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
Claims 1-3, 5, 6, 9-11, 13, 15, 16, 18, 20-22, and 24-28 are currently pending and under prosecution.
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 1-3, 5, 6, 9-11, 13, 15, 16, 18, 20-22, and 24-28 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 WRITTEN DESCRIPTION rejection.
The claims are drawn to a method of inducing mammalian cardiac cell proliferation, the method comprising ectopically introducing an LRRC10 protein in a mammalian cardiac cell to thereby induce proliferation of the cardiac cell. Claim 3 recites that the LRRC10 protein of claim 1 is at least 95% identical to SEQ ID NO: 1. Thus, the claims are drawn to the broad genus of any LRRC10 protein, no structure is recited.
Dependent claim 3 is directed up to a 5% variant of LRRC10, thus this claim encompasses a genus of proteins having up to 5% discrepancy from the disclosed sequence. It is unclear what the mutations will be, and what can be changed without disrupting the function of LRRC10.
The instant specification discloses that the LRRC10 protein refers to the wild-type human LRRC10 protein or homologs or variants having an LRRC10 activity. [0037 of published specification] The instant specification also discloses intravenous injection of AAV9-cTnT-LRRC10, AAV9-cTnT-NLS-LRRC10 (which harbors a nuclear localization signal (NLS) to target LRRC10 in the nucleus). [0129 of the published specification] Thus, the specification discloses introducing an LRRC10 protein via an adenovirus vector comprising the full protein. Additionally, the specification does not provide any examples of any homolog or variant of the LRRC10 protein with less than 100% of the protein that still retains function of the protein.
It is well understood in the art that mutations in amino acids can have structural and functional consequences, as taught by Sotomayor-Vivas et al (Linking protein structural and functional change to mutation using amino acid networks. PLoS One. 2022 Jan 21;17(1)). It is impossible to determine which residue(s) can be mutated for another residue, to still have the same effect and function. With regards to mutations in LRRC10, Siri-Angkul et al (Cardiac L-type calcium channel regulation by Leucine-Rich Repeat-Containing Protein 10. Channels (Austin). 2024 Dec;18(1):2355121. doi: 10.1080/19336950.2024.2355121. Epub 2024 May 19) teaches that variants of LRRC10 have been associated with cardiac diseases. Siri-Angkul teaches that variants of LRRC10 have been identified in dilated cardiomyopathy and sudden unexplained nocturnal cardiac death syndrome. [Abstract, pg 2 ‘Discovery of LRRC10 and its roles in cardiac biology and disease, 2nd column, last paragraph] Thus, variants in the protein may not be able to retain function of the LRRC10 and may further lead to disease progression, structural and functional consequences.
To provide adequate written description and evidence of possession of the claimed LRRC10 protein, the instant specification can structurally describe representative proteins that function as claimed, or describe structural features common to the members of the genus, which features constitute a substantial portion of the genus. Alternatively, the specification can show that the claimed invention is complete by disclosure of sufficiently detailed, relevant identifying characteristics, functional characteristics when coupled with a known or disclosed correlation between function and structure, or some combination of such characteristics (see University of California v. Eli Lilly and Co., 119 F.3d 1559, 43 USPQ2d 1398 (Fed. Cir. 1997) and Enzo Biochem, Inc. V. Gen-Probe Inc.).
Although Applicants may argue that it is possible to screen for LRRC10 proteins that function as claimed, the court found in (Rochester v. Searle, 358 F.3d 916, Fed Cir., 2004) that screening assays are not sufficient to provide adequate written description for an invention because they are merely a wish or plan for obtaining the claimed chemical invention. “As we held in Lilly, “[a]n adequate written description of a DNA … ‘requires a precise definition, such as by structure, formula, chemical name, or physical properties,’ not a mere wish or plan for obtaining the claimed chemical invention.” 119 F.3d at 1566 (quoting Fiers, 984 F.2d at 1171). For reasons stated above, that requirement applies just as well to non-DNA (or RNA) chemical inventions.” Knowledge of screening methods provides no information about the structure of any future LRRC10 proteins variants yet to be discovered that may function as claimed.
