(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 .
Applicants’ arguments and amendments filed on 7/1/2026 have been entered.
Claims 1-8 and 11 have been amended.
Claims 14-20 are new.
In view of Applicants amendments, the 112(b) rejections are withdrawn.
Claims 1-11 and 14-20 are examined in the instant application.
Allowable Subject Matter
Claims 17 and 19 are objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims.
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.
Claim(s) 1, 2 and 8-11 remain rejected and new claims 14 and 20 are rejected under 35 U.S.C. 103 as being unpatentable over Debs et al. (WO 2018/175932) in view of Bloquel et al. (2005, FASEB J., Vol., pgs. 1-22) for reasons of record in the Non-Final Office Action on 4/1/2026 (and repeated as amended below).
Regarding claims 1, 2, 8, 11 and 14, Debs et al. teaches a method of treating ocular pathologies such as wet-aged macular degeneration (WETAMD) and retinopathy in an individual in need thereof by administering to muscle tissue of the patient DNA constructs encoding brolucizumab and bevacizumab, wherein the DNA construct comprises:
a) a bacterial or prokaryotic origin of replication (R6K),
(b) one or more sequences promoting the expression of DNA in the patient's ocular sphere,
(c) a first nucleotide sequence coding for:
a first therapeutic protein (brolucizumab), and
a signal peptide allowing secretion of this first therapeutic protein,
this signal peptide being contiguous with the sequence of the first therapeutic protein, at the N-terminal of said first therapeutic protein,
(d) a promoter allowing expression of this first therapeutic protein in the patient's ocular sphere,
(e) a polyadenylation sequence at 3' of the first nucleotide sequence;
(f) a second nucleotide sequence coding for:
a second therapeutic protein (bevacizumab), different than the first therapeutic protein, and
a signal peptide allowing secretion of this second therapeutic protein,
the signal peptide being contiguous with the sequence of the second therapeutic protein, at the N-terminal of said second therapeutic protein,
(g) a promoter allowing expression of this second therapeutic protein in the patient's ocular sphere, and
(h) a polyadenylation sequence at 3' of the second nucleotide sequence (see Abstract, pg. 1 parag. 2-4, pg. 4 line 28 bridge pg. 5 line 24, Fig. 23, Table 2 and Table 3, Example 1 and pg. 41).
Regarding claim 9, Debs teaches that the DNA construct is circular in shape (pg. 4 line 2).
Regarding claim 10, Debs teaches the DNA construct can be naked (pg. 11 line 3).
Debs does not teach:
electrotransfer to the ciliary muscle.
Regarding the electrotransfer of DNA vectors to the ciliary muscle, Bloquel et al.
teach (emphasis added):
“Due to its small size and particular isolating barriers, the eye is an ideal target for local therapy. Recombinant protein ocular delivery requires invasive and painful repeated injections.
Alternatively, a transfected tissue might be used as a local producer of transgene-encoded
therapeutic protein. We have developed a nondamaging electrically mediated plasmid delivery
technique (electrotransfer) targeted to the ciliary muscle, which is used as a reservoir tissue for
the long-lasting expression and secretion of therapeutic proteins. High and long-lasting reporter
gene expression was observed, which was restricted to the ciliary muscle. Chimeric TNF-α
soluble receptor (hTNFR-Is) electrotransfer led to elevated protein secretion in aqueous humor
and to drastic inhibition of clinical and histological inflammation scores in rats with endotoxin-induced uveitis.” (Abstract lines 1-10).
Importantly, Bloquel teaches that “Local and sustained therapeutic protein production through ciliary muscle electrotransfer is a promising alternative to repeated intraocular protein administration for a large number of inflammatory, degenerative, or angiogenic diseases.” (Abstract, last sentence).
Bloquel concludes by teaching that:
“Our experiments show that the local intraocular production of a chimeric TNF-α soluble receptor by ciliary muscle fibers, resulting from hTNFR-Is/mIgG1 plasmid electrotransfer, significantly reduces the intensity of clinical and histological disease parameters in EIU. This beneficial therapeutic effect resulted from the local production (and secretion) of hTNFR-Is/mIgG1 within the treated eyes, since the reduced disease severity was associated with high hTNFR-Is/mIgG1 ocular level and with decreased TNF-α concentration in the aqueous humor.” (pg. 10 parag. 2 lines 1-6).
