DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application is being examined under the pre-AIA first to invent provisions.
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission of RCE on 2/27/26 and the amendment of claims has been entered.
Election/Restrictions
Applicant’s election without traverse of Group I, claimed in claims 1-8, 21 and 22 was previously acknowledged. Election was made without traverse of 1) a peptide of up to amino acids comprising an alpha domain of alpha lactalbumin’ 2) gastrointestinal tract cancer; 3) HAMLET and 4) SEQ ID NO: 3.
In the reply filed 8/6/25, Applicants amended claims 1-2 and canceled claims 3-7 and 11. Claims 26-28 were added.
In the RCE filed 2/27/26, Applicants amended claim 1 and canceled claims 2, 27 and 28.
Claims 9-10, 12, 16-20 and 24-25 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) /as being drawn to a nonelected group, there being no allowable generic or linking claim.
Claims 1,2, 8-10, 12 and 16-26 are pending.
Claims 1, 8, 21-22 and 26 read on Group I and the elected species and are under consideration.
Claim Rejections - 35 USC § 112-Maintained
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.
The rejection of claims 1, 8, 21-22 and 26 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for reducing formation of colon cancer tumors and treating colon cancer with HAMLET or BAMLET does not reasonably provide enablement for preventing formation of a GI tract cancer in an individual that does not have GI tract cancer, wherein the GI tract cancer has aberrant activation of Wnt/β-catenin signaling and/or shows a loss of APC function is maintained. Please note this rejection has been modified necessitated by amendment of the claims.
The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the invention commensurate in scope with these claims.
As stated in MPEP 2164.01(a), “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.”
The factors to be considered when determining whether a disclosure meets the enablement requirement of 35 USC 112, first paragraph, were described in In re Wands, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988) as:
1. the nature of the invention;
2. the breadth of the claims;
3. the state of the prior art;
4. the relative skill of those in the art;
5. the predictability or unpredictability of the art;
6. the amount of direction or guidance presented [by the inventor];
7. the presence or absence of working examples; and
8. the quantity of experimentation necessary to make and/or use the invention.
(1) The Nature of the Invention
Claim 1 is directed to a method for preventing formation of a GI tract cancer in an individual that does not have a GI tract cancer, wherein the GI tract cancer has aberrant activation of Wnt/β-catenin signaling and/or shows a loss of APC function wherein the method comprises administering to the individual a biologically active complex comprising (a) alpha-lactalbumin; a variant of alpha-lactalbumin comprising an alpha-domain having at least 94% sequence identity to alpha-lactalbumin; or a peptide of up to 50 amino acids comprising (i) an alpha-domain with at least 94% sequence identity to the Alpha 1 or Alpha 2 domain of alpha lactalbumin; or (ii) an alpha domain with at least 94% sequence identity to SEQ ID NO: 2 or SEQ ID NO: 4 and and a fatty acid or a salt thereof, wherein the fatty acid is oleic acid or a salt thereof.
(2) The Breadth of the claims
The claims will be given its broadest reasonable interpretation. The applicable rule for interpreting the claims is that “each claim must be separately analyzed and given its broadest reasonable interpretation in light of and consistent with the written description.” See MPEP 2163(II)(1), citing In re Morris, 127 F.3d 1048, 1053-1054; 44 USPQ2d 1023, 1027 (Fed. Cir. 1997). In view of this rule, Claim 1 is drawn to preventing formation of any GI tract cancer in an individual that does not have a GI tract cancer, wherein the GI tract cancer has aberrant activation of Wnt/β-catenin signaling and/or shows a loss of APC function with the biologically active complex of claim 1. The claims are extremely broad due to the great number of GI tract cancers known in the art.
(3) The state of the prior art and (5) The predictability or unpredictability of the art
The instant application is enabling for treating and reducing formation of colon cancer tumors by administration of HAMLET or BAMLET.
