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 .
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 8/10/26 has been entered.
Applicant’s election without traverse of group I and the species: a first and second virus, Cas nuclease, cardiac progenitor cell, under 30 years of age, and AAV serotype 9 in the reply filed on 1/29/24 is acknowledged.
Claim Objections
Claim 9 is objected to because of the following informalities: the claim appears to inadvertently recite “population or satellite cells” rather than “population of satellite cells”, consistent with the base claim. Appropriate correction is required.
Claim Rejections - 35 USC § 112
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 1-5, 9, 11-13, 16-22, 25, and 26 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. THIS IS A NEW MATTER REJECTION.
Claims 1 and 16 have been amended to require the “replacement of a genomic region associated with a muscular dystrophy with a non-pathological genomic region”.
Although the specification discloses that the modification can comprise replacement of a genomic region associated with a disease or condition with a non-pathological genomic region via homologous recombination [0036], the specification does not disclose replacement of a genomic region associated with any muscular dystrophy.
Disclosure that the subject has been diagnosed with a muscular dystrophy [0038] is not equivalent with disclosing replacement of a genomic region associated with any muscular dystrophy. The specification does not disclose that the “genomic region associated with a muscular dystrophy comprises a genomic mutation associated with Becker muscular dystrophy or Duchenne muscular dystrophy in the DMD gene” as recited in amended claims 3 and 20.
The specification does not disclose genomic mutations associated with Becker muscular dystrophy or Duchenne muscular dystrophy in the DMD gene.
Additionally, the specification does not disclose “or wherein the first and second viruses to be administered in a ratio range of less than 1:1 and down to 1:20”. Disclosure of the ratio being 1:1 or about 1: 20 [0081] is not equivalent to “or wherein the first and second viruses to be administered in a ratio range of less than 1:1 and down to 1:20” (instant claim 11).
The claims recite Cas or a functional Cas variant. The specification does not adequately describe the structure required for the variant to have the function of Cas. The specification does not adequately describe variants of Cas that are functional as Cas.
MPEP §2163.06 notes:
If new matter is added to the claims, the examiner should reject the claims under 35 U.S.C. 112, first paragraph - written description requirement. In re Rasmussen, 650 F.2d 1212, 211 USPQ 323 (CCPA 1981).
MPEP §2163.02 teaches that:
Whenever the issue arises, the fundamental factual inquiry is whether a claim defines an invention that is clearly conveyed to those skilled in the art at the time the application was filed...If a claim is amended to include subject matter, limitations, or terminology not present in the application as filed, involving a departure from, addition to, or deletion from the disclosure of the application as filed, the examiner should conclude that the claimed subject matter is not described in that application.
A review of the specification does not reveal support for where the claim amendments are found. Should applicant disagree, applicants are encouraged to point out with particularity by page and line number where such support might exist for each claim limitation added in the amended claims filed on 8/10/26.
There is no support for this claim limitation in the claimed priority documents. Therefore, the effective filing date of the instant claims is considered, for purposes of prior art, to be 11/3/20, which is the filing date of the instant application.
Claims 1-5, 9, 11-13, 16-22, 25, and 26 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.
Claims 1 and 16 require the “replacement of a genomic region associated with a muscular dystrophy with a non-pathological genomic region”.
Although the specification discloses that the modification can comprise replacement of a genomic region associated with a disease or condition with a non-pathological genomic region via homologous recombination [0036], the specification does not adequately describe replacement of a genomic region associated with any muscular dystrophy.
Without further description of the recited terminology, one would not be able to readily envision which genomic regions are associated in any manner with any muscular dystrophy and which genomic regions are non-pathological.
Disclosure that the subject has been diagnosed with a muscular dystrophy [0038] is not a sufficient description of replacement of a genomic region associated with any muscular dystrophy. The specification does not adequately describe the “genomic region associated with a muscular dystrophy comprises a genomic mutation associated with Becker muscular dystrophy or Duchenne muscular dystrophy in the DMD gene” as recited in amended claims 3 and 20. The specification does not disclose genomic mutations associated with Becker muscular dystrophy or Duchenne muscular dystrophy in the DMD gene.
Without further description of the recited terminology, one would not be able to readily envision which genomic mutations are associated in any manner with Becker muscular dystrophy or Duchenne muscular dystrophy in the DMD gene.
