DETAILED ACTION
Claims 1-16 are pending and under examination in the instant application.
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 .
Information Disclosure Statement
The information disclosure statement filed on 01/05/2024 fails to comply with 37 CFR 1.98(a)(2), which requires a legible copy of each cited foreign patent document; each non-patent literature publication or that portion which caused it to be listed; and all other information or that portion which caused it to be listed. It has been placed in the application file, but the information referred to therein has not been considered. In this case, there is no copy of the cited non-patent literature A3 (ESCOUBAS et al., "Deregulation of CRTCs in Aging and Age-Related Disease Risk," Trends in Genetics, 2017, Volume 33, Issue 5, pp 303-321).
Also, the listing of references in the specification is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered.
Claim Objections
Claim 5 is objected to because of the following informalities:
Claim 5 recites “expression or activity of amphiregulin gene or protein is decreased in the brain as compared with a wild-type animal”. An article should be added.
Appropriate correction is required.
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) 1-4, 6-7, and 11-13 is/are rejected under 35 U.S.C. 102(a)(1) and 102(a)(2) as being anticipated by Yong et al. (KR20170036929A, filed on 09/24/2015, and published on 04/04/2017. Citations are from the English translation of KR20170036929A).
Regarding claim 1, Yong et al. teaches an animal model, in which expression or activity of CREB-regulated transcription coactivator 3 (CRTC3) gene or protein is suppressed (Abstract and claim 6 of Yong et al.).
Although Yong et al. does not specifically teach that the animal model lacks social dominance, since the structure of the claimed animal model in which expression or activity of CRTC3 gene or protein is suppressed
and the structure of the CRTC3-deficient animal model taught by Yong et al. are the same, the claimed property of lacking social dominance is inherently and necessarily present in Yong et al. Accordingly, the mere recitation of its presence in the instant claims is not sufficient to distinguish the instant claims from prior art. “When the structure recited in the reference is substantially identical to that of the claims, claimed properties or functions are presumed to be inherent.” See MPEP 2112.01 or In re Best, 195 USPQ 430, 433 (CCPA 1997).
Regarding claim 2: Following discussion of claim 1, Yong et al. teaches that the expression or activity of CRTC3 gene or protein is specifically suppressed in the brain (page 4, Example 2: CRTC3 Identification of brain tissue changes due to deficiency. 2. Identification of astrocyte activity by immunohistochemical staining).
Regarding claim 3: Following discussion of claim 1, Yong et al. teaches that the expression or activity of CRTC3 gene or protein is specifically suppressed in astrocytes of the brain (Fig. 2, page 4, Example 2: CRTC3 Identification of brain tissue changes due to deficiency. 2. Identification of astrocyte activity by immunohistochemical staining).
Regarding claim 4: Following discussion of claim 1, Yong et al. teaches that the CRTC3 gene is knocked out (page 4, Example 2: CRTC3 Identification of brain tissue changes due to deficiency. 2. Identification of astrocyte activity by immunohistochemical staining).
Regarding claim 6: Following discussion of claim 1, Yong et al. does not specifically teach that the animal model shows no changes in memory-related behavior, sensory-related behavior, or both as compared with a wild-type animal. However, since the structure of the claimed animal model in which expression or activity of CRTC3 gene or protein is suppressed and the structure of the CRTC3-deficient animal model taught by Yong et al. are the same, the claimed functional property of showing no changes in memory-related behavior, sensory-related behavior, or both as compared with a wild-type animal is inherently and necessarily present in Yong et al. Accordingly, the mere recitation of its presence in the instant claims is not sufficient to distinguish the instant claims from prior art. “When the structure recited in the reference is substantially identical to that of the claims, claimed properties or functions are presumed to be inherent.” See MPEP 2112.01 or In re Best, 195 USPQ 430, 433 (CCPA 1997).