The Stony Brook Cancer Center (https://cancer.stonybrookmedicine.edu/GICancer/Types accessed 9/24/25) teaches different types of GI tract cancers to include advanced abdominal. Advanced abdominal cancers refers to a variety of cancers affecting digestive system organs including the stomach, liver, large and small intestines, pancreas, gall bladder and esophagus. Bile duct cancer includes three types” intrahepatic, perihilar and distal. Therefore, the limitation of GI tract cancers includes many different types of cancers that affect different organs of the GI tract.
The Cleveland Clinic (https://my.clevelandclinic.org/health/diseases/15806-pancreatic-cancer accessed 9/24/25) teaches that pancreatic cancer cannot be prevented but there are things to be done to lower the risk, such as not smoking, eating fresh fruit and vegetables and maintaining a healthy weight. There was not teaching or suggestion in the art that administering HAMLET, BAMLET or any other compound/agent would be able to prevent the formation of pancreatic cancer.
Schatoff et al. (Curr. Colorectal cancer Rep (2017) 13:101-110) reviews the difficulty in even treating cancers. Schatoff et al. teach that Wnt signaling pathway is a critical mediator of tissue homeostasis and repair and is frequently co-opted during tumor development. Schatoff et al. teach that almost all colorectal cancers demonstrate hyperactivation of the Wnt pathway. Importantly, Schatoff et al. teach that to date, this vast knowledge has not translated into effective treatment (Abstract and p. 101, 1st col.). Schatoff et al. also states despite the overwhelming evidence that Wnt pathway hyperactivation drives CRC, targeting Wnt therapies have not made headway in the clinic (p. 105, 2nd col). Therefore, even with the knowledge that a cancer exhibits Wnt/β-catenin pathway activation did not provide predictable results for identifying a viable therapeutic intervention. The predictability is even less apparent for prevention, which requires determining whether administration of a particular agent with actually prevent or reduce the occurrence of the cancer.
Giardiello et al. (N Engl J Med 2002;346:1054-1059) teach that familial adenomatous polyposis is caused by germ line mutation in the adenomatous polyposis coli gene and is characterized by development of hundreds of colorectal adenomas and eventually colorectal cancer (Abstract). Giardiello et al. teach that tested whether sulindac can prevent adenomas (Abstract). Giardiello et al. teach that did not prevent the development of adenomas in subjects with familial adenomatous polyposis (Abstract). Therefore, an agent known for treatment of adenomas did not predict that the same agent would prevent the adenomas from developing.
There was no prior art found that discloses HAMLET/BAMLET or another biologically active complex that meets the limitations of claim 1, that are sufficient to prevent formation of all GI tract cancers required by claim 1.
However, the art is supportive of treatment of some cancer types with HAMLET or BAMLET. Storm et al. (“Conserved features of cancer cells define their sensitivity of HAMLET-induced death; c-Myc and glycolysis” Oncogene; epub 6/6/2011, cited on IDS) teach that HAMLET has broad tumoricidal activity to leukemia cell, carcinoma cells, glioma cells,/ bladder cancers and skin papilloma, wherein healthy differentiated cells survive HAMLET challenge (p. 4766, 1st col., 2nd para.). Storm et al. teach HAMLET sensitivity of cancer cells was shown to be dependent on c-Myc oncogene expression and the glycolytic machinery of the cells (Conclusion).
Therefore, the state of the art at the time of the application is that the etiology and treatment/prevention of different cancers is not well understood and therapy is challenging and complex. Adding to the complexity are the many different types of proliferative diseases and cancers known in the art. Therefore, there is uncertainty in prevention. As presented above, even in a genetically defined condition caused by APC mutations, preventative efficacy was not predictable.
It would be unduly burdensome and require undue experimentation to screen patients early in the disease process or even before the disease process to identify the population for “preventing”. Identifying patients for prevention would also be unduly burdensome because risk factors for GI tract cancers includes being male, ethnicity and H. pylori infection to name a few (American Cancer Society https://www.cancer.org/cancer/types/stomach-cancer/causes-risks-prevention/risk-factors.html> accessed 9/24/25). Therefore, if one considers the risk factors, almost everyone is risk and need of prevention.