The MPEP states that for a generic claim, the genus can be adequately described if the disclosure presents a sufficient number of representative species that encompass the genus. See MPEP § 2163. If the genus has a substantial variance, the disclosure must describe a sufficient variety of species to reflect the variation within that genus. See MPEP § 2163. Although the MPEP does not define what constitute a sufficient number of representative species, the courts have indicated what do not constitute a representative number of species to adequately describe a broad genus. In Gostelli, the courts determined that the disclosure of two chemical compounds within a subgenus did not describe that subgenus. In re Gostelli, 872, F.2d at 1012, 10 USPQ2d at 1618. Additionally, in Carnegie Mellon University v. Hoffman-La Roche Inc., Nos. 07-1266, -1267 (Fed. Cir. Sept. 8, 2008), the Federal Circuit affirmed that a claim to a genus described in functional terms was not supported by the specification’s disclosure of species that were not representative of the entire genus. Furthermore, for a broad generic claim, the specification must provide adequate written description to identify the genus of the claim. In Regents of the University of California v. Eli Lilly & Co. the court stated:
"A written description of an invention involving a chemical genus, like a description of a chemical species, 'requires a precise definition, such as by structure, formula, [or] chemical name,' of the claimed subject matter sufficient to distinguish it from other materials." Fiers, 984 F.2d at 1171, 25 USPQ2d 1601; In re Smythe, 480 F.2d 1376, 1383, 178 USPQ 279, 284985 (CCPA 1973) ("In other cases, particularly but not necessarily, chemical cases, where there is unpredictability in performance of certain species or subcombinations other than those specifically enumerated, one skilled in the art may be found not to have been placed in possession of a genus ...") Regents of the University of California v. Eli Lilly & Co., 43 USPQ2d 1398.
The Guidelines for Examination of Patent Applications under the 35 USC § 112, first paragraph, “Written Description” Requirement”, published at Federal Register, Vol. 66, No. 4, pp. 1099-1111 outline the method of analysis of claims to determine whether adequate written description is present. The first step is to determine what the claim as a whole covers, i.e., discussion of the full scope of the claim. Second, the application should be fully reviewed to understand how applicant provides support for the claimed invention including each element and/or step, i.e., compare the scope of the claim with the scope of the description. Third, determine whether the applicant was in possession of the claimed invention as a whole at the time of filing.
To achieve the desired function, it appears that a gRNA is required for claim 1 although it is not required by the instant claim. It appears that a gRNA is required for the Cas nuclease to be functional and for insertion of the donor template, wherein the gRNA is required to be complementary to the DMD gene. Additionally, it appears that a specific donor template that has been determined to treat the specific disease condition is required, rather than any genomic region with any association to any muscular dystrophy. As instantly drafted, the specification does not adequately describe what structure is required for the replacement of any genomic region with any association to any muscular dystrophy with any non-pathological genomic region “corresponding” in any manner to any nucleotide sequence in the donor template. The specification does not adequately describe the structure required for the function.
Thus, having analyzed the claims with regard to the Written Description guidelines, it is clear that the specification does not disclose a representative number of species for genomic regions associated with muscular dystrophy, non-pathological genomic regions corresponding to any nucleotide sequence of a donor template, or genomic regions with any association with any muscular dystrophy that comprise any genomic mutation with any association with Becker muscular dystrophy or Duchenne muscular dystrophy in the DMD gene as claimed. Thus, one skilled in the art would be led to conclude that Applicant was not in possession of the claimed invention at the time the application was filed.
Claims 1-5, 9, 11-13, 16-22, 25, and 26 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for systemic administration of a specific AAV-CRISPR system of the specification comprising a specific donor template, specific gRNAs, and a nucleotide sequence encoding Cas9 with efficient NHEJ and HDR in the liver, does not reasonably provide enablement for a method of replacing any genomic region with any association with any muscular dystrophy with any non-pathological genomic region corresponding to any nucleotide sequence of the donor template via delivery of any first virus that transduces a nucleic acid sequence encoding a Cas nuclease and a second virus that transduces a donor template. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and or use the invention commensurate in scope with these claims.