Thus at the time of filing the ordinary artisan would have found it prima facie obvious to combine the teachings of Debs regarding treating the eye with a composition comprising two DNA vectors encoding therapeutic proteins with the teachings of Bloquel regarding the advantages of electrotransfer DNA delivery to the eye to arrive at the claimed invention.
One of ordinary skill in the art would have been motivated to deliver the DNA vectors of Debs to only the ciliary muscle via electrotransfer for the treatment of a disease such as WETAMD since Bloquel teaches that electrotransfer is a successful alternative to repeated administration to the eye and results in long-term localized expression of the therapeutic protein.
There would have been a reasonable expectation of success that DNA vectors of Debs could be administered to the ciliary muscle via electrotransfer since Bloquel taught successful delivery and expression of therapeutic proteins in the eye via electrotransfer of plasmid DNA to the ciliary muscle.
Thus, the cited art provides the requisite teachings and motivations to make and use the invention as claimed.
Response to Arguments
Applicants’ Arguments
Applicants argue in amendment that the rejection relies on a combination of references
that address fundamentally different gene delivery systems operating in materially different
therapeutic contexts. Debs is directed to systemic intravenous administration of nucleic acid
constructs using cationic liposomes or related polycationic structures, designed to achieve
broad systemic distribution following administration into the bloodstream. That is, the entire
framework of Debs is centered on systemic delivery via circulation and lipid-mediated
transfection, and it does not contemplate localized ocular administration, injection into ocular
muscle tissue, or any form of electrotransfer. Accordingly, Debs reflects a delivery paradigm
fundamentally distinct from localized tissue-specific gene delivery as contemplated in the
present claims.
Bloquel, by contrast, is directed to a highly localized ocular gene delivery technique
involving electrotransfer into the ciliary muscle. Importantly, Bloquel's experimental system is
limited to a simple single-cassette plasmid encoding a single therapeutic protein. There is
no disclosure or suggestion in Bloquel of multi-cassette constructs, nor any indication that
constructs of increased structural complexity would be used or contemplated in the electrotransfer context. Thus, Bloquel likewise reflects a narrowly tailored local delivery
system that is structurally and functionally distinct from systemic vector systems such as
Debs.
Thus, at the outset, the cited references are directed to fundamentally different
delivery paradigms: Debs teaches systemic intravenous liposomal delivery throughout the
body, while Bloquel teaches localized, electrically mediated transfer into ocular muscle
tissue. These are not variations along a shared continuum but distinct technical approaches
with different delivery routes, cellular targets, and mechanistic requirements. See MPEP §
2143.01(V) (modifications that change the principle of operation of a reference weigh against
obviousness), and MPEP § 2143 (a proper obviousness determination requires articulated
reasoning with rational underpinning to support the proposed combination).
Claim 1, however, recites a specific and structurally constrained combination of
features that is not disclosed or suggested in either reference. In particular, the claimed
method recites a DNA construct comprising two distinct expression cassettes, each
encoding a different therapeutic protein and each including its own promoter, signal peptide,
and polyadenylation sequence, combined with administration by injection into the ciliary
muscle followed by electrotransfer into the cells of the ciliary muscle. Neither Debs nor
Bloquel discloses or suggests this combination. Debs does not disclose ocular
administration or electrotransfer at all, and Bloquel does not disclose or suggest dual-
expression cassette constructs or any modification of systemic liposomal vectors of the type
described in Debs.
The combination required by the rejection therefore depends on fundamentally
reconfiguring Debs' systemic IV liposomal gene delivery system into a localized ocular
electrotransfer system as taught by Bloquel. However, nothing in either reference provides
any teaching, suggestion or articulated rationale that would have led a person of ordinary
skill in the art to make such a modification. The systems operate in different biological
compartments and rely on different physical mechanisms of delivery, circulatory distribution
and lipid-mediated uptake on the one hand, and direct tissue injection followed by electrical
permeabilization on the other. In the absence of such articulated reasoning, the rejection
fails to satisfy the requirement under MPEP § 2143 that an obviousness determination be
supported by a reasoned explanation grounded in the prior art as a whole.
