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 .
Nucleotide and/or Amino Acid Sequence Disclosures
REQUIREMENTS FOR PATENT APPLICATIONS CONTAINING NUCLEOTIDE AND/OR AMINO ACID SEQUENCE DISCLOSURES
Items 1) and 2) provide general guidance related to requirements for sequence disclosures.
37 CFR 1.821(c) requires that patent applications which contain disclosures of nucleotide and/or amino acid sequences that fall within the definitions of 37 CFR 1.821(a) must contain a "Sequence Listing," as a separate part of the disclosure, which presents the nucleotide and/or amino acid sequences and associated information using the symbols and format in accordance with the requirements of 37 CFR 1.821 - 1.825. This "Sequence Listing" part of the disclosure may be submitted:
In accordance with 37 CFR 1.821(c)(1) via the USPTO patent electronic filing system (see Section I.1 of the Legal Framework for Patent Electronic System (https://www.uspto.gov/PatentLegalFramework), hereinafter "Legal Framework") as an ASCII text file, together with an incorporation-by-reference of the material in the ASCII text file in a separate paragraph of the specification as required by 37 CFR 1.823(b)(1) identifying:
the name of the ASCII text file;
ii) the date of creation; and
iii) the size of the ASCII text file in bytes;
In accordance with 37 CFR 1.821(c)(1) on read-only optical disc(s) as permitted by 37 CFR 1.52(e)(1)(ii), labeled according to 37 CFR 1.52(e)(5), with an incorporation-by-reference of the material in the ASCII text file according to 37 CFR 1.52(e)(8) and 37 CFR 1.823(b)(1) in a separate paragraph of the specification identifying:
the name of the ASCII text file;
the date of creation; and
the size of the ASCII text file in bytes;
In accordance with 37 CFR 1.821(c)(2) via the USPTO patent electronic filing system as a PDF file (not recommended); or
In accordance with 37 CFR 1.821(c)(3) on physical sheets of paper (not recommended).
When a “Sequence Listing” has been submitted as a PDF file as in 1(c) above (37 CFR 1.821(c)(2)) or on physical sheets of paper as in 1(d) above (37 CFR 1.821(c)(3)), 37 CFR 1.821(e)(1) requires a computer readable form (CRF) of the “Sequence Listing” in accordance with the requirements of 37 CFR 1.824.
If the "Sequence Listing" required by 37 CFR 1.821(c) is filed via the USPTO patent electronic filing system as a PDF, then 37 CFR 1.821(e)(1)(ii) or 1.821(e)(2)(ii) requires submission of a statement that the "Sequence Listing" content of the PDF copy and the CRF copy (the ASCII text file copy) are identical.
If the "Sequence Listing" required by 37 CFR 1.821(c) is filed on paper or read-only optical disc, then 37 CFR 1.821(e)(1)(ii) or 1.821(e)(2)(ii) requires submission of a statement that the "Sequence Listing" content of the paper or read-only optical disc copy and the CRF are identical.
Specific deficiencies and the required response to this Office Action are as follows:
Specific deficiency – Nucleotide and/or amino acid sequences appearing in the specification are not identified by sequence identifiers in accordance with 37 CFR 1.821(d). Specifically, no sequence identification has been provided for the sequences presented on p. 40, lines 23 and 34 of the instant specification.
Required response – Applicant must provide:
A substitute specification in compliance with 37 CFR 1.52, 1.121(b)(3) and 1.125 inserting the required sequence identifiers, consisting of:
A copy of the previously-submitted specification, with deletions shown with strikethrough or brackets and insertions shown with underlining (marked-up version);
A copy of the amended specification without markings (clean version); and
A statement that the substitute specification contains no new matter.
Specific deficiency – Nucleotide and/or amino acid sequences appearing in the drawings are not identified by sequence identifiers in accordance with 37 CFR 1.821(d). Sequence identifiers for nucleotide and/or amino acid sequences must appear either in the drawings or in the Brief Description of the Drawings. Specifically, no sequence identification has been provided for the sequences presented in Figures 1, 3 and 5 of the instant specification.
Required response – Applicant must provide:
Replacement and annotated drawings in accordance with 37 CFR 1.121(d) inserting the required sequence identifiers;
AND/OR
A substitute specification in compliance with 37 CFR 1.52, 1.121(b)(3) and 1.125 inserting the required sequence identifiers into the Brief Description of the Drawings, consisting of:
A copy of the previously-submitted specification, with deletions shown with strikethrough or brackets and insertions shown with underlining (marked-up version);
A copy of the amended specification without markings (clean version); and
A statement that the substitute specification contains no new matter.
DETAILED ACTION
Status of Application/Election/Restrictions
Applicant’s election without traverse of SEQ ID NO:12 for species of VH, SEQ ID NO:13 for species of VL, cognitive dysfunction with Parkinson’s disease (PDD) for species of tauopathy or dementia-related disease, therapeutic drug for PD for species of therapeutic drug, levodopa for species of therapeutic drug of PD in the reply filed on September 9, 2025 is acknowledged.
Claims 1-27, 58, 75 and 86-136 are canceled. Claims 28-39, 41-57, 59-74, and 76-85 are pending in this application. Claims 80-83 and 85 are withdrawn without traverse (filed 09/09/2025) from further consideration pursuant to 37 CFR 1.142(b) as being drawn to nonelected inventions, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on September 9, 2025.
Claims 28-39, 41-57, 59-74, 76-79 and 84 are under examination with respect to SEQ ID NO:12 for VH, SEQ ID NO:13 for VL, cognitive dysfunction with Parkinson’s disease (PDD) for tauopathy or dementia-related disease, therapeutic drug for PD for therapeutic drug and levodopa for therapeutic drug of PD in this office action.
Drawings
The drawings/figures 1, 3 and 5 are objected to because sequence listings included in the specification must not be duplicated in the drawings. See 37 C.F.R. §1.58(a) and §1.83(a). Appropriate correction is required.
See MPEP § 608.02-I ([E9_R-11]) Drawing requirements
If the specification includes a sequence listing or a table, such a sequence listing or table is not permitted to be reprinted in the drawings. 37 CFR 1.83(a) and 1.58(a). If a sequence listing as shown in the drawings has more information than is otherwise contained in the specification, the sequence listing could be included in the specification and the drawings. Applications filed under 35 U.S.C. 371 are excluded from the prohibition from having the same tables and sequence listings in both the description portion of the specification and drawings.
Claim Objections
Claim 84 is objected to because of the following informalities: the recitations “EPI-589, NXN-462, Ferriprox, GM608, OXB-101, NTCELL, Ibiglustat, ENT-01, RG7935, and BIIB054” recited in claim 84 are not unique or common abbreviations in the art. Applicants are required to spell out “EPI-589, NXN-462, Ferriprox, GM608, OXB-101, NTCELL, Ibiglustat, ENT-01, RG7935, and BIIB054” at the first usage. Appropriate correction is required.
Improper Markush Grouping
7. Claims 41-43, 57, 59-60, 74, and 76-77 are rejected on the basis that it contains an improper Markush grouping of alternatives. See In re Harnisch, 631 F.2d 716, 721-22 (CCPA 1980) and Ex parte Hozumi, 3 USPQ2d 1059, 1060 (Bd. Pat. App. & Int. 1984). A Markush grouping is proper if the alternatives defined by the Markush group (i.e., alternatives from which a selection is to be made in the context of a combination or process, or alternative chemical compounds as a whole) share a “single structural similarity” and a common use. A Markush grouping meets these requirements in two situations. First, a Markush grouping is proper if the alternatives are all members of the same recognized physical or chemical class or the same art-recognized class, and are disclosed in the specification or known in the art to be functionally equivalent and have a common use. Second, where a Markush grouping describes alternative chemical compounds, whether by words or chemical formulas, and the alternatives do not belong to a recognized class as set forth above, the members of the Markush grouping may be considered to share a “single structural similarity” and common use where the alternatives share both a substantial structural feature and a common use that flows from the substantial structural feature. See MPEP § 706.03(y).
