DETAILED ACTION
Election/Restrictions
Applicant's election with traverse of Group I and CCT2 inhibitor in the reply filed on March 25 2026 is acknowledged. The traversal is on the ground(s) that the special technical feature of Group I is present and in common with Group II and that they both possess a common technical feature that makes a contribution over the prior art. It is argued that the present genus of 8 CCT inhibitors represent a finite number of species and Applicants should not be required to elect a species. This is not found persuasive because firstly, while the claims do recite 8 different CCT inhibitors, each of these groups is in and of itself a genus. These inhibitors include small molecules, antibodies, peptides, siRNA, etc. as recited in claim 4. Therefore, the examiner cannot agree that there is a finite number of species. Secondly, while applicants contend the common technical feature makes a contribution over the prior art, no evidence or explanation as to what applicants view as the special technical feature and how this feature makes a contribution over the prior art. As set forth in the restriction requirement set forth in the Action mailed on 2/11/26, Khaled et al. teaches treating a subject with a CCT inhibitor.
The requirement is still deemed proper and is therefore made FINAL.
Claims 1-2, 4-8, 10-11, 15, 22, 32-34, 36-39, 41-42 and 46 are pending in the application. Claims 32-34, 36-39, 41-42 and 46 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected invention, there being no allowable generic or linking claim.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 March 25 2026. Accordingly, claims 1-2, 4-8, 10-11, 15 and 22 are being examined on the merits herein.
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 .
Priority
This application is a 371 of PCT/US2022/019165 (03/07/2022) which claims benefit of 63/157,051 (03/05/2021) as reflected in the filing receipt issued on January 24 2024.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on January 3 2024, September 10 2025 and March 25 2026 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Drawings
The drawings are objected to for the following reasons: 37 C.F.R. 1.84 states “Character of lines, numbers, and letters. All drawings must be made by a process which will give them satisfactory reproduction characteristics. Every line, number, and letter must be durable, clean, black (except for color drawings), sufficiently dense and dark, and uniformly thick and well-defined.”
In the current case, the words in Figures 1A-C, 3D, 7A-B, 9A-C, 10A, 12A-B, 15A-B, 16A-D, 17A-B, 17C-D, 18A-C, 24A, 31A-B, 32A-B, 34B, 35C-D, 36A-C and 42A-B are illegible.
Figure 31A-B additionally are objected to because the two graphs for GLUT1 do not contain a description for either the x-axis or the y-axis. The graph does not indicate what is measured.
Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Claim Rejections - 35 USC § 112-Written Description
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1-2, 4, 7-8, 10-11, 15 and 22 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.
The specification discloses chemicals, such as a CT20p peptide and those specifically of SEQ ID NO: 1-6, which meet the written description and enablement provisions of 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph. However, claim(s) 1-2, 4, 7-8, 10-11 is(are) directed to encompass any CCT inhibitor or more specifically any CCT1/CCT2/CCT3/CCT4/CCT5/CCT6/CCT7/CCT8 inhibitor, which only correspond in some undefined way to specifically instantly disclosed chemicals. While claim 4 refers to classes of inhibitors, these recitations are still broad and provide no structural information except for potentially containing amino acids (antibody, peptide, polypeptide) or nucleic acids (siRNA or short hairpin RNA). None of these inhibitors meet the written description provision of 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, due to lacking chemical structural information for what they are and chemical structures are highly variant and encompass a myriad of possibilities. The specification provides insufficient written description to support the genus encompassed by the claim. Note: MPEP 2163.
Vas-Cath Inc. v. Mahurkar, 19 USPQ2d 1111, (Fed. Cir. 1991), makes clear that "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.)