The instant specification fails to describe fails to describe structural features common to the members of the genus, which features constitute a substantial portion of the genus because the instant specification discloses one example, which is the administration of the full LRRC10 protein that functions as claimed. A definition by function does not suffice to define the genus because it is only an indication of what the antigen binding domain does, rather than what it is. The specification fails to provide any structural features coupled to the claimed functional characteristics. Accordingly, in the absence of sufficient recitation of distinguishing identifying characteristics, the specification does not provide an adequate written description of the claimed genus of proteins that function as claimed.
With regards to variants having up to 5% sequence discrepancy from the sequence, Applicants have not established any reasonable structure-function correlation with regards to the sequences that can be altered and still maintain function. The instant claims attempt to claim every variant of the protein would achieve a desired result, wherein the instant specification does not describe sufficient representative examples to support the full scope of the claims.
Applicants have not established any reasonable structure-function correlation with regards to the sequences that can be altered and maintain function. The instant claims attempt to claim every antigen binding domain that would achieve a desired result, i.e., induce proliferation in a cardiac cell, wherein the instant specification dose not describe representative examples to support the full scope of the claims.
Given the lack of representative examples to support the full scope of the claimed protein, the present claims lack adequate written description. The specification does not provide an adequate written description of the claimed genus of LRRC10 protein that that is required to practice the claimed invention.
Claims 1-3, 5, 6, 9-11, 13, 15, 16, 18, 20-22, and 24-28 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 enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
Claim 1 recites a method of inducing mammalian cardiac cell proliferation, the method comprising ectopically introducing an LRRC10 protein in a mammalian cardiac cell to thereby induce proliferation of the cardiac cell. Claim 3 recites that the LRRC10 protein of claim 1 is at least 95% identical to SEQ ID NO: 1.
The claims read on the use of any LRRC10 protein to function as claimed, and claim 3 is directed to up to 5% variant of LRRC10. It is unclear what the mutations will be, and what can be changed without disrupting the function of LRRC10 and can function as claimed. Thus, the claim is drawn to the use of any LRRC10 protein that is required to function as claimed, and lacks support for enablement.
The instant specification discloses that the LRRC10 protein refers to the wild-type human LRRC10 protein or homologs or variants having an LRRC10 activity. [0037 of published specification] The instant specification also discloses intravenous injection of AAV9-cTnT-LRRC10, AAV9-cTnT-NLS-LRRC10 (which harbors a nuclear localization signal (NLS) to target LRRC10 in the nucleus). [0129 of the published specification] Thus, the specification discloses introducing an LRRC10 protein via an adenovirus vector comprising the full protein. The specification does not provide any examples of any homolog or variant of the LRRC10 protein that retains function as claimed.
A search of the art demonstrates that LRRC10 is a heart-restricted leucine-rich repeat protein and does not contain any predicted transmembrane or catalytic domain part of LRR motif. (see Siri-Angkul et al (Cardiac L-type calcium channel regulation by Leucine-Rich Repeat-Containing Protein 10. Channels (Austin). 2024 Dec;18(1):2355121. doi: 10.1080/19336950.2024.2355121. Epub 2024 May 19, pg 2, section “Discovery of LRRC10”). Siri-Angkul further teaches that almost 60^ of the amino acid residues are devoted to the center of the protein and that many variants are associated with cardiac disease in humans, and that when wild type and a variant LRRC10 are compared, it is demonstrated that the variant can potentially act as a disease modifier. [pg 2-3] Thus, demonstrating that the structure of the LRRC10 protein has functional consequences and variants (or homologs) can have potentially have negative effects on the function of the protein.
