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 .
Restriction/Election
Applicant's election with traverse of Group I, claims 53-68, in the reply filed on 01/13/26 is acknowledged. The traversal is on the ground(s) that the claims of group 2 have been amended to be drawn to the method of claim 66, or a product comprising SEQ ID NO: 1 and an additional therapeutic agent. The latter remark is not found persuasive for the product claims, because the combination therapy is not required in claim 53. Which is the independent claim from which claim 66 depends. As such, the only technical feature unifying groups I and II entirely is SEQ ID NO: 1, which is taught by Stemmer et al., as discussed in the restriction requirement. This is not persuasive to overcome the group restriction requirement.
As to the methods of claims 70 and 71, these were amended after the restriction was sent. However, they are dependent on claim 66, which now puts them in the elected method Group I, as additional method limitations, and they will be included.
The requirement is still deemed proper and is therefore made FINAL.
Claims 69 and 72 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected invention, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 01/13/26.
Applicants also elected “neurodegenerative disease,” and “Alzheimer’s disease,” as the species. Upon further consideration, there is no burden to examine the currently presented method claims together. Therefore, claims 53-68, 70 and 71 are currently under examination.
Claim Rejections 35 USC 112(A)
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 53-68, 70 and 71 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 treating, delaying the onset or ameliorating Alzheimer’s Disease (AD) with the full length SEQ ID NO: 1, does not reasonably provide enablement for preventing Alzheimer’s and cognitive decline, or for treating, preventing ameliorating and delaying the onset of all neurological diseases and cognitive decline with any “functional fragment or derivative” of the polypeptide. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and 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:
(1) The breadth of the claims; (2) The nature of the invention; (3) The state of the prior art; (4) The level of one of ordinary skill; (5) The level of predictability in the art; (6) The amount of direction provided by the inventor; (7) The existence of working examples; and (8) 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) (reversing the PTO's determination that claims directed to methods for detection of hepatitis B surface antigens did not satisfy the enablement requirement). In Wands, the court noted that there was no disagreement as to the facts, but merely a disagreement as to the interpretation of the data and the conclusion to be made from the facts. In re Wands, 858 F.2d at 736-40, 8 USPQ2d at 1403-07. The Court held that the specification was enabling with respect to the claims at issue and found that "there was considerable direction and guidance" in the specification; there was "a high level of skill in the art at the time the application was filed;" and "all of the methods needed to practice the invention were well known." 858 F.2d at 740, 8 USPQ2d at 1406. After considering all the factors related to the enablement issue, the court concluded that "it would not require undue experimentation to obtain antibodies needed to practice the claimed invention." Id., 8 USPQ2d at 1407.
(1) The nature of the invention and (5) The breadth of the claims:
The invention is drawn to a method of preventing Alzheimer’s, as the elected species, and also broadly drawn to treating, preventing ameliorating and delaying the onset of all neurological diseases and cognitive decline, in general, with any “functional fragment or derivative” of the SEQ ID NO: 1 polypeptide, its functional fragments and derivatives.
This is very broad in that it encompasses all neurological diseases, which are defined as are conditions that target how the nervous system (brain, spinal cord and nerves) function (evidenced by Cleveland Clinic: Neurological Disorders: What They Are, Symptoms & Types; https://my.clevelandclinic.org/health/diseases/neurological-disorders, last visited 03/07/26). Many have very different symptoms, mechanisms and causes.
(2) The state of the prior art:
The art recognizes that there are hundreds of neurological disorders, such as Alzheimer’s disease, multiple sclerosis and meningitis, for example, which have many different symptoms that affect movement, emotions, cognitive functions and other psychobiological processes with many treatment options that vary based on the type of disease, condition or desired cognitive outcomes (Cleveland Clinic, p. 1). The art also recognizes that there is no way to prevent all neurological disorders, but that risk of injury or damage to the nervous system can reduce their likelihood (Cleveland Clinic, p. 1).
There are currently no cures for neurodegenerative diseases, or anything that serves as a blanket treatment, and options remain limited due to disease heterogeneity, prolonged preclinical and prodromal phases, poor understanding of disease mechanisms, and diagnostic challenges (evidenced by Imam et al. The Global Neurodegeneration Proteomics Consortium: biomarker and drug target discovery for common neurodegenerative diseases and aging. Nature Medicine, Volume 31, August 2025, p. 2556–2566). The art also recognizes that identifying novel biomarkers is crucial for improving early detection, prognosis, staging and subtyping of these conditions. High-dimensional molecular studies in biofluids (‘omics’) offer promise for scalable biomarker discovery, but challenges in assembling large, diverse datasets hinder progress, which makes identification of biomarkers and important part of treating individual diseases, and is not currently available for understanding how to treat every type of neurodegenerative disease with simply one drug (Imam, Abstract).