Regarding claim 7: Following discussion of claim 1, Yong et al. does not specifically teach that the animal model has decreased functional connectivity between prefrontal cortex and parietal cortex in the brain as compared with a wild-type animal. However, since the structure of the claimed animal model in which expression or activity of CRTC3 gene or protein is suppressed and the structure of the CRTC3-deficient animal model taught by Yong et al. are the same, the claimed functional property of decreased functional connectivity between prefrontal cortex and parietal cortex in the brain as compared with a wild-type animal is inherently and necessarily present in Yong et al. Accordingly, the mere recitation of its presence in the instant claims is not sufficient to distinguish the instant claims from prior art. “When the structure recited in the reference is substantially identical to that of the claims, claimed properties or functions are presumed to be inherent.” See MPEP 2112.01 or In re Best, 195 USPQ 430, 433 (CCPA 1997).
Regarding claim 11: Following discussion of claim 1, Yong et al. teaches that the animal is mouse (page 3. Example 1: In patients with Alzheimer's dementia Of CRTC3 Identify expression levels).
Regarding claim 12, Yong et al. teaches a method of producing an animal model, comprising suppressing expression or activity of CREB-regulated transcription coactivator 3 (CRTC3) gene or protein (page 4, Example 2: CRTC3 Identification of brain tissue changes due to deficiency. 2. Identification of astrocyte activity by immunohistochemical staining).
Yong et al. does not specifically teach that a method of producing an animal model lacking social dominance. However, since the steps of the claimed method of suppressing expression or activity of CREB-regulated transcription coactivator 3 (CRTC3) gene or protein and the method steps taught by Yong et al. are the same, the claimed functional property of the claimed animal model lacking social dominance is inherently and necessarily present in Yong et al. Accordingly, the mere recitation of its presence in the instant claims is not sufficient to distinguish the instant claims from prior art. “When the prior art method is the same as a method described in the specification for carrying out the claimed method, it can be assumed the method will inherently perform the claimed process. See In re Best, 562 F. 2d, 1252, 1255, 195 USPQ 430, 433 (CCPA 1977) and Ex parte Novitski, 26 USPQ 2d 1389 (Bd. Pat. App. & inter. 1993). There is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the time of the invention, but only that the subject matter is in fact inherent in the prior art reference. See Schering Corp. v. Geneva Pharm. Inc, 339 F.3d 1373, 1377, 67, USPQ2d 1664, 1668 (Fed. Cir. 2003). See also Toro Co. v. Deere & Co. 355 F.3d 1313, 1320, 69 USPQ2d 1584, 1590 (Fed. Cir. 2004) See MPEP 2112.02.
Regarding claim 13: Following discussion of claim 1, Yong et al. teaches that the suppressing comprises knocking out the CRTC3 gene (page 4, Example 2: CRTC3 Identification of brain tissue changes due to deficiency. 2. Identification of astrocyte activity by immunohistochemical staining).
Claim(s) 1 and 5 are rejected under 35 U.S.C. 102(a)(1) and 102(a)(2) as being anticipated by Yong et al. (KR20170036929A, filed on 09/24/2015, and published on 04/04/2017. Citations are from the English translation of KR20170036929A), as evidenced by Xu et al. (Xu et al., “Individual CREB-target genes dictate usage of distinct cAMP-responsive coactivation mechanisms”. EMBO J. 2007 Jun 20;26(12):2890-903).
Regarding claim 1, the teachings of Yong et al. are set forth in detail above.
Regarding claim 5: Following discussion of claim 1, Yong et al. does not specifically teach that expression or activity of amphiregulin gene or protein is decreased in the brain as compared with a wild-type animal of the animal model. However, Xu et al. provides evidence that amphiregulin is a direct target gene of the cAMP response element-binding protein (CREB), such as CRTC3 (CREB-regulated transcription coactivator 3 (See Table 1 and page 2891, column 2, paragraph 2). Also, since the structure of the claimed animal model in which expression or activity of CRTC3 gene or protein is suppressed and the structure of the CRTC3-deficient animal model taught by Yong et al. are the same, the claimed functional property of decreasing expression or activity of amphiregulin gene or protein in the animal’s brain is inherently and necessarily present in Yong et al. Accordingly, the mere recitation of its presence in the instant claims is not sufficient to distinguish the instant claims from prior art. “When the structure recited in the reference is substantially identical to that of the claims, claimed properties or functions are presumed to be inherent.” See MPEP 2112.01 or In re Best, 195 USPQ 430, 433 (CCPA 1997).