It is noted that pharmaceutical and biological art is generally unpredictable, requiring each embodiment to be individually assessed for physiological activity. Furthermore, “GI tract cancers” encompasses many different types of cancer that have different etiologies and pathologies. Given this fact, historically the development of new drugs has been difficult and time-consuming. Adding to the unpredictability is that many treatment options may show promise in animal models, but may fail to show therapeutic improvement in clinical trials. There is no absolute predictability, even in view of the high level of skill in the art.
Thus, for preventing formation of GI tract cancers, the possibilities are vast. For example, the pathology and etiology pancreatic cancer is distinct from the etiology and pathology of esophageal cancer. With respect to cancer, each type of cancer manifests differently and involves different cell types/organs and it would be highly unpredictable given the art and the breadth of the claims to determine if the biologically active complex of claim 1 would be able to prevent formation of all GI tract cancers with Wnt/ β-catenin and/or APC dysfunction.
(4) The relative skill of those in the art
MPEP 2141.03 states (in part)” A person of ordinary skill in the art is also a person of ordinary creativity, not an automaton.” KSR International Co. v. Teleflex Inc., 127 S.Ct. 1727, 167 LEd2d 705, 82 USPQ2d 1385, 1397 (2007). “[I]n many cases a person of ordinary skill will be able to fit the teachings of multiple patents together like pieces of a puzzle.” Id. Office personnel may also take into account “the inferences and creative steps that a person of ordinary skill in the art would employ.” Id. At 1396, 82 USPQ2d at 1396. The “hypothetical person having ordinary skill in the art’ to which the claimed subject matter pertains would, of necessity have the capability of understanding the scientific and engineering principles applicable to the pertinent art.” Ex parte Hiyamizu, 10 USPQ2d 1393, 1394 (Bd. Pat. App. & Inter. 1988) (disagreeing with the examiner’s definition of one of ordinary skill in the art (i.e. a doctorate level engineer or scientist working at least 40 hours per week in semiconductor research or development), and finding that the hypothetical person is not definable by way of credentials, and that the evidence in the application did not support the conclusion that such a person would require a doctorate or equivalent knowledge in science or engineering). In the instant case, the skill in the art high with respect to physicians and scientists. The level of skill in the art (physicians and scientists) would be high.
(6) The amount of direction or guidance presented (by the inventor) and (7) The presence or absence of working examples
The applicant provided sufficient guidance or direction regarding treating and reducing formation of colon cancer tumors with HAMLET. Applicants provide in vivo data showing the biologically active complex, HAMLET administered to APCMin mice reduced tumor burden and increases survival (Fig. 1). The applicant provided guidance regarding administering HAMLET to the drinking water from the time of weaning until week 17 (controls received drinking water alone). H&E staining of the intestinal segments confirmed fewer and smaller tumors were observed compared to control.
In contrast, the applicant provides little in way of direction or guidance regarding preventing or treating other types of GI tract cancers with the biologically active complex of claim 1.
Therefore, the specification and working examples provided by the applicant support treating and reducing formation of colon tumors with HAMLET/BAMLET.
(8) The quantity of experimentation necessary (to make and/or use the invention)
Owing to the factors listed above, especially in points 6 and 7, the amount of experimentation needed will be extensive in view of the lack of guidance by the inventor.
MPEP 2164.01(a) states, “A conclusion of lack of enablement means that, based on the evidence regarding each of the above factors, the specification, at the time the application was filed, would not have taught one skilled in the art how to make and/or use the full scope of the claimed invention without undue experimentation. In re Wright, 999 F.2d 1557,1562, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993).” That conclusion is clearly justified here.