Univ. of Rochester v. G.D. Searle, 69 USPQ2d 1886, 1892 (CAFC 2004), further supports this by stating that:
The appearance of mere indistinct words in a specification or a claim, even an original claim, does not necessarily satisfy that requirement. A description of an anti-inflammatory steroid, i.e., a steroid (a generic structural term) described even in terms of its functioning of lessening inflammation of tissues fails to distinguish any steroid from others having the same activity or function. A description of what a material does, rather than of what it is, usually does not suffice…. The disclosure must allow one skilled in the art to visualize or recognize the identity of the subject matter purportedly described. (Emphasis added).
With the exception of the above specifically disclosed chemical structures, the skilled artisan cannot envision the detailed chemical structure of the encompassed inhibitor, 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 for isolating it. The chemical structure itself is required. See Fiers v. Revel, 25 USPQ2d 1601, 1606 (Fed. Circ. 1993) and Amgen Inc. V. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016, (Fed. Cir. 1991). In Fiddes v. Baird, 30 USPQ2d 1481, 1483, (Bd. Pat. App. & Int. 1993), claims directed to mammalian FGF's were found unpatentable due to lack of written description for the broad class. The specification provided only the bovine sequence. Finally, University of California v. Eli Lilly and Co., 43 USPQ2d 1398, 1404, 1405 (Fed. Cir. 1997) held that:
...To fulfill the written description requirement, a patent specification must describe an invention and do so in sufficient detail that one skilled in the art can clearly conclude that "the inventor invented the claimed invention." Lockwood v. American Airlines, Inc., 107 F.3d 1565, 1572, 41 USPQ2d 1961, 1966 (Fed. Cir. 1997); In re Gosteli, 872 F.2d 1008, 1012, 10 USPQ2d 1614, 1618 (Fed. Cir. 1989) (" [T]he description must clearly allow persons of ordinary skill in the art to recognize that [the inventor] invented what is claimed."). Thus, an applicant complies with the written description requirement "by describing the invention, with all its claimed limitations, not that which makes it obvious," and by using "such descriptive means as words, structures, figures, diagrams, formulas, etc., that set forth the claimed invention." Lockwood, 107 F.3d at 1572, 41 USPQ2d at 1966.
Furthermore, to the extent that a functional description can meet the requirement for an adequate written description, it can do so only in accordance with PTO guidelines stating that the requirement can be met by disclosing “sufficiently detailed, relevant identifying characteristics,” including “functional characteristics when coupled with a known or disclosed correlation between function and structure.” Univ. of Rochester v. G.D. Searle, 68 USPQ2d 1424, 1432 (DC WNY 2003).
The instant claims recite the use of any CCT inhibitor which can then be used to treat any cancer or any drug-resistant cancer. The state of the art supports that chaperonin containing TCP-1 controls the development of malignant tumors as taught by Zheng et al. (Int J Oncol, 2023). This review article makes it clear that CCT is involved in the growth of numerous malignant tumors (abstract). This reference teaches that exploring genes that can inhibit CCT expression or developing inhibitors against CCT may become the focus of future research. It is taught that miR-148a/152 can inhibit the migration, invention and proliferation of CD44+/CD133+ colon cancer stem cells and promote their apoptosis by inhibiting CCT6a expression. CT20p can induce the death of neuroblastoma cells (page 2, left column, first paragraph). Mk2206, inhibitors the growth of CCT3 overexpressing lung cancer cells (page 2, left column, last paragraph). Therefore, while CCT inhibition is suggested in the art as being desirable and various different groups have identified a couple different inhibitors including CT20p, it does not appear that there is a specific structural relationship between the known inhibitors and any compound whether that is a small molecule, nucleic acid or peptide/antibody that could inhibit any of the CCT. Jia et al. (Toxin, 2024) recognizes that HSF1A is a CCT inhibitor (abstract). Therefore, the state of the art recognizes that there are a couple known CCT inhibitors including CT20p which is taught in the instant specification. But nothing in the art supports a structural-functional relationship between a compound and CCT inhibition.
In contrast, the instant specification, see for example page 24 paragraph 103., describes a variety of cell cycle inhibitors which would be representative of the scope of the claimed inhibitors.