Even assuming arguendo that a skilled artisan could conceptually contemplate
combining these references, one skilled in the art would not have had any reasonable
expectation that the resulting system would function as claimed. In particular, Bloquel's
electrotransfer experiments are conducted using relatively small, single-cassette plasmids
encoding a single therapeutic protein. In contrast, Debs contemplates systemic delivery
systems optimized for entirely different pharmacokinetic and transfection conditions. The
proposed modification would require a fundamental redesign of both systems, and the Office
Action provides no articulated rationale or evidence that a person of ordinary skill in the art
would have had a reasonable expectation of success in modifying a systemic liposomal IV
gene delivery system for use in localized ocular electrotransfer with a structurally and
functionally distinct dual-cassette construct. See MPEP § 2143.02 (a proper obviousness
rejection requires a reasonable expectation of success based on the prior art).
Examiner’s Response
While Applicants arguments have been fully considered they are not found persuasive. While Debs and Bloquel may be drawn to two different means of gene delivery, it much be emphasized that they are both teaching treatment of an ocular pathology. While Debs treatment method relies upon delivery to the muscle, Bloquel teaches an alternative treatment that is direct and with multiple benefits as set forth above. Further, Applicant provides no evidence that the DNA constructs could not be delivered via electrotransfer to a ciliary muscle and Bloquel does not teach any specific limitations in their electrotransfer method regarding size and/or complexity of a DNA construct. Thus the ordinary artisan is provided with an alternative and beneficial means of direct delivery of a DNA construct encoding a therapeutic protein for treatment of an ocular pathology.
Thus for the reasons above and of record the rejection is maintained.
Claim(s) 3 remains rejected under 35 U.S.C. 103 as being unpatentable over Debs et al. (WO 2018/175932) in view of Bloquel et al. (2005, FASEB J., Vol., pgs. 1-22) as applied to claims 1, 2, 8-11, 14 and 20 above, and further in view of Nietz et al. (WO 2019/113225 A1) for reasons of record in the Non-Final Office Action on 4/1/2026 (and repeated as amended below).
Regarding claim 1, Debs et al. teaches a method of treating ocular pathologies such as wet-aged macular degeneration (WETAMD) and retinopathy in an individual in need thereof by administering to muscle tissue of the patient DNA constructs encoding brolucizumab and bevacizumab, wherein the DNA construct comprises:
a) a bacterial or prokaryotic origin of replication (R6K),
(b) one or more sequences promoting the expression of DNA in the patient's ocular sphere,
(c) a first nucleotide sequence coding for:
a first therapeutic protein (brolucizumab), and
a signal peptide allowing secretion of this first therapeutic protein,
this signal peptide being contiguous with the sequence of the first therapeutic protein, at the N-terminal of said first therapeutic protein,
(d) a promoter allowing expression of this first therapeutic protein in the patient's ocular sphere,
(e) a polyadenylation sequence at 3' of the first nucleotide sequence;
(f) a second nucleotide sequence coding for:
a second therapeutic protein (bevacizumab), different than the first therapeutic protein, and
a signal peptide allowing secretion of this second therapeutic protein,
the signal peptide being contiguous with the sequence of the second therapeutic protein, at the N-terminal of said second therapeutic protein,
(g) a promoter allowing expression of this second therapeutic protein in the patient's ocular sphere, and
(h) a polyadenylation sequence at 3' of the second nucleotide sequence (see Abstract, pg. 1 parag. 2-4, pg. 4 line 28 bridge pg. 5 line 24, Fig. 23, Table 2 and Table 3, Example 1 and pg. 41).
Debs does not teach:
A first therapeutic protein is encoded by a nucleotide sequence having at least 75% sequence identity to SEQ ID NO: 1.
Regarding a therapeutic protein, Nietz et al. teach a method to express therapeutic
proteins in the eye to treat a variety of eye diseases and disorders (see Abstract and pg. 1). Specifically, Niets teaches a nucleic acid sequence (SEQ ID NO: 101) which is 99.5% identical to instantly recited SEQ ID NO: 1 and which can be delivered to treat a cone cell disorder by expressing a therapeutic protein (see claims 50 and 58).