Factors to be considered in a determination of lack of enablement include, but are not limited to:
(A) The breadth of the claims;
(B) The nature of the invention;
(C) The state of the prior art;
(D) The level of one of ordinary skill;
(E) The level of predictability in the art;
(F) The amount of direction provided by the inventor;
(G) The existence of working examples; and
(H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988)
The instant claims are directed to a method of modifying the genome of a population of satellite cells in vivo in any postnatal subject comprising replacing any genomic region with any association with any muscular dystrophy with any non-pathological genomic region corresponding to any nucleotide sequence of the donor template via delivery of any first virus that transduces a nucleic acid sequence encoding a Cas nuclease and a second virus that transduces a donor template.
The specification has not drawn an adequate nexus between replacing any possible genomic region with any association with any muscular dystrophy (i.e. the genomic region can cause or have no effect on the condition and meet the instant limitation of being associated to the muscular dystrophy) with any possible non-pathological genomic region (no specific region that has been shown to treat any specific condition) and the predictable outcome of modifying the genome.
For example, not all mutations associated with Duchenne muscular dystrophy in the DMD gene are necessarily deleterious or responsible for the condition. For example, Okubo et al.( Journal of Human Genetics (2017) 62, 931–933) teach that the variant c.2612A4C is a benign polymorphism in Duchenne/Becker muscular dystrophy (page 931).
The specification does not draw an adequate nexus between replacement of any genomic region that comprises any genomic mutation associated with Duchenne muscular dystrophy in the DMD gene with any possible non-pathological genomic region corresponding to any nucleotide sequence in the donor template and the modification of the genome in a predictable manner.
To achieve the desired function, it appears that a gRNA is required for claim 1 although it is not required by the instant claim. It appears that a gRNA is required for the Cas nuclease to be functional and for insertion of the donor template, wherein the gRNA is required to be complementary to the DMD gene. Additionally, it appears that a specific donor template that has been determined to treat the specific disease condition is required, rather than any genomic region with any association to any muscular dystrophy.
The scope of the claims in view of the specification as filed together do not reconcile the unpredictability in the art to enable one of skill in the art to make and/or use the claimed invention, namely a broad method of replacing any genomic region with any association with any muscular dystrophy (i.e. the genomic region can cause or have no effect on the condition and meet the instant limitation of being associated to the muscular dystrophy) with any possible non-pathological genomic region (no specific region that has been shown to treat any specific condition) and the predictable outcome of modifying the genome without the presence of a gRNA encompassing in vivo effects.
MPEP 2164.01
Any analysis of whether a particular claim is supported by the disclosure in an application requires a determination of whether that disclosure, when filed, contained sufficient information regarding the subject matter of the claims as to enable one skilled in the pertinent art to make and use the claimed invention.
Also, MPEP 2164.01(a)
A conclusion of lack of enablement means that, based on the evidence regarding each of the above factors, the specification, at the time the application was filed, would not have taught one skilled in the art how to make and/or use the full scope of the claimed invention without undue experimentation. In re Wright, 999 F.2d 1557,1562, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993).
Given the teachings of the specification as discussed above, one skilled in the art could not predict a priori whether introduction a first virus that transduces a nucleic acid encoding a Cas nuclease and a second virus that transduces a nucleic acid encoding any donor template would result in replacement of a genomic region associated in any manner to any muscular dystrophy with a non-pathological genomic region corresponding to a nucleotide sequence in the donor template
Without further guidance, one of skill in the art would have to practice a substantial amount of trial and error experimentation, an amount considered undue and not routine, to practice the instantly claimed invention.
A conclusion of lack of enablement means that, based on the evidence regarding each of the above factors, the specification, at the time the application was filed, would not have taught one skilled in the art how to make and/or use the full scope of the claimed invention without undue experimentation (see MPEP 2164.01(a)).
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
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) 1-5, 9, 11-13, 16-22, 25, and 26 is/are rejected under 35 U.S.C. 103 as being unpatentable over Zhu et al. (Molecular Therapy: Nucleic Acids Vol. 7 June 2017, 31-41), in view of Tabebordbar et al. (Science, 2016, 351, 6271, 407-411), and Long et al. (Science, 2016, 351, 6271, 400-403).
Zhu et al. teach: In skeletal muscles, satellite cells are acknowledged as bona fide adult MuSCs being responsible for postnatal growth and regeneration of the muscle fiber. Transplantation-based studies have demonstrated the impressive potential of satellite cells in regenerating damaged or diseased muscle and thus highlighted the importance of such adult stem cells as therapeutic targets in treating inherited, acquired, as well as age-associated muscular disorders. However, the application of the CRISPR/Cas9 gene-editing technique in concert with satellite cell remains unseen in spite of the recognized importance and advantages of such adult stem cells (page 32).