Therefore, only the above chemically structurally defined chemicals, but not the full breadth of the claim(s) meet the written description provision of 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph. The species specifically disclosed are not representative of the genus because the genus is highly variant. Applicant is reminded that Vas-Cath makes clear that the written description provision of 35 USC § 112 is severable from its enablement provision. (See page 1115.)
Claim Rejections - 35 USC § 112-Enablement
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1-2, 4-8, 10-11, 15 and 22 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 a cancer associated with an increase or elevated expression of CCT, does not reasonably provide enablement for treating any cancer or drug-resistant cancer with any CCT inhibitor. 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. This is a scope of enablement rejection.
To be enabling, the specification of the patent must teach those skilled in the art how to make and use the full scope of the claimed invention without undue experimentation. In re Wright, 999 F.2d 1557, 1561 (Fed. Cir. 1993). Explaining what is meant by “undue experimentation,” the Federal Circuit has stated:
The test is not merely quantitative, since a considerable amount of experimentation is permissible, if it is merely routine, or if the specification in question provides a reasonable amount of guidance with respect to the direction in which the experimentation should proceed to enable the determination of how to practice a desired embodiment of the claimed invention. PPG v. Guardian, 75 F.3d 1558, 1564 (Fed. Cir. 1996).
The factors that may be considered in determining whether a disclosure would require undue experimentation are set forth by In re Wands, 8 USPQ2d 1400 (CAFC 1988) at 1404 where the court set forth the eight factors to consider when assessing if a disclosure would have required undue experimentation. Citing Ex parte Formal, 230 USPQ 546 (BdApls 1986) at 547 the court recited eight factors:
1) the quantity of experimentation necessary,
2) the amount of direction or guidance provided,
3) the presence or absence of working examples,
4) the nature of the invention,
5) the state of the prior art,
6) the relative skill of those in the art,
7) the predictability of the art, and
8) the breadth of the claims.
These factors are always applied against the background understanding that scope of enablement varies inversely with the degree of unpredictability involved. In re Fisher, 57 CCPA 1099, 1108, 427 F.2d 833, 839, 166 USPQ 18, 24 (1970). Keeping that in mind, the Wands factors are relevant to the instant fact situation for the following reasons:
The breadth of the claims and Nature of the Invention
The claims are very broad in that they claim treating any cancer or any drug-resistant cancer in a subject in need thereof comprising administering a therapeutically effective amount of any CCT inhibitor.
The Relative Skill Level, the State of the Prior Art and The Level of
Predictability in the Art
The relative skill of those in the art is high, that of an MD or PHD. Someone with experience in not only drug design but also medical treatments.
Wang et al. is directed to the role of CCT4/ErbB signaling in nephroblastoma: implications for a biomarker of Wilms tumor. It is taught that when CCT4 is activated, the ERBB signal pathway is inhibited, the apoptosis is enhanced, the expression of MMP3/9 is downregulated, and cancer cells’ invasion and metastasis ability is decreased (section 4. Discussion). Studies have shown that in tumor patients, the activation of the ERBB signal pathway and the upregulation of its related genes can promote the transformation of normal cells into tumor cells. In contrast, inhibition of the ERBB signal pathway can restore tumor cells to a non-transformed state in vitro and inhibit the growth of tumor cells in vivo (section 4. Discussion). It is speculated that the low expression of CCT4 promotes the development of nephroblastoma by regulating cell proliferation (section 4. Discussion). This then suggest that in Wilms Tumor, CCT4 inhibition would lead to the development of nephroblastoma not treatment.
Yao et al. teaches that in hepatocellular carcinoma it was found that there was significant increase in TCP1/CCT2/CCT3/CCT4/CCT5/CCT6A/CCT7/CCT8 expressions but also decreased CCT6B expression (abstract). Indicating there is a difference in expression of CCT.