As to the enablement of preventing cognitive decline, neurodegenerative diseases, specifically Alzheimer’s, and the symptoms associated therewith, the art also recognizes that there is a plethora of etiologies, even within Alzheimer’s and that there is no way to prevent either of the classes of these conditions. A recent systematic review by the National Institute of Aging and the Academies of Science Medicine and Engineering concluded that there were no specific interventions with enough evidence to justify mounting an assertive public health campaign to encourage adopting them for preventing cognitive decline and dementia/Alzheimer’s (Agency for Healthcare Research and Quality. Preventing Cognitive Decline and Dementia: A Way Forward, 2017; p. 2). Based on findings from the systematic review and other supplemental data sources, the committee could only conclude that there were beneficial effects of three interventions were supported by encouraging, but inconclusive, evidence (p. 2). These only include cognitive training, blood pressure management in people with hypertension, and increased physical activity (p. 2). As such, the art recognizes that there is no single way to prevent neurodegenerative diseases, cognitive decline and dementia/Alzheimer’s.
Furthermore, there are many types of neurological disorders that cannot be prevented because they are caused by a particular genetic mutation or spectrum of genetic and other unknown factors. For example, amyotrophic lateral sclerosis (ALS) requires a large body of knowledge, including an understanding of the causes and risk factors for ALS that require identifying a window of opportunity to study those at risk for disease, methods for predicting when the clinical manifestations of ALS will emerge, and viable strategies to intervene by mitigating risk or treating the underlying biology of disease, which is currently not well understood (evidenced by Benatar et al. A roadmap to ALS prevention: strategies and priorities. Journal of Neurology, Neurosurgery & Psychiatry. 2023; 94: 399-402).
Taken together, these evidentiary references make it clear that the state of the art recognizes neurological diseases and cognitive decline overall to be unpreventable, ameliorable, delayed or treatable as a large, heterogeneous class of diseases because they have variant etiologies, require different treatments, and many are poorly understood. Additionally, although some may be treatable, there is no way to prevent them in general, and no way to prevent the elected species, Alzheimer’s disease.
As to the use of “a functional fragment or derivative” of SEQ ID NO: 1 to treat any neurological disease or disorder, the art also recognizes the functional limitations of short peptides, such as poor in vivo stability because they have amide bonds, but lack the stability conferred by secondary or tertiary structures (Wang et al. Therapeutic peptides: current applications and future directions, Signal Transduction and Targeted Therapy volume 7, Article number: 48. 2022). As such, amide bonds can be easily hydrolyzed or destroyed by enzymes upon unprotected exposure to an in vivo environment, making the peptides chemically and physically unstable, with a short half-life and fast elimination, which requires experimentation to find if a particular peptide is functional (abstract, p. 3). This results in fragments of the claimed SEQ ID NO: 1, which is a 14 D-amino acid residue, highly unpredictable as to which parts of the peptide or its derivative will perform the claimed methods of treatment, delay, prevention and amelioration unpredictable.
Note that the references included here are cited here as evidentiary for current and prior art review purposes. They have been cited to show that the state of the art at the filing date of the invention is still contrary to what is enabled by the state of the art now. This evidences a gap in what was and is known in the art as being enabled, compared what was claimed in this application at the effective filing date.
(3) The relative skill of those in the art:
The relative skill of those in the art is high.
(4) The predictability or unpredictability of the art:
As discussed above, treatment, prevention, amelioration of neurodegenerative diseases and cognitive decline is highly unpredictable because the causes and symptoms of them are highly variant, and for many are not well understood.
(6) The amount of direction or guidance presented and (7) The presence or absence of working examples:
Applicants have claimed to be able to treat any neurological disease with any functional fragment or variant of SEQ ID NO: 1; however, the specification only provides examples using dTCApFs, which is the full length D-amino acid sequence of SEQ ID NO: 1, and one example for comparison of T101, which is the full length L-version of the same amino acid. There are no other derivatives or functional fragments disclosed and no guidance is given as to which portion of the peptide are required for functioning in the method of treatment, or what limits the term “derivative.”
Applicants have only shown one in vivo example, which only show that SEQ ID NO: 1 can cross the BBB in mice (example 1).