Zhu et al. teach: It has to be realized that DMD is a chronic and progressive disorder affecting all muscles in the body. Unfortunately, delivery of myogenic stem cells to the site of muscle lesions via systemic circulation like intravenous injection was previously shown to result in only a small portion entering the muscle microvasculature and migrating into dystrophic muscles. Instead, intramuscular injections have been repeatedly proved to ensure a good uptake of satellite cell derived myoblasts in skeletal muscles. Obviously, our approach helps to preserve autonomy and life quality in DMD patients by slowing down or stopping muscle degeneration and increasing force in wasted muscles, but not for a respiratory muscle such as the diaphragm. Efficient systemic delivery of adult stem cells to the whole body muscles will undoubtedly advance stem cell-based therapy for muscular disease (page 38).
Zhu et al. isolated and expanded skeletal muscle stem cells (MuSCs/satellite cells) from mdx mice and then co-infected the cells with two adenoviral vectors, one expressing Cas9 and other expressing a gRNA with a DMD specific donor template. The donor template is a 1314-bp DNA fragment having 591- and 722- bp homology arms around the DMD mutation. Zhu et al. teach that HDR corrected the mutant DMD sequence. The corrected MuSCs were transplanted into mdx mice, producing dystrophin-positive fibers (instant claims 1, 3-5, and 20-22).
Zhu et al. performed the method ex vivo rather than in vivo as instantly claimed. However, Zhu et al. discloses delivery challenges for intravenous injection and expressly teaches: Instead, intramuscular injections have been repeatedly proved to ensure a good uptake of satellite cell derived myoblasts in skeletal muscles. Therefore, it would have been obvious in view of Zhu et al. alone to practice the method in vivo via intramuscular injection in a postnatal subject, a DMD patient (instant claim 1).
It would have been obvious for the administration to be systemic (instant claim 2) and via AAV vectors (instant claims 12 and 25) because Tabebordbar et al. teach: to test the potential for in vivo Dmd targeting by CRISPR/Cas9, we pseudotyped dual AAVs (AAV-SaCas9 + AAV-Ai9 gRNAs; hereafter, AAV-Ai9 CRISPR) to serotype 9 (instant claims 12 and 25), which exhibits robust transduction of mouse skeletal and cardiac muscle, and injected these AAVs into the tibialis anterior (TA) muscles of mdx;Ai9 mice (7.5E+11 vg each). Four weeks later, muscles were harvested to assess genome-editing events. TdTomato fluorescence was detected in muscles injected with AAV Ai9 CRISPR, but not in muscles injected with vehicle alone (Fig. S4A). Co-delivery of AAV9-SaCas9 + AAV9-Dmd23 gRNAs (hereafter AAV-Dmd CRISPR) likewise yielded robust and specific modification of the Dmd locus in TA muscles in vivo (page 3)
Tabebordbar et al. teach: We next evaluated the potential for multisystemic gene editing in vivo using AAV-CRISPR. Dual AAV-Ai9 CRISPR vectors (1.5E+12 vg each) were co-injected intraperitoneally into mdx;Ai9 mice at postnatal day 3 (P3). Three weeks later, widespread tdTomato expression was detected in all cardiac and skeletal muscles analyzed (Fig. S8A) (page 4).
Therefore, it would have been obvious for the system of Zhu et al. to be targeted to cardiac cells, as these cells were known targets for treatment of the same disease taught by Zhu et al., DMD, as evidenced by Tabebordbar et al. (instant claim 16).
Additionally, it would have been obvious to utilize dual AAV9 via intraperitoneal injection for the method of Zhu et al. because Tabebordbar et al. teach that this mode of delivery resulted in Dmd restoration. Tabebordbar et al. teach: Similar systemic dissemination of AAV and excision of exon23 in multiple organs were seen in two adult mice injected intravenously with AAV-Dmd CRISPR at 6 weeks of age (Fig. S9) (page 4).
Since Tabebordbar et al. demonstrate that systemically delivered AAV-CRISPR can reach endogenous Pax7+ satellite cells in a DMD model (page 4), it would have been obvious to utilize the AAV and systemic administration of Tabebordbar et al. to deliver the CRISPR agents of Zhu et al. for replacement of a genomic region in a cardiac cell with a reasonable expectation of success (instant claims 1, 2, 16, and 19). One would reasonably expect for the action of Zhu et al. to occur in cardiac and skeletal muscles, as taught by Tabebordbar et al.