The amount of direction or guidance provided and the presence or absence of working examples
Looking to the instant specification, focus in the treatment methods appear to be with CCT2 and CT20p, see for example the discussion in example 3, example 4 (breast cancer cells), example 5, example 6 and example 7; which is significantly narrower than the breadth of the instant claims.
Example 7 states that targeting CCT (and CCT2 specifically) can be an effective therapeutic approach for breast cancer as well as other cancers in which CCT is highly expressed.
Example 8 states that bioinformatic databases show that pediatric cancers have high levels of CCT2.
The quantity of experimentation necessary
Because of the known unpredictability of the art, and in the absence of experimental evidence, no one skilled in the art would accept the assertion that the instantly claimed agents could be predictably used to treat all cancers with any CCT inhibitor as inferred by the claim and contemplated by the specification. The specification clearly focuses only on CCT2 and repeatedly discusses overexpression (highly expressed/high levels) of CCT2. The state of the art recognizes that there can be different levels of expression of different CCT in different diseases and that low levels of CCT4 (administration of a CCT4 inhibitor would be expected to decrease levels of CCT4) actually promote the development of neuroblastoma. Accordingly, the instant claims do not comply with the enablement requirement of §112, since to practice the invention claimed in the patent a person of ordinary skill in the art would have to engage in undue experimentation, with no assurance of success.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claim(s) 1-2, 4-6, 10-11, 15 and 22 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Khaled et al. (USPGPUB No. 20170165318) as evidenced by Showalter et al. (Scientific Reports, January 21 2020).
The instant application claims a method of treating a cancer or a drug-resistant cancer in a subject in need thereof, comprising administering to the subject a therapeutically effective amount of a chaperonin-containing TCP1 (CCT) inhibitor. As elected the inhibitor is a CCT2 inhibitor. As claimed the inhibitor is a CT20p peptide.
Khaled et al. is directed to method and compositions comprising a CT20 peptide.
Claimed is a method of treating a subject suspected of having a cancer. A therapeutic regimen is initiated if the CCT level in the sample is above a pre-determined threshold level (i.e. there is an elevated CCT level). The therapeutic regimen comprises administering to a subject an effective amount of a composition comprising a CT20 peptide (claim 1). The CT20 peptide comprises an amino acid sequencing having at least 60% identity to SEQ ID NO: 1-6 (claim 2). Cancers include breast cancer (claim 10).
As shown below SEQ ID NO: 1 of Khaled et al. has 100% identity to instantly claimed SEQ ID NO: 1.
PNG
media_image1.png
187
660
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Greyscale
SEQ ID NO: 2 of Khaled et al. has 100% identity to instantly claimed SEQ ID No: 2 as shown below:
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160
740
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Greyscale
SEQ ID NO: 3-6 of Khaled et al. has 100% identity to instantly claimed SEQ ID NO: 3-6.
Therefore, Khaled et al. teaches administering to the same subject (i.e. a subject with cancer such as breast cancer), the same amount (i.e. effective amount), the same inhibitor (i.e. CT20p peptide).
Regarding the claimed CCT2, as evidenced by Showalter et al., CT20p directly interacts with CCT2 (page 2, 2nd complete paragraph).
Regarding claim 10, Khaled et al. claims that the pre-determined range of CCT amounts can be obtained from subject having been diagnosed with metastatic cancer, not having metastatic cancer, or any combination thereof (claim 18). It is taught targeting CCT in cells comprising a CT20 peptide wherein the cells include metastatic cancer cells (paragraph 0084; 0100; 0117; 0124; 0137; 0212; 0243).
Regarding claim 15, Khaled et al. expressly claims the cancer is breast cancer. As evidenced by Showalter et al., CDK2 and CDK4 are increased in breast cancer cells (page 6, last paragraph).
Regarding claim 22, this claim merely recites the drug-resistant cancer and does not actually require the subject to have a drug-resistant cancer. Therefore, this claim does not distinguish the instant claims from the subjects taught in Khaled et al.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102 of this title, 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.