It is also well understood in the art that mutations in amino acids can have structural and functional consequences, as taught by Sotomayor-Vivas et al (Linking protein structural and functional change to mutation using amino acid networks. PLoS One. 2022 Jan 21;17(1)). It is impossible to determine which residue(s) can be mutated for another residue, to still have the same effect and function. With regards to specific mutations in LRRC10, Siri-Angkul et al also teaches that variants of LRRC10 have been associated with cardiac diseases. Thus, variants in the protein may not be able to retain function of the LRRC10.
Applicant is reminded that MPEP 2164.03 teaches “the amount of guidance or direction needed to enable the invention is inversely related to the amount of knowledge in the state of the art as well as the predictability of the art. In re Fisher, 428 F.2d 833, 166 USPQ 18, 24 (CCPA 1970) the amount of guidance or direction refers to that information in the application, as originally filed, that teaches exactly how to make or use the invention. The more that is known in the prior art about the nature of the invention, how to make, and how to use the invention, and the more predictable the art is, the less information needs to be explicitly state in the specification. In contrast, if little is known in the prior art about the nature of the invention and the art is unpredictable, the specification would need more detail as how to make and use the invention in order for it to be enabling. Given lack of guidance in the specification, no one skilled in the art would accept the assertion that the claimed invention would function as contemplated or as claimed based only on the information in the specification and that known in the art at the time the invention was made.
The specification provides insufficient guidance with regard to these issues and provides no working examples which would provide guidance to one skilled in the art and no evidence has been provided which would allow one of skill in the art to predict that the invention will function as contemplated or claimed with a reasonable expectation of success. For the above reasons, it appears that undue experimentation would be required to practice the claimed invention
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claim(s) 1, 2, 5, 6, 16, 20, 21, 24 and 28 are rejected under 35 U.S.C. 102(a)(1) and (a)(2) as being anticipated by Wu et al (CN102166346 A1; Published 8/31/2011).
Wu teaches a method of inducing mammalian cardiac cell proliferation comprising ectopically introducing an LRRC10 protein in a mammalian cardiac cell to induce proliferation of the cardiac cell. Wu teaches that LRRC10 is a small molecule and can be used to treat myocardial hypertrophy. [Abstract] Wu teaches that administering a vector that contains the LRRC10 gene into cardiomyocytes. [0007, 0011-0012, 0019] Wu teaches that LRRC10 overexpression significantly inhibited the increase in cardiomyocyte. [0012] Wu teaches that heart disease is a main risk factor that affects human life and that before heart failure, heart patients will experience a process of hypertrophy and hyperplasia, and that the heart specifically expresses LRRC10. [0004]
Regarding claim 5, Wu teaches and demonstrates expressing the LRRC10 protein from a recombinant nucleic acid encoding the LRRC10 protein within the cell. [0059-0060; Example 4] Regarding claims 6 and 28, Wu teaches introducing an LRRC10 protein via exogenous nucleic acid encoding the LRRC10 in the cardiac cell. [0012, 0015-0018] Regarding claim 9, Wu teaches that the cardiac cell is comprised within a heart. [0074] Regarding claim 16, Wu that medicine containing LRRC10 small molecule can inhibit cardiac hypertrophy and can be used for cardiac hypertrophy caused by pathological stimulation, and that when LRRC10 is introduced it allows for improvement in cardiac structure. [0009, 0012] Regarding claims 20-21 and 24, Wu teaches that the cardiac cell is comprised within a subject, and that they suffered from a cardiac event or chronic heart condition, such as myocardial hypertrophy. [Example 5, 0062]
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.
Claim(s) 1, 2, 5, 6, 9-11, 13, 15, 16, 18, 20-22, and 24-28 rejected under 35 U.S.C. 103 as being unpatentable over Wu et al (CN102166346 A1; Published 8/31/2011), in view of Brody et al (2016) (LRRC10 is required to maintain cardiac function in response to pressure overload. Am J Physiol Heart Circ Physiol. 2016 Jan 15;310(2):H269-78).