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Nietz continues to teach that their therapeutic proteins can be used to treat diseases of the macula (pg. 59 lines 1-7).
Thus at the time of filing the ordinary artisan would have found it prima facie obvious to combine the teachings of Debs and Bloquel regarding treating the eye with a composition comprising two DNA vectors encoding therapeutic proteins with the teachings of Nietz regarding the therapeutic proteins for treating diseases of the eye to arrive at the claimed invention.
One of ordinary skill in the art would have been motivated to deliver the nucleic acid encoding a therapeutic proteins which is 99.5% identical to SEQ ID NO: 1 since Nietz teaches that their therapeutic proteins are effective for treating disease of the eye and in particular diseases of the macula.
There would have been a reasonable expectation of success that nucleic acid encoding a therapeutic protein of Nietz would be effective in treating an ocular pathology since Nietz teaches that their therapeutic proteins are effective for treating a variety of eye diseases.
Thus, the cited art provides the requisite teachings and motivations to make and use the invention as claimed.
Response to Arguments
Applicant does not present any specific arguments regarding this rejection, thus for the reasons above and of record the rejection is maintained.
Claim(s) 4, 5 and 7 remain rejected and new claims 15, 16 and 18 are rejected under 35 U.S.C. 103 as being unpatentable over Debs et al. (WO 2018/175932) in view of Bloquel et al. (2005, FASEB J., Vol., pgs. 1-22) as applied to claims 1, 2, 8-11, 14 and 20 above, and further in view of Adamson et al. (WO 2010136492), Ge et al. (WO 2005116066), Jin et al. (WO2006119510), Krusius et al. (1986, PNAS, Vol. 83, pgs. 7683-7687) and Wang et al. (2015, Invest. Opthamol. Vis. Sci., Vol. 56, pgs. 2971-2979) for reasons of record in the Non-Final Office Action on 4/1/2026 (and repeated as amended below).
Regarding claim 1, Debs et al. teaches a method of treating ocular pathologies such as wet-aged macular degeneration (WETAMD) and retinopathy in an individual in need thereof by administering to muscle tissue of the patient DNA constructs encoding brolucizumab and bevacizumab, wherein the DNA construct comprises:
a) a bacterial or prokaryotic origin of replication (R6K),
(b) one or more sequences promoting the expression of DNA in the patient's ocular sphere,
(c) a first nucleotide sequence coding for:
a first therapeutic protein (brolucizumab), and
a signal peptide allowing secretion of this first therapeutic protein,
this signal peptide being contiguous with the sequence of the first therapeutic protein, at the N-terminal of said first therapeutic protein,
(d) a promoter allowing expression of this first therapeutic protein in the patient's ocular sphere,
(e) a polyadenylation sequence at 3' of the first nucleotide sequence;
(f) a second nucleotide sequence coding for:
a second therapeutic protein (bevacizumab), different than the first therapeutic protein, and
a signal peptide allowing secretion of this second therapeutic protein,
the signal peptide being contiguous with the sequence of the second therapeutic protein, at the N-terminal of said second therapeutic protein,
(g) a promoter allowing expression of this second therapeutic protein in the patient's ocular sphere, and
(h) a polyadenylation sequence at 3' of the second nucleotide sequence (see Abstract, pg. 1 parag. 2-4, pg. 4 line 28 bridge pg. 5 line 24, Fig. 23, Table 2 and Table 3, Example 1 and pg. 41).
Debs does not teach:
a first therapeutic protein is encoded by a nucleotide sequence having at least 85% sequence identity to SEQ ID NO: 3 (claims 4 and 7),
a second therapeutic protein is encoded by a nucleotide sequence having at least 85% sequence identity to SEQ ID NO: 8 (claims 5 and 7),
a signal peptide sequence of SEQ ID NOs: 4 and 13 (claims 4 and 7),
decorin (claim 18).
Regarding a first therapeutic protein in SEQ ID NO: 3 and claim 15, Adamson et
al. teach a method to express a nucleic acid encoding SEQ ID NO: 43, which is 100% identical to instant SEQ ID NO: 3 from an administered DNA vector for the treatment of eye diseases such as WETAMD and uveitis (pg. 5 lines 25-37 and pg. 36 lines 7-14).