The factual inquiries set forth in Graham v. John Deere Co., 383 U.S. 1, 148 USPQ 459 (1966), that are applied for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 7-8, 15 and 22 are rejected under 35 U.S.C. 103 as being unpatentable over Khaled et al. (USPGPUB No. 20170165318) as applied to claims 1-2, 4-6, 10-11, 15 and 22 above in view of Showalter et al. (Scientific Reports, January 21 2020) and Guarducci et al. (Breast Care, 2017).
Applicant Claims
The instant application claims further comprising administering to the subject a therapeutically effective amount of a cell cycle inhibitor wherein the cell cycle inhibitor comprises a CCND1 inhibitor, a CDK2 inhibitor, or a CDK4 inhibitor.
The instant application claims wherein the cancer cells obtained from the subject has an increased level of one or more tumor biomarkers selected from the group consisting of MYC, MYCN, CDK2, CDK4, CCNE1, CCND1, YAP1, and RB1 relative to a reference control. While this claim is rejected in the 102 rejection above, in the event Applicants show that this claim is not anticipated, it is obvious for the reasons set forth below.
The instant application claims the drug-resistant cancer is resistant to a cell cycle inhibitor. While this claim does not expressly require the subject to a have a drug-resistant cancer, in the interest of compact prosecution, the examiner interprets claim 22 as limiting the subject to one having a drug-resistant cancer that is resistant to a cell cycle inhibitor.
Determination of the Scope and Content of the Prior Art
(MPEP §2141.01)
The teachings of Khaled et al. are set forth above. Taught is using an anti-cancer or anti-neoplastic drug that can be used in conjugation with a CT20 peptide (paragraph 0077). It is taught that the cancer can be a drug resistant cancer (paragraph 0084; 0100; 0117; 0124; 0137).
Ascertainment of the Difference Between Scope the Prior Art and the Claims
(MPEP §2141.02)
While Khaled et al. teaches an additional drug can be used in conjugation with a CT20 peptide and the cancer can be a drug resistant cancer, Khaled et al. does not expressly teach a cell cycle inhibitor such as a CDK2 or CDK4 inhibitor or that the drug resistant cancer wherein the cancer is resistant to a cell cycle inhibitor. However, these deficiencies are cured by Showalter et al. and Guarducci et al.
Showalter et al. is directed to investigating chaperonin-containing TCP-1 subunit 2 as an essential component of the chaperonin complex for tumorigenesis. As shown in Figure 1A when comparing breast cancer to normal tissue, there was a statistically significant increase in the majority of the genes expressing CCT subunits (Results, page 2). In support of CCT2 driving cell division, examined the levels of CDK4 and CDK2, kinases that are involved in the G1-S phases of the cell cycle. These CDKs could be potential substrates or interactors of CCT (Table 1). CDK2 and CDK4 are increased in breast cancer cells (page 6, last paragraph). Finding that overexpressing CCT2 promoted the proliferation of breast cancer and breast epithelial cells is among the first to demonstrate that an increase in cancer cell growth and upregulation of select CDKs as well as other CCT subunits resulted from overexpressing this single CCT subunit (Discussion, page 8).
Guarducci et al. is directed to mechanisms of resistance to CDK4/6 inhibitors in breast cancer and potential biomarkers of response. Palbociclib (PD0332991), abemaciclib (LY2835219) and ribociclib (LEE011) are selective ATP-competitive, orally administered inhibitors of CDK4 and CDK6. These compounds have been extensively studied in vitro and in vivo and are currently in different stages of clinical development (page 304, last paragraph). Amplification of CCNEI was found in MCF7 with acquired resistance to palbociclib. Silencing of CCNE1 or CDK2 resulted in substantial increase cell-cycle arrest and reduction in cell growth in combination with palbociclib even though in this model p13K inhibition was unable to re-sensitive cells to palbociclib (paragraph bridging columns 306). Gene expression data showed elevated expression of CCND3, CCNE1 and CDKN2D at C1D15 in resistant tumors, suggesting a persistent E2F activity in non-responding tumors (page 307, right column, first paragraph).