The teachings of Wu are recited above. However, Wu does not explicitly the limitations of claims 10, 11, 13, 15, 18, 22, and 25-27, wherein the heart comprises a cardiac injury, such as myocardial infarct or a functional defect, such as reduced ejection fraction.
Brody teaches that LRRC10 is required to maintain cardiac function in response to pressure overload. Brody teaches that in LRRC10 knockout mice, there was an increase in dilation and cardiomyopathy, increase in heart weight and pressure overload stimulation. [pg 269, 1st and 2nd column] Brody teaches cardiac hypertrophy can be induced by a number of cardiovascular diseases, such as myocardial infarction. [pg. 269, 2nd column, 2nd paragraph] Brody teaches that LRRC10 knockout mice, these mice had decreased ejection fraction, increased left ventricular internal diameter, compared with wild type mice. [pg H272, 1ST column, 3rd paragraph] Brody teaches that pressure overload occurs in response to cardiovascular diseases, including hypertension, and when prolonged, becomes maladaptive and can progress to heart failure. Brody demonstrates that LRRC10 is important for the response of the heart to mechanical stress and pressure overload hypertrophy. [pg H275, 2nd column Discussion]
It is noted that claim 10 requires the heart comprises a cardiac injury, claims 11 and 12 require that the cardiac injury is a myocardial lesion, such as myocardial infarct or increased left ventricular internal diameters, or a functional defect, such as reduced ejection fraction, respectively. One of skilled in the art could have pursued applying the method of Wu wherein the heart comprises a cardiac injury (myocardial lesion or functional defect), because: (1) Wu teaches a method of inducing mammalian cardiac cell proliferation comprising ectopically introducing an LRRC10 protein in a mammalian cardiac cell to induce proliferation of the cardiac cell, (2), Wu that medicine containing LRRC10 small molecule can inhibit cardiac hypertrophy and can be used for cardiac hypertrophy caused by pathological stimulation, and that when LRRC10 is introduced it allows for improvement in cardiac structure, (3) Wu teaches that the cardiac cell is comprised within a subject, and that they suffered from a cardiac event or chronic heart condition, such as myocardial hypertrophy, (4) Brody teaches that LRRC10 is required to maintain cardiac function in response to pressure overload and in LRRC10 knockout mice, there was an increase in dilation and cardiomyopathy, increase in heart weight and pressure overload stimulation, (3) Brody teaches cardiac hypertrophy can be induced by a number of cardiovascular diseases, such as myocardial infarction, and (4) Brody teaches that LRRC10 knockout mice, these mice had decreased ejection fraction, increased left ventricular internal diameter, compared with wild type mice. Thus, given the known role of LRRC10 in cardiac remodeling and proliferation, especially after cardiac events and injury, and given the known method of administering an LRRC10 to a subject to improve cardiac remodeling, one of skilled in the art could have pursued introducing an LRRC10 protein in a cardiac cell after a cardiac injury or event, with a reasonable expectation of success.
Claim(s) 1-3, 5, 6, 16, 20, 21, 24 and 28 are is rejected under 35 U.S.C. 103 as being unpatentable over Wu et al (CN102166346 A1; Published 8/31/2011), Brody et al (2016) (LRRC10 is required to maintain cardiac function in response to pressure overload. Am J Physiol Heart Circ Physiol. 2016 Jan 15;310(2):H269-78), as applied to claims 1, 2, 5, 6, 9-11, 13, 15, 16, 18, 20-22, and 24-28 above, and further in view of Ota et al. (Complete sequencing and characterization of 21,243 full-length human cDNAs. Nat Genet 36, 40–45, 2004).
The teachings of Wu are recited above. However, the art does not explicitly teach that the LRRC10 protein is at least 95% identical to SEQ ID NO: 1.
Ota et al teaches the complete sequences of full length human CDNAs, and teaches the full sequence of the human LRRC10 protein, which is 100% identical to the instantly claimed SEQ ID NO: 1. Ota teaches this protein plays an important role inc ariac development and/or cardiac function. Please see sequence alignment and information below.