The Markush grouping of different antibodies recognizing SEQ ID NO:2 comprising different SEQ ID NOs: for VH and VL of the antibody is improper because the alternatives defined by the Markush grouping do not share both a single structural similarity and a common use for the following reasons:
The recited alternative species do not share a single structural similarity, as each species of antibodies has a different chemical structure because it comprises different amino acid sequences for a VH and a VL of the antibody, which has a different binding activity to different epitopes. Thus, the antibodies do not share a single structural similarity or biological activity. See MPEP § 706.03(y).
To overcome this rejection, Applicant may set forth each alternative (or grouping of patentably indistinct alternatives) within an improper Markush grouping in a series of independent or dependent claims and/or present convincing arguments that the group members recited in the alternative within a single claim in fact share a single structural similarity as well as a common use.
Claim Rejections - 35 USC § 101
8. 35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claims 28-39, 41-57, 59-74, 76-79 and 84 are rejected under 35 U.S.C. 101 because the claimed invention is directed to a judicial exception (i.e., a law of nature, a natural phenomenon, or an abstract idea) without significantly more. The claim(s) recite(s) determining whether a test animal is affected with tauopathy or a dementia-related disease including Parkinson’s disease (PD) at present or maybe affected in the future based on different expression levels of a polypeptide consisting of SEQ ID NO:1 detected in the sample of the test animal and a correlation between the presence of a polypeptide consisting of SEQ ID NO:1 or variant thereof in the test animal” sample as compared to a control level and the presence of tauopathy or a dementia-related disease or PD in patients. This correlation is a consequence of natural phenomenon in the sample of the animals including humans having tauopathy or a dementia-related disease excluding Alzheimer’s disease or PD, which is a judicial exception. The instant claims claim determining a test subject having or at risk of developing tauopathy or a dementia-related disease (excluding AD) or PD based on a correlation between the presence of an increased level of the polypeptide of SEQ ID NO:2 or variant thereof in the test animal’s sample as compared to a control level and the presence of a tauopathy or a dementia-related disease or PD in patients, which is similar to the claims that were directed to a discovery of a law of nature by the Supreme Court in Mayo Collaborative Servs. v. Prometheus Labs. Inc., 566 U.S. 66, 101 USPQ2d 1961 (2012) and Cleveland Clinic Foundation v. True Health Diagnostics, LLC, 859 F.3d 1352, 1361, 123 USPQ2d 1081, 1087 (Fed. Cir. 2017) (Step 2A Prong 1: YES).
This judicial exception is not integrated into a practical application because the invention provides no improvement to any other technology or technical field (see MPEP 2106.05(a)) or transform into a different technology (see MPEP 2106.05(b)-(c)), does not apply or use a judicial exception to effect a particular treatment or prophylaxis for a disease or medical condition (see Vanda Memo) and does not apply or use the judicial exception in some other meaningful way beyond generally linking the use of the judicial exception to a particular technological environment, such that the claim as a whole is more than a drafting effort designed to monopolize the exception (see MPEP 2106.05(e) and Vanda Memo). The claims 28-39, 41-57 and 59-61 do not contain the treating step. The claims 62-74 and 76-85 do not necessarily contain the treating step because the limitation “(iii) administering…a therapeutic or prophylactic drug…when the amount of the polypeptide…is higher than the control” is a contingent limitation and only required or exists under a condition that the test animal/patient has been identified as having or at risk of developing tauopathy or a dementia-related disease or PD based on an increased level of the claimed polypeptide of SEQ ID NO:1 or variant thereof in the test animal’s/patient’s sample higher than the control. Even if the step of administering is required, the treatment is not specific and the use of a therapeutic or prophylactic drug for tauopathy or a dementia-related disease or the use of Levodopa for PD is purely conventional or routine practice in the field as evidenced by xx. Thus, the invention does not apply or integrate a judicial exception into a practical application such as a particular treatment or prophylaxis for a disease or medical condition (see Vanda Memo) and in some other meaningful way beyond generally linking the use of the judicial exception to a particular technological environment, such that the claim as a whole is more than a drafting effort designed to monopolize the exception (see MPEP 2106.05(e) and Vanda Memo) (Step 2A Prong 2: NO).
The claim(s) does/do not include additional elements that are sufficient to amount to significantly more than the judicial exception because the claims recite elements/steps in addition to the judicial exception(s) that are well-understood, purely conventional or routine in the relevant field, the elements/steps recited in the claims in addition to the judicial exception(s) that are insignificant extra-solution activity, e.g., are merely appended to the judicial exception(s) and amount to nothing more than a mere field of use.
The additional elements “detecting a polypeptide consisting of SEQ ID NO:1 or variant” “quantifying the polypeptide in a sample..” in independent claim 28, 45 and 62 and claims 37, 54 , 71, the additional elements “human” in claims 34, 51, 68, “different samples including blood, CSF, saliva, lacrimal fluid or urine” in claims 35, 52, 69, the additional elements “detecting other diagnosis markers” in claims 36, 70, “detected using an antibody” in claims 38, 55 and 72 are insignificant extra-solution activities for collecting data and are merely appended to the judicial exception(s) and amount to nothing more than mere field of use view of MPEP 2106.05(d)-(h) and Cleveland Clinic Foundation v. True Health Diagnostics, LLC, 859 F.3d 1352, 1355, 1362, 123 USPQ2d 1081, 1082-83, 1088 (Fed. Cir. 2017).
The addition elements “(i)… quantifying….(ii)… comparing the amount ….with the amount….from a healthy animal…’, and (iii)… determining based on the results of (ii)….when the amount of …(i) is higher than the control” in claims 29, 46-47, 50 and 63, and the additional elements “quantified in (i) is not less than 1.1 times of the control value” or “higher than the cultoff value” “45-85 units or 45-85ng/ml” in claims 30-33, 48-49 and 64-67 are mental steps, which is a judicial exception.
The additional elements “the antibody further recognizes the polypeptide of SEQ ID NO:2”in claims 56 and 73, and “the antibody has a heavy chain variable region….at least 90% homology with… SEQ ID NO:12…..and a light chain variable region….at least 90% homology with ….SEQ ID NO:13” and “(5) an antibody comprising the VH of SEQ ID NO:12 and the VL of SEQ ID NO:13” in claims 41-43, 57, 59-60, 74 and 76-77 are well known and routine practice in the art to detect the polypeptide of SEQ ID NO:1 or SEQ ID NO:2 and has been used for diagnosing Alzheimer’s disease (AD) as evidenced by Hashimoto (US10393757, issued Aug 27, 2019, priority Dec 28, 2010; see abstract; col. 6-19, Examples 1-4, claims 1-2, in particular) and Ono et al. (US12000844, issued Jun 4, 2024, priority Aug 7, 2018; see claims 1-17).
The combination of the judicial exception with additional elements is insufficient to ensure that the claims amount to significantly more than the exception itself because these additional elements or steps are mere field of use that impose no meaningful limit on the performance of the method and are no more than well-understood, purely conventional, and routinely taken by others in order to apply the natural principle (Step2B: NO).
Thus, claims 28-39, 41-57, 59-74, 76-79 and 84 are not patent eligible because the claimed invention of claims 28-39, 41-57, 59-74, 76-79 and 84 is directed to a judicial exception (i.e., a law of nature, a natural phenomenon, or an abstract idea) without significantly more.