Regarding claim 16, the specification teaches that SEQ ID NO: 3 is aflibercept (pg. 9 line 14).
SEQ ID NO: 3 (SEQ ID NO: 43)
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Regarding a second therapeutic protein in SEQ ID NO: 8, Ge et al. teach
method to express a nucleic acid encoding SEQ ID NO: 1, which is 99.7%% identical to instant
SEQ ID NO: 8 from an administered DNA vector for the treatment of eye diseases such as diabetic retinopathy and WETAMD (pg. 1 lines 8-16, pg. 11 parag. 2).
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Regarding a signal peptide of SEQ ID NO: 4, Jin et al. teach a method of treating
eye disorders such an ocular surface inflammatory disorder, macular degeneration and proliferative vitreoretinopathy using a DNA vector comprising a signal peptide (SEQ ID NO: 101) which is 100% identical to instant SEQ ID NO: 4.
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(iiia) Regarding a signal peptide of SEQ ID NO: 13, Ge et al. teach a method of
treating eye disorders such an diabetic retinopathy and WETAMD using a DNA vector comprising a signal peptide (SEQ ID NO: 1) which is 100% identical to instant SEQ ID NO: 13.
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Regarding decorin, Krusius et al. teach the identification and sequencing of the
nucleic and amino acid sequences as well as the characterization of the protein PG40 (see Abstract and Fig. 2).
It should be noted that PG40 and decorin are synonyms for the same protein. In this regard Wang et al. teach that decorin is a therapeutic protein which can prevent the breakdown of the epithelial barrier in the retina (see Abstract).
Specifically, Wang teaches that “diabetic macular edema (DME) is one of the primary causes of visual impairment in patients with diabetes mellitus.1 Breakdown of the blood-retina barrier (BRB) caused by the disruption of tight junctions appears to be the main factor responsible for DME” (pg. 2791 col. 1 lines 1-5).
Wang continues to teach that that their results “indicate that decorin is able to prevent the HG plus hypoxia-induced breakdown of RPE cell monolayer, and this beneficial effect is mainly mediated by inhibition of p38 MAPK activation.” (pg. 2976 col. 2 parag. 1 lines 4-6).
Thus at the time of filing the ordinary artisan would have found it prima facie obvious to combine the teachings of Debs and Bloquel regarding treating the eye with a composition comprising two DNA vectors encoding therapeutic proteins with the teachings of Adamson, Ge and Jin regarding therapeutic proteins and signal peptides for treating diseases of the eye and with the teachings of Krusius and Wang regarding the therapeutic value of decorin to arrive at the claimed invention.
One of ordinary skill in the art would have been motivated to deliver the nucleic acids encoding the therapeutic proteins of Adamson and Ge since both Adamson and Ge teach that their therapeutic proteins are effective for treating a variety of ocular pathologies. Further motivation is provided to use the signal peptides of Jin and Ge since both Jin and Ge teach use of their signal peptides in method of delivery a DNA vector for the treatment of an ocular pathology. Further motivation is provided by Krusius to use decorin as a therapeutic protein for treating an ocular pathology.
There would have been a reasonable expectation of success that the nucleic acids encoding therapeutic proteins of Adamson and Ge would be effective in treating an ocular pathology since both Adamson and Ge teach that their therapeutic proteins are effective for treating a variety of ocular pathologies
Thus, the cited art provides the requisite teachings and motivations to make and use the invention as claimed.
Response to Arguments
Applicant does not present any specific arguments regarding this rejection, thus for the reasons above and of record the rejection is maintained.
Claim(s) 1 and 6 remain rejected under 35 U.S.C. 103 as being unpatentable over Debs et al. (WO 2018/175932) in view of Bloquel et al. (2005, FASEB J., Vol., pgs. 1-22) as applied to claims 1, 2, 8-11, 14 and 20 above, and further in view of Krusius et al. (1986, PNAS, Vol. 83, pgs. 7683-7687) and Wang et al. (2015, Invest. Opthamol. Vis. Sci., Vol. 56, pgs. 2971-2979) for reasons of record in the Non-Final Office Action on 4/1/2026 (and repeated as amended below).