It is noted that claim 3 requires that the LRRC10 protein is at least 95% identical to SEQ ID NO: 1. This limitation would have been obvious to those of ordinary skill in the art because: (1) Wu teaches a method of inducing mammalian cardiac cell proliferation comprising ectopically introducing LRRC10 protein in a mammalian cardiac cell to induce proliferation of the cardiac cell, (2) Wu demonstrates that administering a medicine containing the LRRC10 protein allows for improvement in cardiac structure, and (2) Ota teaches the full sequence of the LRRC10 protein. Given the known function of LRRC10 protein in cardiac development, and given the known fact that introducing the full length of LRRC10 protein results in improved cardiac function and structure, one of skilled in the art could have pursued introducing the full length of LRRC10 protein comprising SEQ ID NO: 1 to function as claimed, with a reasonable expectation of success.
SEQUENCE ALIGNMENT: SEQ ID NO: 3
RESULT 1
LRC10_HUMAN
ID LRC10_HUMAN Reviewed; 277 AA.
AC Q5BKY1; Q6ZVY4;
DT 27-SEP-2005, integrated into UniProtKB/Swiss-Prot.
DT 12-APR-2005, sequence version 1.
DT 28-JAN-2026, entry version 149.
DE RecName: Full=Leucine-rich repeat-containing protein 10;
GN Name=LRRC10;
OS Homo sapiens (Human).
OC Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia;
OC Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae;
OC Homo.
OX NCBI_TaxID=9606;
RN [1]
RP NUCLEOTIDE SEQUENCE [LARGE SCALE MRNA].
RC TISSUE=Pericardium;
RX PubMed=14702039; DOI=10.1038/ng1285;
RA Ota T., Suzuki Y., Nishikawa T., Otsuki T., Sugiyama T., Irie R.,
RA Wakamatsu A., Hayashi K., Sato H., Nagai K., Kimura K., Makita H.,
RA Sekine M., Obayashi M., Nishi T., Shibahara T., Tanaka T., Ishii S.,
RA Yamamoto J., Saito K., Kawai Y., Isono Y., Nakamura Y., Nagahari K.,
RA Murakami K., Yasuda T., Iwayanagi T., Wagatsuma M., Shiratori A., Sudo H.,
RA Hosoiri T., Kaku Y., Kodaira H., Kondo H., Sugawara M., Takahashi M.,
RA Kanda K., Yokoi T., Furuya T., Kikkawa E., Omura Y., Abe K., Kamihara K.,
RA Katsuta N., Sato K., Tanikawa M., Yamazaki M., Ninomiya K., Ishibashi T.,
RA Yamashita H., Murakawa K., Fujimori K., Tanai H., Kimata M., Watanabe M.,
RA Hiraoka S., Chiba Y., Ishida S., Ono Y., Takiguchi S., Watanabe S.,
RA Yosida M., Hotuta T., Kusano J., Kanehori K., Takahashi-Fujii A., Hara H.,
RA Tanase T.-O., Nomura Y., Togiya S., Komai F., Hara R., Takeuchi K.,
RA Arita M., Imose N., Musashino K., Yuuki H., Oshima A., Sasaki N.,
RA Aotsuka S., Yoshikawa Y., Matsunawa H., Ichihara T., Shiohata N., Sano S.,
RA Moriya S., Momiyama H., Satoh N., Takami S., Terashima Y., Suzuki O.,
RA Nakagawa S., Senoh A., Mizoguchi H., Goto Y., Shimizu F., Wakebe H.,
RA Hishigaki H., Watanabe T., Sugiyama A., Takemoto M., Kawakami B.,
RA Yamazaki M., Watanabe K., Kumagai A., Itakura S., Fukuzumi Y., Fujimori Y.,
RA Komiyama M., Tashiro H., Tanigami A., Fujiwara T., Ono T., Yamada K.,
RA Fujii Y., Ozaki K., Hirao M., Ohmori Y., Kawabata A., Hikiji T.,
RA Kobatake N., Inagaki H., Ikema Y., Okamoto S., Okitani R., Kawakami T.,
RA Noguchi S., Itoh T., Shigeta K., Senba T., Matsumura K., Nakajima Y.,
RA Mizuno T., Morinaga M., Sasaki M., Togashi T., Oyama M., Hata H.,
RA Watanabe M., Komatsu T., Mizushima-Sugano J., Satoh T., Shirai Y.,
RA Takahashi Y., Nakagawa K., Okumura K., Nagase T., Nomura N., Kikuchi H.,
RA Masuho Y., Yamashita R., Nakai K., Yada T., Nakamura Y., Ohara O.,
RA Isogai T., Sugano S.;
RT "Complete sequencing and characterization of 21,243 full-length human
RT cDNAs.";
RL Nat. Genet. 36:40-45(2004).