Claim Rejections - 35 USC § 112
9. The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 28-39, 41-57, 59-74, 76-79 and 84 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor, or for pre-AIA the applicant regards as the invention.
Claims 28-39, 41-57, 59-74, 76-79 and 84 are indefinite because:
i. Claims 28, 34-39, 41-45, 50-57, 59-62, 68-74, 76-79 and 84 are incomplete for omitting essential elements/steps, such omission amounting to a gap between the steps. See MPEP § 2172.01. The omitted elements/steps are: steps of quantifying, comparing and determining, and specific elements including specific controls for comparison and specific parameters/criteria used for comparing and determining the presence or the susceptibility of tauopathy or a dementia-related disease, which are essential and required by the claimed method in view of p. 62-66 and p. 91-93 of the instant specification.
Based on p. 62-66 and p. 91-93 of the instant specification, the following steps are required by the claimed method in order to determine the presence or susceptibility of the disease, including the step of quantifying the amount of S38AA in the test subject, the step of comparing the amount of S38AA in the test subject with the amount of S38AA in a “healthy control” and the step of determining based on a criteria: an “increased” level of S38AA in the test subject when compared to the level of S38AA in the healthy control is indicative of the presence of the disease.
However, the instant claims only recite a single step of detecting the claimed polypeptide of SEQ ID NO:1 or variant thereof in a sample, and do not recite or include the steps set forth above, or any steps or elements related to how to determine, such as steps of measuring or quantifying, comparing with a specific control or value, and determining the presence or susceptibility of the disease based on a specific amount or a specific comparison, such as an increased or decreased amount of the claimed polypeptide in the test subject when compared to a healthy control is indicative of the presence of the disease or the susceptibility of developing the disease in the future. Thus, a skilled artisan cannot envision what other steps and elements are, and what parameters or criteria are and can used for determining the presence or susceptibility of the claimed disease. It is unclear what other steps, elements, parameters and criteria are, and thus can be used and included within the scope of the claims for determining whether the test animal is affected with tauopathy or a dementia-related disease or may be affected with tauopathy or dementia-related disease in the future, which render the claims indefinite.
ii. The term “may be affected…in the future” recited in instant claims 28-29, 31 is uncertain and indefinite. It is unclear whether detection of the presence of the claimed polypeptide in a test subject means that the subject has the claimed disease or will not have the disease, which render the claims indefinite.
iii. The term “higher than…” or “smaller than…” recited in claims 29, 31, 46-47 and 63 is a relative term which renders the claim indefinite. The term “higher than” is not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention. Applicant fails to set forth the metes and bounds of what is encompassed within the definition of “higher than…” or “smaller than…”. Since the metes and bounds are unknown, a skilled artisan cannot envision what would be considered as “higher than the control value…” or “smaller than the control value” recited in the claim. Thus, the claims are indefinite.
iv. The limitations “cutoff value” in claim 65 and “the cutoff value is 45-85 units” in claim 66 are unclear because the term “cutoff value” or “the cutoff value is 45-85 units” is not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention. Applicant fails to set forth the metes and bounds of what is encompassed within the definition of “cutoff value” or “the cutoff value is 45-85 units”. Since the metes and bounds are unknown, a skilled artisan cannot envision what would be considered as “cutoff value” or “the cutoff value is 45-85 units” recited in the claim. Thus, the claims are indefinite.
v. The rest of claims are indefinite as depending from an indefinite claim.
Claim Rejections - 35 USC § 112
10. 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 28, 34-39, 41-45, 50-57, 59-62, 68-74, 76-79 and 84 are rejected under 35 U.S.C. 112(a) or pre-AIA 35 U.S.C. 112, first paragraph, as based on a disclosure which is not enabling. The disclosure does not enable one of ordinary skill in the art to practice the invention without steps of quantifying, comparing and determining and without specific parameters and criteria of how to determine, which are critical or essential to the practice of the invention but not included in the claim(s). See In re Mayhew, 527 F.2d 1229, 188 USPQ 356 (CCPA 1976). Based on p. 62-66 and p. 91-93 of the instant specification, the step of quantifying the amount of S38AA in a sample of the test subject, the step of comparing the amount of S38AA detected in the test subject to the amount of S38AA detected in a healthy control and the step of determining based on an increased level in the test subject when compared to that of the healthy control is indicative of the presence of the disease are required for the claimed method. However, the instant claims do not recite or include any steps or elements of how to determine, such as steps of measuring or quantifying, comparing with a specific control or value, and determining the presence or susceptibility of the disease based on a specific amount or a specific comparison, such as an increased or decreased amount of the claimed polypeptide in the test subject when compared to a healthy control is indicative of the presence of the disease or the susceptibility of developing the disease in the future. However, the instant claims do not recite or include specific elements/steps of how to determine the presence or susceptibility of tauopathy or a dementia-related disease because instant claims only recite a single step of detecting the claimed polypeptide of SEQ ID NO:1 or variant thereof in a sample. There are no steps of quantifying, comparing and determining, and there are no specific parameters/criteria of how to compare and determine the presence or the susceptibility of the disease recited in the claims. The instant claims do not recite any specific amount or comparison, such as an increased or decreased amount when compared to a healthy control is indicative of the presence of the disease or the susceptibility of developing the disease in the future. Thus, a skilled artisan cannot envision what other steps and elements are, and what specific parameters or criteria are used to determine the presence or susceptibility of the claimed disease. Thus, it is unpredictable what other steps, elements, parameters and criteria can be used and included in the claims in order to determine whether the test animal is affected with tauopathy or a dementia-related disease or may be affected with tauopathy or dementia-related disease in the future. Accordingly, a skilled artisan does not know how to use the claimed method of determining whether the test animal is affected or susceptible to the claimed tauopathy or dementia-related disease without steps of quantifying, comparing and determining and without further knowledges or guidance of specific elements of parameters/criteria for comparison and/or determining the presence or the susceptibility of tauopathy and a dementia-related disease.
Claim Rejections - 35 USC § 112
11. Claims 62-74, 76-79 and 84 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 alleviating symptoms of Parkinson’s disease (PD) by administering a therapeutic drug to PD patients who are diagnosed with PD and with an increased level of S38AA/SLC38A10/SNAT10 (SEQ ID NO:1) compared to healthy controls, does not reasonably provide enablement for a method for treating or preventing all forms of tauopathy or dementia related disease excluding AD by the claimed method as broadly claimed. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
“There are many factors to be considered when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any necessary experimentation is ‘undue’. These factors 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)”. See MPEP § 2164.01.
Claims 62-74, 76-79 and 84 are drawn to a method of treating or preventing tauopathy or a dementia-related disease excluding AD comprising detecting a polypeptide of SEQ ID NO:1 or variant thereof and quantifying and determining whether the test subject has an increased level of the claimed polypeptide of SEQ ID NO:1 or variant thereof compared to a healthy control, and administering a therapeutic or prophylactic drug including Levodopa for tauopathy and dementia-related disease including PD to the tested subject who has an increased level of the claimed polypeptide of SEQ ID NO:1 or variant thereof compared to a healthy control.
The claims encompass a method of preventing all forms of tauopathy and dementia-related diseases using any given agent. However, neither the specification nor the prior art provides guidance to enable a skilled artisan to practice the claimed invention without undue experimentation because currently, all forms of tauopathy or dementia-related diseases cannot be prevented.