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, 8-10, and 14-16 is/are rejected under 35 U.S.C. 103 as being unpatentable over Yong et al. (KR20170036929A, filed on 09/24/2015, and published on 04/04/2017. Citations are from the English translation of KR20170036929A), in view of Won et al. (KR20190125098A, filed on 04/27/2018, and published on 11/06/2019. Citations are from the English translation of KR20190125098A).
Regarding claim 1, the teachings of Yong et al. are set forth in detail above.
Regarding claim 8: Following discussion of claim 1, Yong et al. fails to teach that the animal model is a model for a disease related to lack or reduction of social dominance.
However, Won et al. teaches an animal model lacking social dominance that can be used to screen for a therapeutic agent for a mental illness and administering a candidate drug for treatment of the psychiatric disease to the animal model lacking social dominance and determining whether social dominance of the animal model is improved (page 2, paragraph 9 and page 3, paragraph 8).
Therefore, it would have been prima facie obvious to one of the ordinary skills in the art before the effective filing date of the claimed invention to have used the animal model of Yong et al. for a mental disorder, such as a disease related to lack or reduction of social dominance with a reasonable expectation of success. One would have been motivated to have done so in order to identify whether social dominance of the animal model is improved and the symptoms are alleviated as taught by Won et al.
Regarding claims 9-10: Following discussion of claim 8, Won et al. teaches that the disease is autism spectrum disorder (ASD), social anxiety disorder (SAD), Schizophrenia, and Major depressive disorder (MDD) (page 1, last 2 lines).
Regarding claim 14: Following discussion of claim 1, Yong et al. teaches in the abstract a method for screening a pharmaceutical composition for treating a cranial nerve disease by providing a pharmaceutical composition for treating a disease and confirming the promotion or activity level of CRTC3 expression can be provided, but fails to teach that the method for screening a therapeutic agent is for a psychiatric disease and comprises administering a candidate drug for treatment of a psychiatric disease to the animal model lacking social dominance and determining whether social dominance of the animal model is improved.
However, Won et al. teaches a screening method of a psychological disorder therapeutic agent, comprising the step of identifying whether the symptoms of the mental disorders are alleviated by for example, a social dominance tube test, wherein a candidate drug is administered to an animal model lacking social dominance to alleviate the symptoms of mental illness (page 2, paragraph 9 and page 3, paragraph 8).
Therefore, it would have been prima facie obvious to one of the ordinary skills in the art before the effective filing date of the claimed invention to have administered a candidate drug to the animal model lacking social dominance of Yong et al. to alleviate the symptoms of the psychiatric disorder with a reasonable expectation of success. One would have been motivated to have done so in order to identify whether the symptoms of the psychiatric disorder are alleviated and whether social dominance of the animal model is improved.
Regarding claim 15: Following discussion of claim 14, Won et al. further teaches that the psychiatric disease is accompanied by symptoms of lack or reduction of social dominance (page 2, paragraph 11).
Regarding claim 16: Following discussion of claim 14, Won et al. further teaches that the determining is performed by a behavioral test for evaluating social dominance or electroencephalogram (EEG) analysis (page 3, paragraph 8).
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to HANAN ISAM ABUZEINEH whose telephone number is (571)272-9596. The examiner can normally be reached Mon- Fri 8:30-5:00.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, CHRISTOPHER BABIC can be reached at (571)272-8507. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
Hanan Isam Abuzeineh
/H.I.A./Examiner, Art Unit 1633
/CHRISTOPHER M BABIC/Supervisory Patent Examiner, Art Unit 1633