RN [2]
RP NUCLEOTIDE SEQUENCE [LARGE SCALE MRNA].
RC TISSUE=Heart;
RX PubMed=15489334; DOI=10.1101/gr.2596504;
RG The MGC Project Team;
RT "The status, quality, and expansion of the NIH full-length cDNA project:
RT the Mammalian Gene Collection (MGC).";
RL Genome Res. 14:2121-2127(2004).
CC -!- FUNCTION: May play important roles in cardiac development and/or
CC cardiac function. {ECO:0000250}.
CC -!- SUBCELLULAR LOCATION: Nucleus {ECO:0000250}.
CC -!- SEQUENCE CAUTION:
CC Sequence=BAC85724.1; Type=Erroneous initiation; Evidence={ECO:0000305};
CC ---------------------------------------------------------------------------
CC Copyrighted by the UniProt Consortium, see
SQ SEQUENCE 277 AA; 31642 MW; 95F326D838980589 CRC64;
Query Match 100.0%; Score 1448; Length 277;
Best Local Similarity 100.0%;
Matches 277; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 MGNTIRALVAFIPADRCQNYVVRDLREMPLDKMVDLSGSQLRRFPLHVCSFRELVKLYLS 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 MGNTIRALVAFIPADRCQNYVVRDLREMPLDKMVDLSGSQLRRFPLHVCSFRELVKLYLS 60
Qy 61 DNHLNSLPPELGQLQNLQILALDFNNFKALPQVVCTLKQLCILYLGNNKLCDLPSELSLL 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 DNHLNSLPPELGQLQNLQILALDFNNFKALPQVVCTLKQLCILYLGNNKLCDLPSELSLL 120
Qy 121 QNLRTLWIEANCLTQLPDVVCELSLLKTLHAGSNALRLLPGQLRRLQELRTIWLSGNRLT 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 QNLRTLWIEANCLTQLPDVVCELSLLKTLHAGSNALRLLPGQLRRLQELRTIWLSGNRLT 180
Qy 181 DFPTVLLHMPFLEVIDVDWNSIRYFPSLAHLSSLKLVIYDHNPCRNAPKVAKGVRRVGRW 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 DFPTVLLHMPFLEVIDVDWNSIRYFPSLAHLSSLKLVIYDHNPCRNAPKVAKGVRRVGRW 240
Qy 241 AEETPEPDPRKARRYALVREESQELQAPVPLLPPTNS 277
|||||||||||||||||||||||||||||||||||||
Db 241 AEETPEPDPRKARRYALVREESQELQAPVPLLPPTNS 277
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SARAH A ALSOMAIRY whose telephone number is (571)272-0027. The examiner can normally be reached Monday-Friday 7:30 AM to 5:30 PM.
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/SARAH A ALSOMAIRY/ Examiner, Art Unit 1646
/Zachariah Lucas/ Supervisory Patent Examiner, Art Unit 1600
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