Neither the specification nor the prior art provides guidance as to how to prevent a person from having any form of tauopathy or dementia-related diseases including AD and PD caused by all possible mechanisms. Any individual has a potential to develop any form of tauopathy or dementia-related diseases including AD and PD caused by all possible mechanisms. Applicant fails to teach how to identify or predict when and which person would be susceptible to such a disease or developing the disease, and predict when the person would need administration of the claimed therapeutic drug or prophylactic drug to prevent the disease before the disease occurs. Neither the specification nor the prior art teaches that administration of the claimed therapeutic drug or prophylactic drug can prevent a person from getting any form of tauopathy or dementia-related diseases including AD and PD caused by all possible mechanisms. The cause of the disease can be due to a genetic mutation, which is a natural process. The causes of different forms of tauopathy or dementia-related diseases including AD and PD caused by all possible mechanisms are different. For example, there are many factors involved in molecular mechanisms contributing to the formation of -amyloid deposits and neurofibrillary tangles in AD. They include genetic mutations affecting the processing of APP or other molecules involved in protein processing and targeting in view of Henstridge et al. (see p. 94, Henstridge et al., Nat. Rev. Neurosci. 2019; 20: 94-107), Tayebati (see p. 106, 1st col, 2nd paragraph, Tayebati, Mech. Ageing Dev. 2006. 127: 100-8) and Sarter (see p. 645, abstract, Sarter, Neurosci. and Biobehav. Rev. 2004. 28: 645-650). Moore et al. teach that the pathogenesis of PD can be familial and associated with different gene deficits including a-synuclein, parkin, PINK1, LRRK, NR4A2 etc. (see p. 59-71, Moore et al., Annu. Rev. Neurosci. 2005; 28:57-87), due to oxidative stress resulting production of ROS and mitochondrial dysfunction or could be due impairment of ubiquitin-proteasome system (see p. 72-74, in particular). Potashkin et al. teach that current animal models do not replicate the true pathophysiology occurring in idiopathic PD and thus the results from animal models often do not translate to the clinic (see p.1, abstract; Potashikin et al., Parkinson’s Disease, 2011; 658083; doi:104061/2011/658083). If the cause is due to genetic deficits or mutations, it is impossible to prevent a person from getting or developing any form of tauopathy or dementia-related diseases including AD and PD caused by all possible mechanisms because the gene mutation or gene deficiency is a natural process result. The specification fails to provide sufficient guidance as to enable one of skill in the art to practice the invention as it pertains to a method of prevention. Further, Applicant also fails to provide specific guidance as to what specific amount of the claimed therapeutic drug or prophylactic drug can be used and thus would be effective to prevent all forms of tauopathy or dementia-related diseases including AD and PD caused by all possible mechanisms. Thus, a skilled artisan cannot contemplate a right amount to prevent the disease or to prevent a person from getting the disease.
Therefore, in view of the breadth of the claims, the lack of guidance in the specification, the limited examples, the unpredictability of inventions, and the current status of the art, undue experimentation would be required by one of skill in the art to perform in order to practice the full scope of the claimed invention as it pertains to a method for treating or preventing tauopathy or dementia-related diseases including AD and PD caused by all possible mechanisms using the claimed therapeutic drug or prophylactic drug.
Claim Rejections - 35 USC § 112
12. Claims 28-39, 41-57, 59-74, 76-79 and 84 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 pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention.
To provide adequate written description and evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, methods of making the claimed product, or any combination thereof.
Claims 28-39, 41-57, 59-74, 76-79 and 84 encompass detecting a genus of polypeptide variants consisting of an amino acid sequence resulting from substitution, deletion, addition or insertion of one or more amino acids in the SEQ ID NO:1 in a genus of tauopathy or dementia-related diseases.
Claims 38-39, 41-42, 55-57, 59, 72-74 and 76 encompass using a genus of antibody for detecting the claimed polypeptide of SEQ ID NO:1 or variants thereof in a genus of tauopathy or dementia-related diseases. Claims 41-42, 57, 59, 74 and 76 encompass using a genus of antibody comprising recited SEQ ID NOs: for VH and VL in a random order and wherein the VH and VL are not necessarily paired.
Applicant has not disclosed sufficient species for the broad genus of polypeptide variant, the broad genus of the broad genus of antibody and the broad genus of antibody with recited SEQ ID NOs: for VH and VL in a random order for detecting the claimed polypeptide or variant thereof.
In making a determination of whether the application complies with the written description requirement of 35 U.S.C. 112, first paragraph, it is necessary to understand what Applicant is in possession of and what Applicant is claiming.
M.P.E.P. § 2163 instructs:
An invention described solely in terms of a method of making and/or its function may lack written descriptive support where there is no described or art-recognized correlation between the disclosed function and the structure(s) responsible for the function. . . .
An applicant may show possession of an invention by disclosure of drawings or structural chemical formulas that are sufficiently detailed to show that applicant was in possession of the claimed invention as a whole. . . .
An applicant may also show that an invention is complete by disclosure of sufficiently detailed, relevant identifying characteristics which provide evidence that applicant was in possession of the claimed invention, i.e., complete or partial structure, other physical and/or chemical properties, functional characteristics when coupled with a known or disclosed correlation between function and structure, or some combination of such characteristics.”
This standard has not been met in this case. The specification only describes detecting S38AA long fragment (SEQ ID NO:2) or S38AA short fragment (SEQ ID NO:1) in plasma of patients using SDS-PAGE and liquid chromatography mass spectrometry (LC-MS/MS) or using ELISA to quantify S38AA long fragment and S38AA short fragment in the patients diagnosed with progressive, supranuclear palsy (PSP), corticobasal degeneration (CBD), multiple system atrophy (MSA), cognitive dysfunction associated with Parkinson’s disease (PDD) (elected) or multiple sclerosis (MS) (See figures 7-9) and also describes different anti-S38AA monoclonal antibodies (1)-(10) recited in the specification. However, the claims are not limited to detection of S38AA long fragment (SEQ ID NO:2) and S38AA short fragment (SEQ ID NO:1) and methods set forth above but also encompass detecting a genus of structurally and functionally undefined polypeptide variants in a genus of tauopathy or dementia-related diseases, and a genus of structurally and functionally undefined antibodies including recited SEQ ID NOs: for VH and VL in a random order.
Applicant is not in possession of detecting a genus of structurally and functionally undefined polypeptide variants in a genus of tauopathy or dementia-related diseases, and a genus of structurally and functionally undefined antibodies including recited SEQ ID NOs: for VH and VL in a random order. The specification provides no well-established structural and functional correlation between the claimed polypeptide of SEQ ID NO:1 or 2 in PSP, CBD, MSA, PDD and MS, and the recited polypeptides and variants of SEQ ID NO:1 in all forms of tauopathy or dementia-related diseases. The specification fails to provide sufficient description as to what structures or sequences for the claimed genus of variant peptides of SEQ ID NO:1 or the claimed genus of antibodies with recited VH and VL in a random order to generate specific anti-S38AA antibodies that can detect the claimed variants in all forms of tauopathy or dementia-related diseases.
It is well established in the art that the formation of an intact antigen-binding site generally requires the association of the complete heavy and light chain variable regions of a given antibody, each of which consists of three CDRs which provide the majority of the contact residues for the binding of the antibody to its target epitope.