Regarding claim 1, Debs et al. teaches a method of treating ocular pathologies such as wet-aged macular degeneration (WETAMD) and retinopathy in an individual in need thereof by administering to muscle tissue of the patient DNA constructs encoding brolucizumab and bevacizumab, wherein the DNA construct comprises:
a) a bacterial or prokaryotic origin of replication (R6K),
(b) one or more sequences promoting the expression of DNA in the patient's ocular sphere,
(c) a first nucleotide sequence coding for:
a first therapeutic protein (brolucizumab), and
a signal peptide allowing secretion of this first therapeutic protein,
this signal peptide being contiguous with the sequence of the first therapeutic protein, at the N-terminal of said first therapeutic protein,
(d) a promoter allowing expression of this first therapeutic protein in the patient's ocular sphere,
(e) a polyadenylation sequence at 3' of the first nucleotide sequence;
(f) a second nucleotide sequence coding for:
a second therapeutic protein (bevacizumab), different than the first therapeutic protein, and
a signal peptide allowing secretion of this second therapeutic protein,
the signal peptide being contiguous with the sequence of the second therapeutic protein, at the N-terminal of said second therapeutic protein,
(g) a promoter allowing expression of this second therapeutic protein in the patient's ocular sphere, and
(h) a polyadenylation sequence at 3' of the second nucleotide sequence (see Abstract, pg. 1 parag. 2-4, pg. 4 line 28 bridge pg. 5 line 24, Fig. 23, Table 2 and Table 3, Example 1 and pg. 41).
Debs does not teach:
a first therapeutic protein is encoded by a nucleotide sequence having at least 70% sequence identity to SEQ ID NO: 6.
Regarding the expression of a therapeutic protein, Krusius et al. teach the
identification and sequencing of the nucleic and amino acid sequences as well as the characterization of the protein PG40 (see Abstract and Fig. 2).
Krusius teaches a nucleotide sequence encoding a protein which is 100% identical to instant SEQ ID NO: 6.
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It should be noted that PG40 and decorin are synonyms for the same protein. In this regard Wang et al. teach that decorin is a therapeutic protein which can prevent the breakdown of the epithelial barrier in the retina (see Abstract).
Specifically, Wang teaches that “diabetic macular edema (DME) is one of the primary causes of visual impairment in patients with diabetes mellitus.1 Breakdown of the blood-retina barrier (BRB) caused by the disruption of tight junctions appears to be the main factor responsible for DME” (pg. 2791 col. 1 lines 1-5).
Wang continues to teach that that their results “indicate that decorin is able to prevent the HG plus hypoxia-induced breakdown of RPE cell monolayer, and this beneficial effect is mainly mediated by inhibition of p38 MAPK activation.” (pg. 2976 col. 2 parag. 1 lines 4-6).
Thus at the time of filing the ordinary artisan would have found it prima facie obvious to combine the teachings of Debs and Bloquel regarding treating the eye with a composition comprising two DNA vectors encoding therapeutic proteins with the teachings of Wang regarding the therapeutic potential of decorin for treating diseases of the eye to arrive at the claimed invention.
One of ordinary skill in the art would have been motivated to deliver a nucleic acid encoding a protein encoding decorin (SEQ ID NO:6) to the eye since Wang teaches that decorin has potential therapeutic efficacy for treating the breakdown of the retinal pigment epithelial barrier resulting from diabetes.
There would have been a reasonable expectation of success that the nucleic acid encoding the therapeutic protein decorin could be used in the method of Debs and Bloquel since the nucleic and amino acid sequences for decorin were known in the art and that the protein decorin has potential therapeutic efficacy in treating an ocular pathology of the eye.
Thus, the cited art provides the requisite teachings and motivations to make and use the invention as claimed.
Response to Arguments
Applicant does not present any specific arguments regarding this rejection, thus for the reasons above and of record the rejection is maintained.
Conclusion
No claims are allowed. SEQ ID NOs: 2, 7 and 9-12 are free of the prior art.
THIS ACTION IS MADE FINAL. 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 DAVID A MONTANARI whose telephone number is (571)272-3108. The examiner can normally be reached M-Tr 8-6.
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DAVID A. MONTANARI
Examiner
Art Unit 1632
/ANOOP K SINGH/Primary Examiner, Art Unit 1632
Prosecution Insights