The instant breadth of the claim is broader than the disclosure, specifically, the instant claims are directed to preventing cancer but the specification, prior art or instant disclosure does not provide support for this.
In conclusion, the instant application is enabled for reducing formation of colon cancer tumors and treating colon cancer with HAMLET or BAMLET, but does not reasonably provide enablement for preventing formation of gastrointestinal tract cancers with the biologically active complex of claim 1.
Response to Arguments
Applicant's arguments filed 8/6/25 have been fully considered but they are not persuasive. Applicants argue that the Examiners assertion of lack of enablement is regarding GI tract cancers generally. However, the amended claims are directed to cancer unified by shared molecule features, APC dysfunction and/or aberrant Wnt/β-catenin signaling. Applicants argue that APC loss and aberrant Wnt/β-catenin activation are well established causative drivers of defined GI tract malignancies. Applicants argue that the specification ties biological activity to suppression of the Wnt/β-catenin pathway (reduced β-catenin staining in treated tumors, reduced cyclin D1,VEGF…, identification of HAMLET as a new Wnt pathway modifier and whole genome profiling confirming downregulation of Wnt pathway genes) and the disease features of claim 1 reflect the cancer mechanisms disclosed in the application. Applicants argue that the specification discloses both treatment and prevention. Applicants argue that APC loss and aberrant Wnt activation are initiating events in the tested model and further emphasized the prophylactic significance of the findings. Applicants argue the experimental record confirms that the claimed biologically active complexes directly modulate this very pathway in vivo (see Declaration). Applicants argue that in light of the mechanistic alignment, a person of ordinary skill in the art would not need to engage in undue experimentation to apply the disclosed pathway modulating complexes to GI tract cancers characterized by the same APC/Wnt abnormality. Applicants argue that the Declaration by Dr. Svanborg confirms that BAMLET administration in ApcMin/+ mice resulting in reduced tumor burden in a genetically APC driven model, β-catenin levels were reduced in treated tissues, gene expression patterns confirmed suppression of Wnt/β-catenin signaling and given this mechanistic alignment PHOSITA would not require undue experimentation. Applicants argue that the data in Exhibit A further demonstrate that the claimed biologically active complexes reduced β-catenin staining in the lung, liver and kidney tissue, downregulation of Wnt/β-catenin associated gene expression networks, reduction of proliferative foci and extended survival relative to sham treated animals. Applicants argue that the data establishes that suppression of Wnt/β-catenin pathway by the claimed biological active complexes is conserved and reproducible across tissues. Applicants argue that structural genus of claim 1 are directly supported by the specification, with multiple representative complexes disclosed. Applicants further argue that undue experimentation is not required because the prior art strongly supports predictability within the defined pathway context. Applicants argue that the working examples in the specification demonstrate reduction of β-catenin levels, suppression of β-catenin dependent proteins…and improved survival of APC driven mice. Applicants argue that the Declaration confirms this data established mechanistic alignment between the claimed complexes and APC/Wnt driven tumorigenesis and would not require undue experimentation for PHOSITA to practice the invention. Applicants argue that enablement does not require proof for every conceivable cancer subtype or every theoretical variant, it requires that the specification teach those skill in the art how to practice the claimed invention without undue experimentation.