Additionally, Tabebordbar et al. teach that after systemic AAV delivery, satellite cells were transduced and genome edited (Figure 4). Figure 4 is titled “Satellite cells in dystrophic muscles are transduced and targeted with systemically disseminated AAV-CRISPR”.
Therefore, Zhu et al. teaches correcting DMD mutations in satellite/MuSCs using two viral vectors, one carrying Cas9 and the other carrying the guide/donor sequences. Tabebordbar et al. teaches that in the same disease state, DMD, Crispr components can in fact be delivered systemically via AAV to reach an edit endogenous satellite cells, including Pax7+ satellite cells. Tabebordbar et al. demonstrates editing in skeletal muscle, cardiac muscle, and endogenous muscle stem cells, supporting systemic editing.
One of ordinary skill in the art would have adapted Zhu’s method to the systemic AAV delivery approach of Tabebordbar et al. because Tabebordbar et al. demonstrated that systemically administered AAV genome-editing vectors could transduce and edit endogenous satellite cells in vivo, thereby providing a way to treat without ex vivo manipulation. Zhu et al. acknowledges the delivery challenges and teaches: Efficient systemic delivery of adult stem cells to the whole body muscles will undoubtedly advance stem cell-based therapy for muscular disease (page 38).
Zhu et al. teach selecting cells that are Pax7+ (see Figure 1) (instant claim 9).
Zhu et al. teach incorporation of two gRNAs (Figure 2 and page 39) (instant claim 11).
Zhu et al. does not expressly disclose the ratio of the first and second viruses. However, it would have been obvious for the first and second viruses to be administered in a ratio range of less than 1:1 and down to 1:20. However, this is not required in claims 11 and 26, but is rather recited in the alternative. Zhu et al. teaches incorporation of two gRNAs.
Since Zhu et al. offers motivation to treat DMD via delivery of the construct of Zhu et al. for genome correction of DMD and that MuSCs can engraft and generate dystrophin-positive muscle after transplantation, it would have been obvious to select a patient that is a juvenile and would benefit from the long term benefits of the method as a matter of design choice. Any DMD patient that has the mutation would have been an obvious choice (instant claims 13 and 18).
Additionally, Long et al. teach: CRISPR/Cas9-mediated genome editing holds clinical potential for treating genetic diseases, such as Duchenne muscular dystrophy (DMD),which is caused by mutations in the dystrophin gene. To correct DMD by skipping mutant dystrophin exons in postnatal muscle tissue in vivo, we used adeno-associated virus–9 (AAV9) to deliver gene-editing components to postnatal mdx mice, a model of DMD. Different modes of AAV9 delivery were systematically tested, including intraperitoneal at postnatal day 1 (P1), intramuscular at P12, and retro-orbital at P18. Each of these methods restored dystrophin protein expression in cardiac and skeletal muscle to varying degrees, and expression increased from 3 to 12 weeks after injection. Postnatal gene editing also enhanced skeletal muscle function, as measured by grip strength tests 4 weeks after injection. This method provides a potential means of correcting mutations responsible for DMD and other monogenic disorders after birth (abstract).
In view of the teachings of Long et al., one would have been motivated to practice the method of Zhu et al. in a postnatal juvenile subject with a reasonable expectation of enhanced skeletal muscle function. Long et al. teach that using AAV9 CRISPR delivery treats DMD after birth.
Response to Arguments
The rejection has been amended in response to the claim amendments. Arguments regarding references that are no longer cited are not being responded to. Applicant argues that the specification demonstrates an unexpected and surprising result of in vivo HDR-editing in the postnatal heart via systemic AAV delivery of CRISPR/Cas9. The specification does not demonstrate any unexpected result commensurate in scope with the instant claims. The instant claims are obvious in view of the cited references and there was motivation to treat a juvenile, as evidenced by Long et al. It is noted that the only claim that requires treatment of a juvenile is instant claim 13.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Amy R Hudson whose telephone number is (571)272-0755. The examiner can normally be reached M-F 8:00am-6:00pm.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Neil Hammell can be reached on 571-270-5919. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/AMY ROSE HUDSON/Primary Examiner, Art Unit 1636
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