Finding of Prima Facie Obviousness Rationale and Motivation
(MPEP §2142-2143)
Regarding claims 7-8, It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Khaled et al., Showalter et al. and Guarducci et al. and administer a CDK2 or CDK4 inhibitor in patients with breast cancer. One skilled in the art would have been motivated to additionally administer these agents as CDK4 inhibitors are known to treat breast cancer as taught by Guarducci et al. Furthermore, Guarducci et al. teaches silencing of CDK2 results in substantial increase in cell-cycle arrest and reduction in cell growth in combination with palbociclib (CDK4 inhibitor). Since Khaled et al. suggests that additional drugs can be administered with the CT20p, there is a reasonable expectation of success. Furthermore, as a general principle it is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose, the idea of combining them flows logically from their having been individually taught in the prior art. See In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) MPEP 2144.06.
Regarding claim 15, Showalter et al. teaches CDK2 and CDK4 are increased in breast cancer cells. Guarducci et al. teaches amplification of CCNEI was found in MCF7 with acquired resistance to palbociclib (CDK4 inhibitor). Gene expression data showed elevated expression of CCND3, CCNE1 and CDKN2D at C1D15 in resistant tumors, suggesting a persistent E2F activity in non-responding tumors. Based on these teachings, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Khaled et al., Showalter et al. and Guarducci et al. and measure tumor biomarkers such as CDK2, CDK4 or CCNE1. One skilled in the art would have expected an increase in these biomarkers as Showalter et al. teaches CDK2/CDK4 are increased in breast cancer cells and Guarducci et al. teaches CCNE1 having elevated expression in resistant tumors.
Regarding claim 22, Khaled et al. teaches administration to cancer cells which are drug resistant. Guarducci et al. teaches that cells can become resistant to CDK4 inhibitors (aka a cell cycle inhibitor). Guarducci et al. also teaches that silencing of CCNE1 or CDK2 resulted in substantial increase cell-cycle arrest and reduction in cell growth in combination with palbociclib even though in this model p13K inhibition was unable to re-sensitive cells to palbociclib. Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Khaled et al., Showalter et al. and Guarducci et al. and administer a combination of CT20p peptide, a CDK2 inhibitor and palbociclib (a CDK4 inhibitor) in cancer cells resistant to a cell cycle inhibitor. One skilled in the art would have been motivated to administer this combination to a subject with cancer that has become resistant to palbociclib with a reasonable expectation of success as Guarducci et al. teaches silencing of CDK2 can sensitize cells to palbociclib.
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 1-2, 4-6 and 22 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 9 of U.S. Patent No. 10973925 as evidenced by Showalter et al. (Scientific Reports, January 21 2020). Although the conflicting claims are not identical, they are not patentably distinct from each other because both sets of claims overlap in scope.
The instant application claims a method of treating a cancer or a drug-resistant cancer in a subject in need thereof, comprising administering to the subject a therapeutically effective amount of a chaperonin-containing TCP1 (CCT) inhibitor. As elected the inhibitor is a CCT2 inhibitor. As claimed the inhibitor is a CT20p peptide.
Patent ‘925 claims a method of treating prostate cancer comprising administer to a subject diagnosed with cancer an effective amount of a nanoparticle comprising a CT20 peptide wherein the peptide is selected from the group consisting of SEQ ID NO: 1-6.
Therefore, Patent ‘925 claims administration to the same subject (e.g. someone with cancer) an effective amount of the same CT20 peptide.
As shown below at least SEQ ID No: 1 of Patent ‘925 has 100% identity to instantly claimed SEQ ID NO: 1
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Regarding the claimed CCT2, as evidenced by Showalter et al., CT20p directly interacts with CCT2 (page 2, 2nd complete paragraph).
