necessitated by the instant amendment. See below.
The claim rejections under 35 USC 102 have been withdrawn due to the instant amendment. However, a new claim rejection under 35 U.S.C. 103 necessitated by the instant amendment is presented below.
Claim Rejections - 35 USC § 112 (New Rejection)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 26-32 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
The scope of “gene product”
The instant claims are directed to the method of administering the vector comprising an expression construct comprising a nucleic acid encoding a gene product, and the gene product hyperpolarizes horizontal cells, improves the function of photoreceptor cells, and mediates potassium conductance. The claims do not particularly limit what these gene products are, but disclose functional limitations. The scope of the genus that meets the claimed functional limitation is broad. The genus of the claimed gene product not only encompasses a potassium channel but also includes any protein that would activate the potassium channel, like potassium channel activating proteins (PCAs). For example, protein kinase C (PKC) is known to act on ATP-sensitive K channel (Light et al., 2000).
The instant specification has described one set of proteins, i.e. membrane proteins such as ion channels including a light-controlled membrane protein linked to potassium channel, e.g. BLINK1 and BLINK2, photoactivated adenylyl cyclases (PACs) linked to a small cyclic nucleotide-gated potassium channel (e.g. NgPAC1, bPAC, TpPAC, OaPAC or Ic-PAC). Considering the functionality of mediating potassium conductance, a light-sensitive potassium channel would be the only example given in the specification. However, the instant specification failed to provide sufficient written description whether the specific gene product which is limited to potassium channels would be able to improve any retinal dystrophy.
Regarding the intended purpose of improving symptoms of a retinal dystrophy, the instant specification shows only a single example of expressing hM4Di (a modified form of the human M4 muscarinic (hM4) receptor using a horizontal cell specific Gja10 promoter in a AAV vector expressed in Cnga3 KO mice. The showing of the effect in an animal model (Cnga3-/- mouse) using a single example of a hM4 expressing vector, however, does not sufficiently provide support for the claimed functionality for the gene product as claimed because the hM4 receptor does not meet the claimed results of mediating potassium conductance.
The scope of “retinal dystrophy”
According to the instant specification, the terms “retinal disorders” or “retinal dystrophies” may be defined as diseases of the retina, i.e. any retinal disease. As discussed above, the instant specification shows the effect of expressing hM4 receptor in Cnga3 knockout mice, and the mouse model corresponds to achromatopsia in human. There is no other disclosure that the expression of hM4 receptor would necessarily produce therapeutically effective outcome in any other retinal disorders belonging to the genus of “retinal dystrophy”. Furthermore, there is no disclosure that any of the gene product having the claimed functionality would be able to improve any of the known retinal dystrophy, let alone the specific retinal dystrophy listed in claim 27.
The instant claims disclose different types of retinal dystrophy as listed in claim 27, and the cone dystrophy with different characteristics, and it appears the different characteristics required by the claims would limit different types of retinal disease. However, Cnga3 knockout mice shown in the instant specification would only represent achromatopsia but this does not sufficiently represent the entire scope of the retinal dystrophy as claimed.
M.P.E.P. §2163 recites, “The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant, identifying characteristics, i.e., structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the applicant was in possession of the claimed genus…when there is substantial variation within the genus, one must describe a sufficient variety of species to reflect the variation within the genus. For inventions in an unpredictable art, adequate written description of a genus which embraces widely variant species cannot be achieved by disclosing only one species within the genus.”
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 26-32 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 26 discloses a new limitation directed to “the expression of the gene product in horizontal cells”. It is not clear if this wherein clause requires a step of administering the vector specifically into horizontal cells, or any route of administration would result in the expression of the gene product in horizontal cells; or it is referring to the characteristics of the gene product but does not require to be administered into the horizontal cells. Clarification is required.
Claim 32 discloses “the administration of the vector to horizontal cells” in the wherein clause. There is no antecedent basis for this phrase in claim 26. Claim 26 is directed to the administering a vector to a subject. There is no disclosure of administering the vector into horizontal cells. Clarification is required.
Applicant is advised to amend claim 26 to disclose the specific step of administering the vector into the horizontal cells of the subject to overcome the rejection.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Claim(s) 26-32 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Balya et al. (WO2009/127705A1; of record).
Balya et al. teach a method of treating a patient suffering blindness by administering a nucleic acid construct comprising a gene encoding a light-gated ion channel or pump (p.7, 2nd para.).
Balya et al. teach that “blindness” is meant total or partial loss of vision associated with macular degeneration, glaucoma and/or retinitis pigmentosa (p.6).
Balya et al. teach the nucleic acid molecule encodes for a hyperpolarizing light-gated ion channel or pump gene (Abstract; p.24, last para.; p.28, Claim 1).
Balya et al. teach that the nucleic acid molecule/construct comprises a cell specific promoter for controlling the expression of the light-gated ion channel or pump gene, and the nucleic acid molecule expressed in horizontal cells (p.3, 3rd para.).
Balya et al. teach that the photoreceptor cells (rod and cones) themselves have lost photosensitivity but not “dead” can be used to express the light-gated ion channel or pump gene (p.8, 2nd para.). This teaching is considered that the rod and/or cone cells have reduced function of photoreceptors, and thus, would meet the limitation of claims 27-28.
Regarding the gene product hyperpolarizing horizontal cells (claim 26), Balya et al. teach that the light-gated ion channel is hyperpolarizing as discussed above. As the light-gated ion channel of Balya et al. is expressed in horizontal cells as discussed above, these teachings of Balya et al. meet the limitation.