The amino acid sequences and conformations of each of the heavy and light chain CDRs are critical in maintaining the antigen binding specificity and affinity which is characteristic of the parent immunoglobulin. It is expected that all of the heavy and light chain CDRs in their proper order and in the context of framework sequences which maintain their required conformation, are required in order to produce a protein having antigen-binding function and that proper association of heavy and light chain variable regions is required in order to form functional antigen binding sites. MacCallum et al. (J. Mol. Biol.,1996; 262: 732-745) teaches that although CDR3 of the heavy and light chain dominate, a number of residues outside the standard CDR definitions make antigen contacts (see p. 733, right col) and non-contacting residues within the CDRs coincide with residues as important in defining canonical backbone conformations (see page 735, left col.). Pascalis et al. (The Journal of Immunology, 2002; 169: 3076-3084) teaches that grafting of the CDRs into a human framework was performed by grafting CDR residues and maintaining framework residues that were deemed essential for preserving the structural integrity of the antigen binding site (see page 3079, right col.) and that although abbreviated CDR residues were used in the constructs, some residues in all 6 CDRs were used for the constructs (see page 3080, left col.). The fact that not just one CDR is essential for antigen binding or maintaining the conformation of the antigen binding site because although CDR H3 is at the center of most if not all antigen interactions, clearly other CDRs play an important role in the recognition process (page 199, left col.) and this is demonstrated in this work by using all CDRs except L2 and additionally using a framework residue located just before the H3 (see page 202, left col.; Casset et al., BBRC, 2003; 307: 198-205). Vajdos et al. (J. Mol. Biol. 2002; 320: 415-428) also teaches that antigen binding is primarily mediated by the CDRs more highly conserved framework segments which connect the CDRs are mainly involved in supporting the CDR loop conformations and in some cases framework residues also contact antigen (page 416, left col.). Holm et al.(Mol. Immunol., 2007; 44: 1075-1084) teaches that although residues in the CDR3 of the heavy chain were involved in antigen binding, unexpectedly a residue in CDR2 of the light chain was also involved (abstract). Chen et al. (J. Mol. Bio., 1999; 293: 865-881) teaches that the antigen binding site is almost entirely composed of residues from heavy chain CDRs, CDR-H1, H2, H3 (page 866). Wu et al. (J. Mol. Biol., 1999; 294:151-162) teaches that it is difficult to predict which framework residues serve a critical role in maintaining affinity and specificity due in part to the large conformational change in antibodies that accompany antigen binding (page 152 left col.) but certain residues have been identified as important for maintaining conformation. The specification fails to provide sufficient descriptive information, such as definitive structural or functional features of the claimed genus of polypeptide variants or antibodies with a random order. Furthermore, the prior art does not provide compensatory structural or correlative teachings sufficient to enable one of skill to identify what other binding members might be. Since the common characteristics/features of other polypeptide variants or antibodies with a random order and their correlation with other forms of tauopathy or dementia-related diseases are unknown, a skilled artisan cannot envision the functional correlations of the genus with the claimed invention. Accordingly, in the absence of sufficient recitation of distinguishing identifying characteristics, the specification does not provide adequate written description of the genus of polypeptide variants, antibodies in a random order or tauopathy or dementia-related diseases.
Based on MPEP § 2161.01 and §2163, “to satisfy the written description requirement, a patent specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. See, e.g., Moba, B.V. v. Diamond Automation, Inc., 325 F.3d 1306, 1319, 66 USPQ2d 1429, 1438 (Fed. Cir. 2003); Vas-Cath, Inc. v. Mahurkar, 935 F.2d at 1563, 19 USPQ2d at 1116”.
Vas-Cath Inc. v. Mahurkar, 19USPQ2d 1111, clearly states “applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the ‘written description’ inquiry, whatever is now claimed.” (See page 1117.) The specification does not “clearly allow persons of ordinary skill in the art to recognize that [he or she] invented what is claimed.” (See Vas-Cath at page 1116).
As discussed above, the skilled artisan cannot envision the detailed chemical structure of the encompassed genus of polypeptide variants, antibodies in a random order or tauopathy or dementia-related diseases and therefore conception is not achieved until reduction to practice has occurred, regardless of the complexity or simplicity of the method of isolation. Adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method of isolating it. The compound itself is required. See Fiers v. Revel, 25 USPQ2d 1601 at 1606 (CAFC 1993) and Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016. One cannot describe what one has not conceived. See Fiddes v. Baird, 30 USPQ2d 1481 at 1483.
Therefore, the claimed methods have not met the written description provision of 35 U.S.C. §112, first paragraph. Applicant is reminded that Vas-Cath makes clear that the written description provision of 35 U.S.C. §112 is severable from its enablement provision (see page 1115). Applicant is directed to the Guidelines for the Examination of Patent Applications Under the 35 U.S.C. 112, ¶ 1 "Written Description" Requirement. See MPEP § 2161.01 and 2163.
Conclusion
13. NO CLAIM IS ALLOWED.
14. The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
US10393757 teaches a method of diagnosing AD based on the level of S38AA comprising the sequence of SEQ ID NO:2, which is 100% identical to instant SEQ ID NO:1 (see the sequence alignment below).
SEQ ID NO:1
US-13-997-854-2
Filing date in PALM: 2013-06-25
Sequence 2, US/13997854
Patent No. 10393757
GENERAL INFORMATION
APPLICANT: Hashimoto et al.
TITLE OF INVENTION: Diagnostic drug and diagnostic method of Alzheimer's disease
FILE REFERENCE: 713766
CURRENT APPLICATION NUMBER: US/13/997,854
CURRENT FILING DATE: 2013-06-25
PRIOR APPLICATION NUMBER: PCT/JP2011/080517
PRIOR FILING DATE: 2011-12-28
PRIOR APPLICATION NUMBER: JP 2010-293891
PRIOR FILING DATE: 2010-12-28
NUMBER OF SEQ ID NOS: 12
SEQ ID NO 2
LENGTH: 1119
TYPE: PRT
ORGANISM: Homo sapiens
ALIGNMENT:
Query Match 100.0%; Score 2278; Length 1119;
Best Local Similarity 100.0%;
Matches 433; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 617 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 676
Qy 61 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 677 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 736
Qy 121 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 737 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 796
Qy 181 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 797 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 856
Qy 241 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 857 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 916
Qy 301 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 917 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 976
Qy 361 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 977 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 1036
Qy 421 PNRDLKLQAGSDL 433
|||||||||||||
Db 1037 PNRDLKLQAGSDL 1049
WO2020032027 teaches a method of diagnosing AD based on the level of S38AA comprising the sequence of SEQ ID NO:1 or 2, which is 100% identical to instant SEQ ID NO:1 (see the sequence alignment below).
BHI48718
(NOTE: this sequence has 1 duplicate in the database searched.
See complete list at the end of this report)
ID BHI48718 standard; protein; 433 AA.
XX
AC BHI48718;
XX
DT 02-APR-2020 (first entry)
XX
DE Human S38AA protein short fragment (617-1050), SEQ 1.
XX
KW S38AA protein; alzheimers disease; neuroprotective; nootropic;
KW prophylactic to disease; protein detection; screening; therapeutic.
XX
OS Homo sapiens.
XX
CC PN WO2020032027-A1.
XX
CC PD 13-FEB-2020.
XX
CC PF 06-AUG-2019; 2019WO-JP030904.
XX
PR 07-AUG-2018; 2018JP-00148924.
XX
CC PA (SUMU ) SUMITOMO DAINIPPON PHARMA CO LTD.
XX
CC PI Ono A, Teranishi Y, Kusumoto M, Hashimoto M, Kashiwabara S;
XX
DR WPI; 2020-14032F/019.
XX
CC PT New polypeptide useful in kit and agent for detecting Alzheimer's
CC PT disease, assisting determination of degree of progression of
CC PT Alzheimer's disease and screening agent for preventing or treating
CC PT Alzheimer's disease.
XX
CC PS Claim 1; SEQ ID NO 1; 91pp; Japanese.