Regarding claim 22, this claim merely recites the drug-resistant cancer and does not actually require the subject to have a drug-resistant cancer. Therefore, this claim does not distinguish the instant claims from the subjects taught in Patent ‘925.
Claims 7-8 and 15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 9 of U.S. Patent No. 10973925 as evidenced by Showalter et al. (Scientific Reports, January 21 2020) as applied to claims 1-2, 4-6 and 22 above and in further view of Alvarez-Fernandez et al. (Cancer Cell, 2020). Although the conflicting claims are not identical, they are not patentably distinct from each other because both sets of claims overlap in scope.
The instant application claims further comprising administering to the subject a therapeutically effective amount of a cell cycle inhibitor wherein the cell cycle inhibitor comprises a CCND1 inhibitor, a CDK2 inhibitor, or a CDK4 inhibitor.
The instant application claims wherein the cancer cells obtained from the subject has an increased level of one or more tumor biomarkers selected from the group consisting of MYC, MYCN, CDK2, CDK4, CCNE1, CCND1, YAP1, and RB1 relative to a reference control.
The teachings of Patent ‘925 are set forth above.
While Patent ‘925 claims treating prostate cancer, Patent ‘925 does not claim further administering a therapeutically effective amount of a cell cycle inhibitor. However, this deficiency is cured by Alvarez-Fernandez et al.
Alvarez-Fernandez et al. is directed to mechanism of sensitivity and resistance to CDK4/6 inhibition. CDK4/6 inhibitors also inhibit cell proliferation and cooperate with AR inhibitors in preclinical models of prostate cancer, although this effect seems to be independent on AR activity at least in castration-resistant prostate cancer (page 517, left column). In prostate cancer models, ERK activation is associated to acquired resistance to palbociclib, resulting in sensitization to MEK inhibitors (page 518, left column). CDK4 or CDK6 overexpression leads to resistance to CDK4/6 inhibitors (page 521, left column).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Patent ‘925 and Alvarez-Fernandez et al. and administer a CDK4 inhibitor in combination with the CT20p peptide. One skilled in the art would have been motivated to administer both as both are taught as treating prostate cancer. As a general principle it is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose, the idea of combining them flows logically from their having been individually taught in the prior art. See In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) MPEP 2144.06.
Regarding claim 15, as taught by Alvarez-Fernandez et al. CDK4 overexpression can lead to resistance of CDK4/6 inhibitors. Therefore, in subject with a drug-resistant cancer, one skilled in the art would expect CDK4 overexpression. Thus, cells obtained from a subject who has developed drug-resistant cancer would be expected to have increased level of CDK4.
Claims 1-2, 4-6, 11 and 22 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-13 of U.S. Patent No. 11129868 as evidenced by Showalter et al. (Scientific Reports, January 21 2020). Although the conflicting claims are not identical, they are not patentably distinct from each other because both sets of claims overlap in scope.
The instant claims are set forth above.
Patent ‘868 claims a method of treating a subject having a breast tumor the method comprises initiating a therapeutic regimen wherein the therapeutic regimen comprises administering to the subject an effective amount of a composition comprising a CT20 peptide wherein the CT20 peptide comprises an amino acid sequence of SEQ ID NO: 1 (claim 1). The therapeutic regimen further comprises administration of an anti-cancer agent (claim 2).
Therefore, Patent ‘868 claims administration to the same subject (e.g. someone with cancer) an effective amount of the same CT20 peptide.
As shown below at least SEQ ID No: 1 of Patent ‘868 has 100% identity to instantly claimed SEQ ID NO: 1
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Regarding the claimed CCT2, as evidenced by Showalter et al., CT20p directly interacts with CCT2 (page 2, 2nd complete paragraph).
Regarding claim 15, Patent ‘868 claims the cancer is breast cancer. As evidenced by Showalter et al., CDK2 and CDK4 are increased in breast cancer cells (page 6, last paragraph).