As to the diseases, the examples only provide in vitro data for disease models of Parkinson’s (example 2) and Alzheimer’s (example 5), and some support for treating cognitive decline (examples 3-4).
This does not support the claims to treating, preventing, ameliorating and delaying the onset of all neurological disorders and cognitive decline in all individuals.
(8) The quantity of experimentation necessary:
As discussed above, the predictability of what will be treatable by administering any one of the peptide agonists or antagonists is low, and it would require a large amount of experimentation to identify which subjects are at risk for which neurodegenerative disorders and types/causes of cognitive decline. The experimentation on patient classes that may be treatable with certain portions of SEQ ID NO: 1 and its derivatives effectively. This makes the quantity of is undue for one of ordinary skill in the art.
Claim Rejections 35 USC 102(A)(1)
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.
Claim(s) 53-68 and 71 are rejected under 35 U.S.C. 102(A)(1) as being anticipated by Stemmer et al. (Molecular and Clinical Oncology. Vol. 8: 22-29, 2018; See ISR)
Stemmer teaches a human study was performed to investigate the safety/efficacy of dTCApFs, which is a hormone peptide that enters cells through the T1/ST2 receptor in advanced/metastatic solid tumors, to determine its safety profile (abstract). Stemmer teaches that the study enrolled 17 patients with pathologically confirmed locally advanced/metastatic solid malignancies, who experienced treatment failure or were unable to tolerate previous standard therapies, and who had cancers, such as pancreatic and colon cancer (abstract). This reference teaches that dTCApFs was administered in rounds of 1-3 cycles, which increased levels of cytokine induction into the ER in T1/ST2-positive tumors and effectively reduced them (abstract).
Claim Interpretation
The claims are drawn to a method of preventing neurological disorders, cognitive decline and their symptoms, or to improving cognitive function, memory and its underlying mechanisms. This means that the patient class of claims 53 includes any subject, as any subject would be “in need” of a method of preventing cognitive decline and neurodegeneration, as well as improving cognitive function and memory in claim 67, as this also does not limit the patient class to any particular condition or disorder. Therefore, art teaching a method of administering SEQ ID NO: 1 to a subject, meets the limitation of preventing these conditions or improving these conditions, as the prior peptide would necessarily encompass this capability upon administration to a subject.
The MPEP states: "[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. IRECO Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977). In In re Crish, 393 F.3d 1253, 1258, 73 USPQ2d 1364, 1368 (Fed. Cir. 2004), the court held that the claimed promoter sequence obtained by sequencing a prior art plasmid that was not previously sequenced was anticipated by the prior art plasmid which necessarily possessed the same DNA sequence as the claimed oligonucleotides. The court stated that "just as the discovery of properties of a known material does not make it novel, the identification and characterization of a prior art material also does not make it novel." Id.
Here, the same composition is being administered to the same patient class (any subject).
As such, the teachings of Stemmer, which administers SEQ ID NO: 1 to subjects in need thereof, meets the limitations of claim 1, drawn to preventing cognitive decline and neurodegenerative diseases. Similarly, claims 54-56 are met because the “results in” amelioration/reduction/improvement are also an inherent mechanisms of this known method, absent any guidance as to dosages, patient class, or specifics regarding the method of prevention. Claims 57 and 58 are met because Alzheimer’s would also be prevented by administering SEQ ID NO: 1 to a subject. Claim 59 is met for the same preventative reasons as claim 53. Claim 60 is met because Stemmer teaches a peptide 100% identical to SEQ ID NO: 1. Claims 62-64 are also drawn to inherent biological functions that are modulated by administration of the same composition to the same patient class. Claim 65 is met because SEQ ID NO: 1 is in a pharmaceutical formulation when administered (p. 23, Col. 1). Claim 67 is met for the same reason as claim 53; however, it is drawn to improving at least one of cognitive decline, long term memory, etc., which also does not limit the patient class from including any subject, so the same patient class is receiving the same composition as it is in Stemmer, and the “improves” is inherent, absent evidence to the contrary. Claim 68 is met because Stemmer teaches a sequence 100% identical to SEQ ID NO: 1. As to claims 66 and 71, the subjects had previously received chemotherapy and pain killers (Spanning p. 23-24), which are additional agents that were administered consecutively, as there is no time frame provided in the claims and no additional agent named in the claims. For these reasons, the limitations of claims 53-68 and 71 are met by Stemmer.
Claim Rejections 35 USC 103(A)
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.