XX
CC The present invention relates to a novel polypeptide useful for
CC detecting, preventing or treating Alzheimer's disease in a subject. The
CC invention further claims: (1) an antibody (Ab1) that specifically
CC recognizes the polypeptide; (2) a nucleic acid encoding the polypeptide;
CC (3) a kit comprising the antibody; (4) a method for detecting the
CC polypeptide involving contacting the test sample with the antibody; (5)
CC an agent comprising one or more anti-S38AA antibody (Ab2) capable of
CC measuring the amount of the polypeptide; (6) a method for determining the
CC possibility of an animal suffering from Alzheimer's disease; (7) a method
CC for assisting the determination of the degree of progression of
CC Alzheimer's disease; and (8) a method for selecting a candidate substance
CC for an agent for preventing or treating Alzheimer's disease. The
CC polypeptide is useful in kit and agent for detecting Alzheimer's disease,
CC assisting the determination of the degree of progression of Alzheimer's
CC disease and for screening agent for preventing or treating Alzheimer's
CC disease. The polypeptide enables highly accurate and reliable detection
CC of Alzheimer's disease.
XX
SQ Sequence 433 AA;
Query Match 100.0%; Score 2278; Length 433;
Best Local Similarity 100.0%;
Matches 433; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 60
Qy 61 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 120
Qy 121 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 180
Qy 181 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 240
Qy 241 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 300
Qy 301 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 360
Qy 361 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 361 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 420
Qy 421 PNRDLKLQAGSDL 433
|||||||||||||
Db 421 PNRDLKLQAGSDL 433
BHI48719
(NOTE: this sequence has 1 duplicate in the database searched.
See complete list at the end of this report)
ID BHI48719 standard; protein; 651 AA.
XX
AC BHI48719;
XX
DT 02-APR-2020 (first entry)
XX
DE Human S38AA protein long fragment (399-1050), SEQ 2.
XX
KW S38AA protein; alzheimers disease; neuroprotective; nootropic;
KW prophylactic to disease; protein detection; screening; therapeutic.
XX
OS Homo sapiens.
XX
CC PN WO2020032027-A1.
XX
CC PD 13-FEB-2020.
XX
CC PF 06-AUG-2019; 2019WO-JP030904.
XX
PR 07-AUG-2018; 2018JP-00148924.
XX
CC PA (SUMU ) SUMITOMO DAINIPPON PHARMA CO LTD.
XX
CC PI Ono A, Teranishi Y, Kusumoto M, Hashimoto M, Kashiwabara S;
XX
DR WPI; 2020-14032F/019.
XX
CC PT New polypeptide useful in kit and agent for detecting Alzheimer's
CC PT disease, assisting determination of degree of progression of
CC PT Alzheimer's disease and screening agent for preventing or treating
CC PT Alzheimer's disease.
XX
CC PS Disclosure; SEQ ID NO 2; 91pp; Japanese.
XX
CC The present invention relates to a novel polypeptide useful for
CC detecting, preventing or treating Alzheimer's disease in a subject. The
CC invention further claims: (1) an antibody (Ab1) that specifically
CC recognizes the polypeptide; (2) a nucleic acid encoding the polypeptide;
CC (3) a kit comprising the antibody; (4) a method for detecting the
CC polypeptide involving contacting the test sample with the antibody; (5)
CC an agent comprising one or more anti-S38AA antibody (Ab2) capable of
CC measuring the amount of the polypeptide; (6) a method for determining the
CC possibility of an animal suffering from Alzheimer's disease; (7) a method
CC for assisting the determination of the degree of progression of
CC Alzheimer's disease; and (8) a method for selecting a candidate substance
CC for an agent for preventing or treating Alzheimer's disease. The
CC polypeptide is useful in kit and agent for detecting Alzheimer's disease,
CC assisting the determination of the degree of progression of Alzheimer's
CC disease and for screening agent for preventing or treating Alzheimer's
CC disease. The polypeptide enables highly accurate and reliable detection
CC of Alzheimer's disease.
XX
SQ Sequence 651 AA;
Query Match 100.0%; Score 2278; Length 651;
Best Local Similarity 100.0%;
Matches 433; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 219 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 278
Qy 61 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 279 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 338
Qy 121 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 339 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 398
Qy 181 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 399 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 458
Qy 241 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 459 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 518
Qy 301 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 519 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 578
Qy 361 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 579 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 638
Qy 421 PNRDLKLQAGSDL 433
|||||||||||||
Db 639 PNRDLKLQAGSDL 651
WO2003016493 teaches a transporter and ion channel protein 5, TRICH-5 comprising the sequence of instant SEQ ID NO:1 (see the sequence alignment below).
SEQ ID NO:1
ABG75823
(NOTE: this sequence has 14 duplicates in the database searched.
See complete list at the end of this report)
ID ABG75823 standard; protein; 1119 AA.
XX
AC ABG75823;
XX
DT 15-JUN-2007 (revised)
DT 10-MAY-2003 (first entry)
XX
DE Transporters and ion channels protein 5, TRICH-5.
XX
KW Human; transporter and ion channel; TRICH; gene therapy;
KW cell proliferative disorder; transport disorder; neurological disorder;
KW muscle disorder; immunological disorder; amyotrophic lateral sclerosis;
KW cystic fibrosis; diabetes; Parkinson's disease; prostate cancer;
KW cardiac disorder; angina; Alzheimer's disease; amnesia; epilepsy;
KW schizophrenia; sickle cell anaemia; infertility; hyperglycaemia;
KW hypoglycaemia; hypercholesterolaemia; stroke; multiple sclerosis;
KW motor neuron disorder; prion disease; metabolic disease;
KW developmental disorder; central nervous system; cardiomyopathy;
KW hypertension; asthma; AIDS; allergy; anaemia; atherosclerosis;
KW atopic dermatitis; diabetes mellitus; osteoarthritis; osteoporosis;
KW rheumatoid arthritis; psoriasis; infection; trauma; hepatitis; cancer;
KW leukemia; lymphoma; BOND_PC; hypothetical protein LOC124565 isoform a;
KW hypothetical protein LOC124565 isoform a [Homo sapiens]; MGC15523;
KW FLJ35718.
XX
OS Homo sapiens.
XX
CC PN WO2003016493-A2.
XX
CC PD 27-FEB-2003.
XX
CC PF 16-AUG-2002; 2002WO-US026323.
XX
PR 17-AUG-2001; 2001US-0313242P.
PR 21-SEP-2001; 2001US-0324782P.
PR 02-OCT-2001; 2001US-0328184P.
PR 26-OCT-2001; 2001US-0345937P.
PR 01-NOV-2001; 2001US-0335698P.
PR 13-NOV-2001; 2001US-0332804P.
PR 27-NOV-2001; 2001US-0333922P.
PR 26-APR-2002; 2002US-0375637P.
PR 03-MAY-2002; 2002US-0377444P.
PR 11-JUN-2002; 2002US-0388180P.
XX
CC PA (INCY-) INCYTE GENOMICS INC.
XX
CC PI Tang YT, Lal PG, Yue H, Baughn MR, Nguyen DB, Yao MG, Greene BD;
CC PI Borowsky ML, Lee S, Emerling BM, Xu Y, Becha SD, Gorvad AE;
CC PI Azimzai Y, Yue H, Elliott VS, Lee EA, Yang J, Lehr-Mason PM;
CC PI Ramkumar J, Lee SY, Faris M, Turner C, Furness M, Buchbinder JL;
CC PI Walia NK, Li JX, Forsythe IJ, Griffin JA, Gietzen KJ, Swarnakar A;
CC PI Hafalia AJA, Lindquist EA, Jiang X, Jackson AA, Wilson AD, Jin P;
CC PI Khare R, Marquis JP;
XX
DR WPI; 2003-268319/26.
DR N-PSDB; ABX12008.
DR PC:NCBI; gi83921602.
XX
CC PT Novel human transporter and ion channel polypeptides and polynucleotides
CC PT for diagnosing, preventing or treating cell proliferative, transport,
CC PT neurological, muscle and immunological disorders.
XX
CC PS Claim 1; Page 195-198; 253pp; English.