These arguments are not persuasive because as indicated above, GI tract cancers include different types of cancers that differ in etiology and pathology, it would be highly unlikely and require undue experimentation to determine if the biological complex of claim 1 could prevent formation of GI tract cancers, even those limited to aberrant Wnt/β-catenin and/or loss of APC function. The applicant provided sufficient guidance or direction regarding treating and reducing formation of colon cancer tumors with HAMLET. Applicants provide in vivo data showing the biologically active complex, HAMLET administered to APCMin mice reduced tumor burden and increases survival (Fig. 1). The applicant provided guidance regarding administering HAMLET to the drinking water from the time of weaning until week 17 (controls received drinking water alone). H&E staining of the intestinal segments confirmed fewer and smaller tumors were observed compared to control. However, this data does not establish that prevention is established across Wnt/β-catenin or loss of APC function among the GI tract cancers. The APC min model represents a particular APC driven intestinal neoplasm model and does not reproduce other important aspects of other GI tract cancers. Importantly, APC mutation and Wnt/β-catenin activation are not the only factors in cancer development and growth. For example, other genetic signaling and alterations in that signaling can affect tumor growth and development. Showing that HAMLET and BAMLET suppresses Wnt/β-catenin signaling in a specific model does not establish that HAMLET and BAMLET would prevent other GI tract cancers encompassed by the claim. The argument of reduced β-catenin staining among other tissues does not establish that cancer was prevented. Gene expression in live or kidney or other organs may show that HAMLET or BAMLET may affect the pathway, however that does not establish that cancer was prevented. The identification of a common pathway does not eliminate unpredictability association with prevention. This is established by Giardiello, that discloses sulindac which is known to exhibit activity against APC tumors, yet failed to prevent adenomas development. The Examiner maintains that it would be unduly burdensome and require undue experimentation to screen patients early in the disease process or even before the disease process to identify the population for “preventing”. Identifying patients for prevention would also be unduly burdensome because risk factors for GI tract cancers includes being male, ethnicity and H. pylori infection to name a few (American Cancer Society). Therefore, if one considers the risk factors, almost everyone is risk and need of prevention. For the reasons presented above, the rejection is maintained.
Response to Amendment
The Declaration under 37 CFR 1.132 filed is insufficient to overcome the rejection of claims. The Declaration discloses that BAMLET and HAMLET demonstrated tumoricidal activity in multiple cancer cell lines and reduced tumor burdens in animal models, including models relevant to intestinal tumor development. The Declaration states that the enclosed data demonstrates in the tissues examined, administration of BAMLET was associated with reduced β-catenin staining and modulation of gene expression patters consistent with downregulation of Wnt/ β-catenin signaling. The Declaration states that aberrant activation of Wnt/ β-catenin signaling and loss of APC function are well known in the scientific literature as drivers of colorectal carcinogenesis and are implication in additional GI tract cancers. The Declaration states that based on the pathway modulation observed and the reduction in tumor burden in the experimental systems provided, the data supports the biological plausibility that administration of such complexes may have preventative utility in GI tract cancers characterized by aberrant Wnt/ β-catenin signaling or loss of APC. The Declaration states that the conclusions are based on demonstrated in vivo reduction of tumor burden in genetically defined APC driven model, direct evidence of β-catenin pathway modulation and established scientific understanding that aberrant Wnt/ β-catenin activation is a causative driver in defined GI tract cancers. Given this mechanistic alignment, PHOSITA would not be required to engage in undue experimentation.
The Declaration and Exhibit A were considered in detail but remain unpersuasive. The Examiner is not disputing that HAMLET and BAMLET have antitumor activity or that Wnt/β-catenin and APC function are important for some GI tract cancers. In fact, the evidence may establish the plausibility of HAMLET and BAMLET in the treatment of cancers with aberrant Wnt/ β-catenin signaling or APC dysfunction. However, biological plausibility in treatment specific cancers does not establish the plausibility in preventing such cancers. The Examiner is of the position that the disclosure does not enable one of ordinary skill in the art to achieve prevention of the claimed GI tract cancers without undue experimentation. In particular, the Declaration and Exhibit A disclose that HAMLET and BAMLET kill cancer cells, however the cells are already transformed (they are already cancer). The evidence provided that they reduce tumor burden demonstrates an effect on existing tumors and does not establish that the tumors were prevented from occurring. Evidence that HAMLET And BAMLET reduce β-catenin staining demonstrates the ability to affect the pathway, but does not establish that the agents will prevent the cancer from occurring. As presented above, the state of the art establishes this point. Giardiello et al. teach that an agent known for treatment of the cancer was unable to prevent the cancer from forming. Therefore, demonstration that the agents have antitumor activity does not predict efficacy in preventing tumors. The disclosure and Exhibit A provide sufficient guidance regarding prevention of colon cancer in a specific model. However, in order to determine if HAMLET and BAMLET would be able to prevent all GI tract cancers involving Wnt/β-catenin signaling and/or APC function would require substantial testing and importantly identification of subjects in need of prevention. The Examiner maintains that it would be unduly burdensome and require undue experimentation to screen patients early in the disease process or even before the disease process to identify the population for “preventing”. Identifying patients for prevention would also be unduly burdensome because risk factors for GI tract cancers includes being male, ethnicity and H. pylori infection to name a few (American Cancer Society). Therefore, if one considers the risk factors, almost everyone is risk and need of prevention. In conclusion, establishing that HAMLET and BAMLET modulate a cancer pathway that is known, is not equivalent to demonstrating modulating that pathway would prevent the cancer from occurring. For the reasons presented above, the rejection is maintained.