Claims 53-68, 70 and 71 are rejected under 35 U.S.C. 103 as being unpatentable over Stemmer, as applied to claims 53-68 and 71 above, and in further view of Couvineau et al. (Frontiers in Endocrinology, September 2018, Vol. 9, No. 573).
The teachings of Stemmer have been described supra.
The difference between the prior art and the instant claims is that the prior art does not teach that Orexin receptor agonists were also administered to the subjects.
Couvineau teaches that Orexins (OxA and OxB) are hypothalamic neuropeptides involved in central nervous system (CNS) to control the sleep/wake process, which is mediated by two G protein-coupled receptor subtypes, OX1R, and OX2R. in addition to these central effects, orexins also play a role and are present in various peripheral organs, such as the intestine, pancreas, adrenal glands, kidney, adipose tissue and reproductive tract (abstract). This reference further teaches that the anti-tumoral role of orexins is mediated by a signaling pathway involving the presence of two immunoreceptor tyrosine-based inhibitory motifs in both orexin receptors subtypes, the recruitment of the phosphotyrosine phosphatase (SHP2) and the induction of mitochondrial apoptosis, making these receptor antagonists (abstract). This reference further teaches that studies have shown orexin’s role in the CNS, as well as it efficacy in colon, pancreatic, prostate and other cancers (throughout article). For example, an in vivo study using xenografted mouse model revealed that daily intraperitoneal injection of OxA induced a strong reduction of tumor volume and in colon cancer (p. 3, Col. 2; p. 4, Fig. 2).
As such, it would have been obvious to one of ordinary skill in the art at the effective filing date of the invention to have taken the OxA of Couvineau and administered it as an additional agent in the method of Stemmer because both are used for the same purpose of treating cancer, specifically colon cancer. One would be motivated to add an Orexin antagonist to this treatment because Couvineau teaches that they have been found to be highly effective in treating colon cancer. As such, there is a reasonable expectation of success that the orexin antagonist of Couvineau can be effectively combined with the method of Stemmer to treat cancer.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 53-68 and 70 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims of U.S. Patent No. 10,933,117 Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of 109 teach the following:
1. A method of treatment of cancer in a patient in need thereof, comprising administering to said patient a therapeutically effective amount of an isolated peptide comprising the amino acid sequence denoted by SEQ ID NO. 1 or a pharmaceutically acceptable salt of said isolated peptide in combination with doxorubicin, wherein said isolated peptide reduces the standard of care administered dose of doxorubicin.
2. The method according to claim 1, wherein the administered dose of doxorubicin is lower than the standard of care dose of doxorubicin by at least about 1%-50%, about 5%-45%, about 10%-40%, about 15%-35% or about 20%-30%.
3. The method according to claim 1, wherein said isolated peptide and doxorubicin are administered concomitantly or consecutively.
4. The method according to claim 1, wherein said cancer is pancreatic cancer, ovarian cancer, spindle cell neoplasm of neural origin, spindle cell neoplasm, metastatic colorectal cancer, colon cancer, colorectal cancer, colon adenocarcinoma, rectal cancer, rectal adenocarcinoma, lung cancer, non-small cell lung carcinoma, spinal cord neoplasm, breast cancer, skin cancer, renal cancer, multiple myeloma, thyroid cancer, prostate cancer, adenocarcinoma, head and neck cancer, gastrointestinal cancer, stomach cancer, cancer of the small intestine, hepatic carcinoma, liver cancer or malignancies of the female genital tract.
5. The method according to claim 1, wherein said isolated peptide consists of the amino acid sequence denoted by SEQ ID NO. 1 or a pharmaceutically acceptable salt thereof.
6. The method according to claim 1, wherein said isolated peptide or a pharmaceutically acceptable salt thereof is administered at a dose of about 5 mg/m.sup.2 to about 100 mg/m.sup.2.
7. The method according to claim 1, wherein said isolated peptide or a pharmaceutically acceptable salt thereof is administered at a frequency of once, twice or thrice per week.
8. The method according to claim 1, wherein said method further comprises administering at least one additional anti-cancer agent.
This meets the limitations of instant claims 53-64 because it is the same drug being given to the same patient class, so it will inherently have the same preventative effects on any subject, including those with cancer. Claim 65 is met because claim 5 teaches a pharmaceutical composition. Instant claims 66 and 71 are met because claim 1 teaches administering doxorubicin and claim 3 teaches that administration is concurrent or consecutive. Claims 67 and 68 are met for the same reasons, as above, because the same patient class in need of improving cognitive function, memory, etc. is any subject, as the specification does not carve out which specific subjects are in need of such treatment.