XX
CC The invention discloses isolated polypeptides chosen from human
CC transporter and ion channel polypeptides, TRICH 1-26, a biologically
CC active or immunogenic fragment and the nucleic acids encoding them. Also
CC disclosed are isolated antibodies raised against the TRICH proteins,
CC methods for detecting a target polynucleotide in a sample and a
CC microarray where at least one element is a TRICH polynucleotide. The
CC proteins are useful for screening for agonists or antagonists, which can
CC then be used for treating a disease or condition associated with
CC decreased or overexpression of functional TRICH in a patient, for
CC screening for a compound that modulates the activity of the polypeptide
CC or that binds to the polypeptide or as an immunogen for preparing
CC antibodies. The polynucleotides are useful for screening for compounds
CC which alter expression of a target polynucleotide or for assessing
CC toxicity of a test compound. The polypeptides, polynucleotides,
CC modulators and antibodies are useful for diagnosis, treatment (e.g. gene
CC therapy) and prevention of cell proliferative, transport, neurological,
CC muscle and immunological disorders, such as amyotrophic lateral
CC sclerosis, cystic fibrosis, diabetes, Parkinson's disease, prostate
CC cancer, cardiac disorders, angina, Alzheimer's disease, amnesia,
CC epilepsy, schizophrenia, sickle cell anaemia, infertility,
CC hyperglycaemia, hypoglycaemia, hypercholesterolaemia, stroke, multiple
CC sclerosis, motor neuron disorder, prion disease, metabolic disease of the
CC nervous system, developmental disorders of the central nervous system,
CC cardiomyopathy, hypertension, asthma, AIDS, allergies, anaemia,
CC atherosclerosis, atopic dermatitis, diabetes mellitus, osteoarthritis,
CC osteoporosis, rheumatoid arthritis, psoriasis, infections, trauma,
CC hepatitis and cancers, including leukemia and lymphoma. The sequences
CC presented in ABG75819-ABG75844 are the TRICH proteins of the invention
CC
CC Revised record issued on 15-JUN-2007 : Enhanced with precomputed
CC information from BOND.
XX
SQ Sequence 1119 AA;
Query Match 100.0%; Score 2278; Length 1119;
Best Local Similarity 100.0%;
Matches 433; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 617 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 676
Qy 61 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 677 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 736
Qy 121 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 737 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 796
Qy 181 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 797 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 856
Qy 241 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 857 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 916
Qy 301 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 917 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 976
Qy 361 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 977 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 1036
Qy 421 PNRDLKLQAGSDL 433
|||||||||||||
Db 1037 PNRDLKLQAGSDL 1049
WO200218435 teaches a human gene 7 encoded secreted protein, HMVBP38comprising the sequence of instant SEQ ID NO:1 (see the sequence alignment below).
AAE20799
(NOTE: this sequence has 8 duplicates in the database searched.
See complete list at the end of this report)
ID AAE20799 standard; protein; 973 AA.
XX
AC AAE20799;
XX
DT 01-JUL-2002 (first entry)
XX
DE Human gene 7 encoded secreted protein HMVBP38, SEQ ID NO:61.
XX
KW Human; secreted protein; gene therapy; human immunodeficiency virus; HIV;
KW immune disease; autoimmune disease; anaemia; multiple sclerosis; cancer;
KW rheumatoid arthritis; hyperproliferative disorder; melanoma; neoplasm;
KW sezary syndrome; Gaucher's disease; neurological disease; cardiac arrest;
KW Alzheimer's disease; Parkinson's disease; Charcot-Marie-Tooth disease;
KW cardiovascular disorder; cerebrovascular disorder; tachycardia; angina;
KW thrombosis; ocular disorder; corneal infection; wound healing; cardiant;
KW vascular; thrombolytic; cytostatic; nootropic.
XX
OS Homo sapiens.
XX
FH Key Location/Qualifiers
FT Peptide 1..34
FT /label= Signal_peptide
FT Protein 35..973
FT /label= Mature_secreted_protein
XX
CC PN WO200218435-A1.
XX
CC PD 07-MAR-2002.
XX
CC PF 17-JAN-2001; 2001WO-US001567.
XX
PR 28-AUG-2000; 2000US-0228084P.
XX
CC PA (HUMA-) HUMAN GENOME SCI INC.
XX
CC PI Rosen CA, Komatsoulis GA, Baker KP, Birse CE, Soppet DR;
CC PI Olsen HS, Moore PA, Wei P, Ebner R, Duan DR, Shi Y, Choi GH;
CC PI Fiscella M, Ni J;
XX
DR WPI; 2002-281060/32.
DR N-PSDB; AAD33243.
XX
CC PT Isolated nucleic acid molecule encoding a human secreted protein is used
CC PT in preventing, treating or ameliorating e.g. Alzheimer's disease, cardio-
CC PT /cerebrovascular disorders and multiple sclerosis.
XX
CC PS Claim 11; Page 451-454; 504pp; English.
XX
CC AAD33237-AAD33280 represent cDNAs corresponding to 18 human secreted
CC protein genes, and AAE20793-AAE20836 represent the proteins they encode.
CC AAE20837-AAE20847 represent human secreted protein fragments. The genes
CC and their corresponding secreted proteins are useful for preventing,
CC treating or ameliorating medical conditions, e.g., by protein or gene
CC therapy. Pathological conditions can be diagnosed by determining the
CC amount of the new protein in a sample or by determining the presence of
CC mutations in the new genes. Specific uses are described for each of the
CC 18 genes, based on the tissues in which they are most highly expressed,
CC and include developing products for the diagnosis or treatment of immune
CC or autoimmune diseases (e.g. HIV (human immunodeficiency virus)
CC infections, anaemia, rheumatoid arthritis and multiple sclerosis),
CC cancers and hyperproliferative disorders (e.g. melanomas, neoplasms of
CC the breast or liver, Sezary syndrome and Gaucher's disease), neurological
CC diseases (e.g. Alzheimer's disease, Parkinson's disease and Charcot-
CC Marie-Tooth disease), cardiovascular or cerebrovascular disorders (e.g.
CC cardiac arrest, tachycardia, angina and thrombosis), infections caused by
CC bacteria, viruses and fungi and ocular disorders (e.g. corneal
CC infections). Secreted proteins of the invention can also be used to
CC promote wound healing, maintain organs before transplantation, support
CC cell culture of primary tissues, modulate differentiation of embryonic
CC stem cells, induce mesodermal tissue to differentiate in embryos,
CC modulate mammalian characteristics (e.g. height and weight), modulate the
CC catabolism, anabolism, energy storage, mental state, biorhythms, cardiac
CC rhythms, reproductive potential, hormonal levels appetite, memory and
CC stress. They can also be used as an additive to increase or decrease
CC storage capabilities and nutritional content of food. The present
CC sequence represents a human secreted protein of the invention
XX
SQ Sequence 973 AA;
Query Match 99.8%; Score 2274; Length 973;
Best Local Similarity 99.8%;
Matches 432; Conservative 0; Mismatches 1; Indels 0; Gaps 0;
Qy 1 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 472 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 531
Qy 61 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 532 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 591
Qy 121 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 592 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 651
Qy 181 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 240
|||||||||||||||||||||||||||||||||| |||||||||||||||||||||||||
Db 652 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQGKLRDGQKDAAPRAAGTVKELPKGPE 711
Qy 241 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 712 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 771
Qy 301 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 772 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 831
Qy 361 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 832 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 891
Qy 421 PNRDLKLQAGSDL 433
|||||||||||||
Db 892 PNRDLKLQAGSDL 904
US20210165002 teaches a method of diagnosing AD based on the level of S38AA comprising the sequence of SEQ ID NO:1 or 2, which is 100% identical to instant SEQ ID NO:1 (see the sequence alignment below).