Double Patenting-Maintained
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.
The rejection of claims 1, 8 and 26 on the grounds of nonstatutory double patenting as being unpatentable over claims 7-8 of U.S. Patent No. 11,103,561 is maintained. Although the claims at issue are not identical, they are not patentably distinct from each other because the USPN claims a method of preventing or treating a proliferative disease, comprising administering an effective amount of the composition of claim 1, wherein the proliferative disease is colon cancer. Colon cancer is a GI tract cancer and a carcinoma. As evidenced by the instant specification, colon cancer is a carcinoma. The USPN uses the colon cancer model of APCmin (Fig. 1). As evidenced by the USPN, aberrant activation of Wnt/B-catenin signaling is fundamental to the pathogenesis of colon cancer (bottom of col. 10). Therefore, the claims of the USPN anticipate the instant claims.
The rejection of claims 1, 8, 21-22 and 26 on the grounds of nonstatutory double patenting as being unpatentable over claims 1-11 of U.S. Patent No. 11,865,161 is maintained. Although the , claims at issue are not identical, they are not patentably distinct from each other because the USPN claims a method for preventing formation of colon cancer comprising administering a biologically active complex comprising alpha-lactalbumin, a variant of alpha-lactalbumin or a peptide of up to 50 amino acids comprising the alpha domain of alpha-lactalbumin and a fatty acid or salt thereof (claim 1). The USPN also claims the fatty acid is oleic acid, the biologically active complex is HAMLET or BAMLET, is SEQ ID NO: 3 or 5, wherein the variant of alpha-lactalbumin comprises the sequence of native mature alpha lactalbumin wherein all of the cysteines have mutated. Colon cancer is a GI tract cancer and a carcinoma. The USPN uses the colon cancer model of APCmin (Fig. 1). As evidenced by the USPN, aberrant activation of Wnt/B-catenin signaling is fundamental to the pathogenesis of colon cancer (col. 11, lines 26-27). Therefore, the USPN anticipates the instant claims.
Response to Arguments
Applicant's arguments filed 2/27/26 have been fully considered but they are not persuasive. Applicants request that double patenting rejection over USPN 11,103,561 and 11,865,161 be held in abeyance until claims are indicated allowable.
This argument is not persuasive as no allowable subject matter has been indicated. The claims remain rejection.
New Rejection
Claims 1, 8, 21-22 and 26 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 7-9, 13-14, 16-18, 22-30 of copending Application No. 19/117,750 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the copending application claims preventing or treating cancer comprising administering alpha lactalbumin and fatty acid or lipid or salt thereof. The compound is identical to instant claimed compound. The copending application claims the compound is administered to the GI tract , where the cancer is a GI tract cancer, wherein the fatty acid is oleic acid.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to TARA L MARTINEZ whose telephone number is (571)270-1470. The examiner can normally be reached Mon-Fri 8:00-5:00.
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/TARA L MARTINEZ/Primary Examiner, Art Unit 1654
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