Regarding the gene product mediating potassium conductance, Balya et al. do not particularly teach the limitation. However, the light-gated ion channel of Balya et al. is considered to meet the claimed gene product because it is inherent that halorhodopsin, an example of light-gated ion channel of Balya et al. is capable of mediating potassium conductance according to Parrish et al. (see entire document).
As the light-gated ion channel of Balya et al. that mediates potassium conductance is considered to meet the claimed gene product, and the light-gated ion channel of Balya et al. is capable of hyperpolarizing the cells, and it is expressed in horizontal cells, and such administration results in vision improvement, it is considered that the same results of improving the function of photoreceptor cells are expected.
Regarding claim 29, Balya et al. do not particularly teach the limitation. However, macular degeneration taught by Balya et al. is characterized by loss of cone photoreceptors in macula according to the instant specification (p.3, 2nd full para. of the instant specification).
The wherein clauses of claims 30-31 are directed to the results of the claimed method, and these limitations do not require any additional active step to be performed. Thus, they do not limit the claimed method of treating. Furthermore, as the molecule being expressed would hyperpolarize the cells, the same outcome as claimed would be expected from the method of Balya et al.
Regarding claim 32, it is considered that the limitation is inherently met as the vector encodes hyperpolarizing light-gated ion channel (supra).
Thus, the reference anticipates the claimed invention.
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.
Claim(s) 26-32 is/are rejected under 35 U.S.C. 103 as being unpatentable over Balya et al. (WO2009/127705A1; of record) in view of Cosentino et al. (2015, Science; IDS ref.)
Balya et al. teach a method of treating a patient suffering blindness by administering a nucleic acid construct comprising a gene encoding a light-gated ion channel or pump (p.7, 2nd para.).
Balya et al. teach that “blindness” is meant total or partial loss of vision associated with macular degeneration, glaucoma and/or retinitis pigmentosa (p.6).
Balya et al. teach the nucleic acid molecule encodes for a hyperpolarizing light-gated ion channel or pump gene (Abstract; p.24, last para.; p.28, Claim 1).
Balya et al. teach that the nucleic acid molecule/construct comprises a cell specific promoter for controlling the expression of the light-gated ion channel or pump gene, and the nucleic acid molecule expressed in horizontal cells (p.3, 3rd para.).
Balya et al. teach that the photoreceptor cells (rod and cones) themselves have lost photosensitivity but not “dead” can be used to express the light-gated ion channel or pump gene (p.8, 2nd para.). This teaching is considered that the rod and/or cone cells have reduced function of photoreceptors, and thus, would meet the limitation of claims 27-28.
Regarding the gene product hyperpolarizing horizontal cells (claim 26), Balya et al. teach that the light-gated ion channel is hyperpolarizing as discussed above. As the light-gated ion channel of Balya et al. is expressed in horizontal cells as discussed above, these teachings of Balya et al. meet the limitation.
Regarding the gene product mediating potassium conductance (claim 26), Balya et al. do not teach the limitation.
Cosentino et al. teach a light-gated potassium channel including BLINK1 that hyperpolarizing of cells (entire document).
It would have been obvious to a person skilled in the art to utilize BLINK1 as the light-gated ion channel for the method of Balya et al. with a reasonable expectation of success. A person of ordinary skilled in the art would have been motivated to do so because Balya et al. require a light-gated ion channel for the purpose of improving vision loss or blindness, and BLINK1 is a light-gated channel according to Cosentino et al., and one skilled in the art would recognize that the BLINK1 is an art-recognize alternative to the light-gated ion channel of Balya et al.
Regarding claim 29, Balya et al. do not particularly teach the limitation. However, macular degeneration is characterized by loss of cone photoreceptors in macula according to the instant specification (p.3, 2nd full para. of the instant specification).
The wherein clauses of claims 30-31 are directed to the results of the claimed method, and these limitations do not require any additional active step to be performed. Thus, they do not limit the claimed method of treating. Furthermore, as the molecule being expressed would hyperpolarize the cells, the same outcome as claimed would be expected from the method of Balya et al.
Regarding claim 32, it is considered that the limitation is inherently met as the vector encodes hyperpolarizing light-gated ion channel (supra).
Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill before the effective filing date of the claimed invention.
Response to Arguments
Applicant’s arguments with respect to claim(s) 26-32 have been considered but are moot because the new ground of rejection. As indicated above, the 112 rejections and 102 rejections based on De Silva, Boesze-Battaglia or Ye have been withdrawn due to the instant amendment.
Regarding the claim rejection based on Balya et al. which is maintained and modified as above, applicant argued that Balya et al. describe a method of treating blindness by making cells light-sensitive in order to act as replacement photoreceptors in a damaged retina, and the skilled person is taught to use a gene product to modulate a cell of the retina so that the same cell acts as a light-sensitive photoreceptor cell. The Examiner respectfully disagrees with this argument. As discussed in the claim rejection, Balya et al. disclose that the light-gated ion channel is expressed in not only photoreceptor cells but also horizontal cells. As discussed in the new rejection above, the teachings of Balya et al. anticipate the claimed invention and also render them obvious.
Conclusion
No claims are allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to TAEYOON KIM whose telephone number is (571)272-9041. The examiner can normally be reached 9-5 EST Monday-Friday.
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/TAEYOON KIM/Primary Examiner, Art Unit 1631