Claims 53-68 and 70 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims of U.S. Patent No. 11,813,305. Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of ‘317 teach the following:
1. A method of treatment of cancer in a patient in need thereof, comprising administering to said patient a therapeutically effective amount of an isolated peptide comprising the amino acid sequence denoted by SEQ ID NO. 1 or a pharmaceutically acceptable salt of said isolated peptide in combination with an anti-cancer agent, wherein said isolated peptide reduces the standard of care administered dose of said anti-cancer agent, and wherein said anti-cancer agent is an anti-PDL1 antibody.
2. The method of claim 1, wherein the administered dose of said anti-cancer agent is lower than the standard of care dose of said anti-cancer agent by at least 1%-50%.
3. The method of claim 1, wherein said cancer is selected from the group consisting of pancreatic cancer, ovarian cancer, spindle cell neoplasm of neural origin, spindle cell neoplasm, metastatic colorectal cancer, colon cancer, colorectal cancer, colon adenocarcinoma, rectal cancer, rectal adenocarcinoma, lung cancer, non-small cell lung carcinoma, spinal cord neoplasm, breast cancer, skin cancer, renal cancer, multiple myeloma, thyroid cancer, prostate cancer, adenocarcinoma, head and neck cancer, gastrointestinal cancer, stomach cancer, cancer of the small intestine, hepatic carcinoma, liver cancer and malignancies of the female genital tract.
4. The method of claim 1, wherein said isolated peptide consists of the amino acid sequence denoted by SEQ ID NO. 1 or a pharmaceutically acceptable salt thereof.
5. The method of claim 1, wherein said isolated peptide or a pharmaceutically acceptable salt thereof is administered at a dose of between 5 mg/m.sup.2 and 100 mg/m.sup.2.
6. The method of claim 1, wherein said isolated peptide or a pharmaceutically acceptable salt thereof is administered at a frequency of once, twice or trice per week.
7. The method of claim 1, wherein said method further comprises administering at least one additional anti-cancer agent.
This meets the limitations of instant claims 53-64 because it is the same drug (SEQ ID NO: 1) being given to the same patient class, so it will inherently have the same preventative effects on any subject, including those with cancer, as is taught by claim 1 of ‘317. Claim 65 is met because claim 5 teaches a pharmaceutical composition. Instant claims 66 and 71 are met because claim 1 of ‘317 teaches administering anti-PD-1 antibody administration in combination, which would necessarily be either concurrent or concomitant, if administered as a combination therapy. Claims 67 and 68 are met for the same reasons, as above, because the same patient class in need of improving cognitive function, memory, etc. is any subject, as the specification does not carve out which specific subjects are in need of such treatment, as is taught by claim 1.
Claims 53-68, 70 and 71 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims of U.S. Patent No. 10,933,117, as applied to claims 53-68 and 71 above, and in further view of Couvineau (see above citation).
The teachings of ‘117 have been described supra.
The difference between the ‘117 and the instant claims is that the prior art does not teach that Orexin receptor agonists were also administered to the subjects.
The teachings of Couvineau have also been described supra.
It would have been obvious to one of ordinary skill in the art at the effective filing date of the invention to have taken the OxA of Couvineau and administered it as an additional agent in the method of ‘117 because both are used for the same purpose of treating cancer, specifically colon cancer. One would be motivated to add an Orexin antagonist to this treatment because Couvineau teaches that they have been found to be highly effective in treating colon cancer. As such, there is a reasonable expectation of success that the orexin antagonist of Couvineau can be effectively combined with the method of ‘117 to treat cancer.
Claims 53-68, 70 and 71 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims of U.S. Patent No. 11,813,305, as applied to claims 53-68 and 71 above, and in further view of Couvineau (see above citation).
The teachings of ‘305 have been described supra.
The difference between ‘305 and the instant claims is that the instant claims do not teach adding orexin.
The teachings of Couvineau have also been described supra.
It would have been obvious to one of ordinary skill in the art at the effective filing date of the invention to have taken the OxA of Couvineau and administered it as an additional agent in the method of ‘305 because both are used for the same purpose of treating cancer, specifically colon cancer. One would be motivated to add an Orexin antagonist to this treatment because Couvineau teaches that they have been found to be highly effective in treating colon cancer. As such, there is a reasonable expectation of success that the orexin antagonist of Couvineau can be effectively combined with the method of ‘305 to treat cancer.
Conclusion
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/JEANETTE M LIEB/Primary Examiner, Art Unit 1654