SEQ ID NO:1
US-17-265-805-1
(NOTE: this sequence has 1 duplicate in the database searched.
See complete list at the end of this report)
Sequence 1, US/17265805
Publication No. US20210165002A1
GENERAL INFORMATION
APPLICANT: Sumitomo Dainippon Pharma Co., Ltd.
TITLE OF INVENTION: DIAGNOSTIC DRUG AND DIAGNOSTIC METHOD FOR ALZHEIMER'S DISEASE
FILE REFERENCE: 752249
CURRENT APPLICATION NUMBER: US/17/265,805
CURRENT FILING DATE: 2021-02-03
PRIOR APPLICATION NUMBER: PCT/JP2019/030904
PRIOR FILING DATE: 2019-08-06
PRIOR APPLICATION NUMBER: JP 2018-148924
PRIOR FILING DATE: 2018-08-07
NUMBER OF SEQ ID NOS: 23
SEQ ID NO 1
LENGTH: 433
TYPE: PRT
ORGANISM: Homo sapiens
Query Match 100.0%; Score 2278; Length 433;
Best Local Similarity 100.0%;
Matches 433; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 60
Qy 61 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 120
Qy 121 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 180
Qy 181 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 240
Qy 241 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 300
Qy 301 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 360
Qy 361 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 361 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 420
Qy 421 PNRDLKLQAGSDL 433
|||||||||||||
Db 421 PNRDLKLQAGSDL 433
US-17-265-805-2
(NOTE: this sequence has 1 duplicate in the database searched.
See complete list at the end of this report)
Sequence 2, US/17265805
Publication No. US20210165002A1
GENERAL INFORMATION
APPLICANT: Sumitomo Dainippon Pharma Co., Ltd.
TITLE OF INVENTION: DIAGNOSTIC DRUG AND DIAGNOSTIC METHOD FOR ALZHEIMER'S DISEASE
FILE REFERENCE: 752249
CURRENT APPLICATION NUMBER: US/17/265,805
CURRENT FILING DATE: 2021-02-03
PRIOR APPLICATION NUMBER: PCT/JP2019/030904
PRIOR FILING DATE: 2019-08-06
PRIOR APPLICATION NUMBER: JP 2018-148924
PRIOR FILING DATE: 2018-08-07
NUMBER OF SEQ ID NOS: 23
SEQ ID NO 2
LENGTH: 651
TYPE: PRT
ORGANISM: Homo sapiens
Query Match 100.0%; Score 2278; Length 651;
Best Local Similarity 100.0%;
Matches 433; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 219 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 278
Qy 61 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 279 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 338
Qy 121 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 339 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 398
Qy 181 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 399 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 458
Qy 241 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 459 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 518
Qy 301 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 519 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 578
Qy 361 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 579 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 638
Qy 421 PNRDLKLQAGSDL 433
|||||||||||||
Db 639 PNRDLKLQAGSDL 651
US20090181380 teaches human genes including a sequence comprising the sequence of instant SEQ ID NO:1 (see the sequence alignment below).
SEQ ID NO:1
US-12-158-262A-1833
(NOTE: this sequence has 20 duplicates in the database searched.
See complete list at the end of this report)
Sequence 1833, US/12158262A
Publication No. US20090181380A1
GENERAL INFORMATION
APPLICANT: Genizon BioSciences, Inc.
TITLE OF INVENTION: GENEMAP OF THE HUMAN GENES ASSOCIATED WITH CROHN'S DISEASE
FILE REFERENCE: GENI-011/01WO
CURRENT APPLICATION NUMBER: US/12/158,262A
CURRENT FILING DATE: 2008-12-04
PRIOR APPLICATION NUMBER: US 60/751,420
PRIOR FILING DATE: 2005-12-19
NUMBER OF SEQ ID NOS: 21498
SEQ ID NO 1833
LENGTH: 1119
TYPE: PRT
ORGANISM: Homo sapiens
Query Match 100.0%; Score 2278; Length 1119;
Best Local Similarity 100.0%;
Matches 433; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 617 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 676
Qy 61 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 677 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 736
Qy 121 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 737 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 796
Qy 181 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 797 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 856
Qy 241 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 857 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 916
Qy 301 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 917 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 976
Qy 361 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 977 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 1036
Qy 421 PNRDLKLQAGSDL 433
|||||||||||||
Db 1037 PNRDLKLQAGSDL 1049
US20070083334 teaches biomolecules including a sequence comprising the sequence that is 99.8% identical to instant SEQ ID NO:1 (see the sequence alignment below).
SEQ ID NO:1
US-11-443-428A-811148
Sequence 811148, US/11443428A
Publication No. US20070083334A1
GENERAL INFORMATION
APPLICANT: Mintz, Liat
APPLICANT: Xie, Hanqing
APPLICANT: Dahari, Dvir
APPLICANT: Levanon, Erez
APPLICANT: Freilich, Shiri
APPLICANT: Beck, Nili
APPLICANT: Zhu, Wei-Yong
APPLICANT: Wasserman, Alon
APPLICANT: Hermesh, Chen
APPLICANT: Azar, Idit
APPLICANT: Bernstein, Jeanne
TITLE OF INVENTION: METHODS AND SYSTEMS USEFUL FOR ANNOTATING BIOMOLECULAR SEQUENCES
FILE REFERENCE: 02/23929
CURRENT APPLICATION NUMBER: US/11/443,428A
CURRENT FILING DATE: 2006-05-31
NUMBER OF SEQ ID NOS: 1034312
SEQ ID NO 811148
LENGTH: 585
TYPE: PRT
ORGANISM: Homo sapiens
Query Match 99.8%; Score 2274; Length 585;
Best Local Similarity 99.8%;
Matches 432; Conservative 0; Mismatches 1; Indels 0; Gaps 0;
Qy 1 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 83 GLAVGGGEKAKGGPPPGNAAGDTGQPAEDSDHGGKPPLPAEKPAPGPGLPPEPREQRDVE 142
Qy 61 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 143 RAGGNQAASQLEEAGRAEMLDHAVLLQVIKEQQVQQKRLLDQQEKLLAVIEEQHKEIHQQ 202
Qy 121 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 203 RQEDEEDKPRQVEVHQEPGAAVPRGQEAPEGKARETVENLPPLPLDPVLRAPGGRPAPSQ 262
Qy 181 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQAKLRDGQKDAAPRAAGTVKELPKGPE 240
|||||||||||||||||||||||||||||||||| |||||||||||||||||||||||||
Db 263 DLNQRSLEHSEGPVGRDPAGPPDGGPDTEPRAAQGKLRDGQKDAAPRAAGTVKELPKGPE 322
Qy 241 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 323 QVPVPDPAREAGGPEERLAEEFPGQSQDVTGGSQDRKKPGKEVAATGTSILKEANWLVAG 382
Qy 301 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 383 PGAETGDPRMKPKQVSRDLGLAADLPGGAEGAAAQPQAVLRQPELRVISDGEQGGQQGHR 442
Qy 361 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 443 LDHGGHLEMRKARGGDHVPVSHEQPRGGEDAAVQEPRQRPEPELGLKRAVPGGQRPDNAK 502
Qy 421 PNRDLKLQAGSDL 433
|||||||||||||
Db 503 PNRDLKLQAGSDL 515
15. Any inquiry concerning this communication or earlier communications from the examiner should be directed to CHANG-YU WANG whose telephone number is (571)272-4521. The examiner can normally be reached on Monday-Thursday, 7:00am-5:00pm EST.
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, Jeffrey Stucker can be reached on 571-272-0911. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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Chang-Yu Wang
January 14, 2026
/CHANG-YU WANG/Primary Examiner, Art Unit 1675