Regarding claim 22, this claim merely recites the drug-resistant cancer and does not actually require the subject to have a drug-resistant cancer. Therefore, this claim does not distinguish the instant claims from the subjects taught in Patent ‘868.
Claims 7-8, 10 and 15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-13 of U.S. Patent No. 11129868 as evidenced by Showalter et al. (Scientific Reports, January 21 2020) as applied to claims 1-2, 4-6, 11 and 22 above and in view of Alvarez-Fernandez et al. Although the conflicting claims are not identical, they are not patentably distinct from each other because both sets of claims overlap in scope.
The instant claims are set forth above.
While Patent ‘868 claims treating breast cancer with a CT20p peptide, Patent ‘848 does not claim further administering a cell cycle inhibitor or that the cells have a higher level of CDK4 biomarker. However, this deficiency is cured by Alvarez-Fernandez et al.
Alvarez-Fernandez et al. is directed to mechanism of sensitivity and resistance to CDK4/6 inhibition. Table 1 teaches CDK4/6 inhibitors in active clinical trials. These include Palbociclib which is approved for metastatic breast cancer, among others. In breast cancers, amplification or overexpression of CCNE1 is correlated (Table 2).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Patent ‘868 and Alvarez-Fernandez et al. and administer a CDK4 inhibitor in combination with the CT20p peptide. One skilled in the art would have been motivated to administer both as both are taught as treating breast cancer. As a general principle it is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose, the idea of combining them flows logically from their having been individually taught in the prior art. See In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) MPEP 2144.06.
Regarding claim 10, Alvarez-Fernandez et al. teaches administration to metastatic breast cancer.
Regarding claim 15, Alvarez-Fernandez et al. teaches that overexpression of CCNE1 is correlated to breast cancer. Thus, in breast cancer subjects one would expect overexpression of this biomarker.
Claims 1-2, 4-6 and 22 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-13 of U.S. Patent No. 12178840 as evidenced by Showalter et al. (Scientific Reports, January 21 2020). Although the conflicting claims are not identical, they are not patentably distinct from each other because both sets of claims overlap in scope.
The instant claims are set forth above.
Patent ‘840 claims a method of treating a subject having lung cancer comprising initiating a therapeutic regimen wherein the therapeutic regimen comprises administering to the subject an effective amount of a composition comprising a CT20 peptide wherein the CT20 peptide comprises an amino acid sequence of SEQ ID NO: 1 (claim 1). The therapeutic regimen further comprises administration of an anti-cancer agent (claim 2).
Therefore, Patent ‘840 claims administration to the same subject (e.g. someone with cancer) an effective amount of the same CT20 peptide.
As shown below at least SEQ ID No: 1 of Patent ‘840 has 100% identity to instantly claimed SEQ ID NO: 1
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Regarding the claimed CCT2, as evidenced by Showalter et al., CT20p directly interacts with CCT2 (page 2, 2nd complete paragraph).
Regarding claim 22, this claim merely recites the drug-resistant cancer and does not actually require the subject to have a drug-resistant cancer. Therefore, this claim does not distinguish the instant claims from the subjects taught in Patent ‘840.
Claims 7-8 and 15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-13 of U.S. Patent No. 12178840 as evidenced by Showalter et al. (Scientific Reports, January 21 2020) as applied to claims 1-2, 4-6 and 22 above in further view of Alvarez-Fernandez et al. Although the conflicting claims are not identical, they are not patentably distinct from each other because both sets of claims overlap in scope.
The instant claims are set forth above.
The teachings of Patent ‘840 are set forth above.
While Patent ‘840 claims treating lung cancer with CT20p peptide, Patent ‘840 does not claim further administering a cell cycle inhibitor. However, this deficiency is cured by Alvarez-Fernandez et al.
Alvarez-Fernandez et al. is directed to mechanism of sensitivity and resistance to CDK4/6 inhibition. Table 1 shows that Trilaciclib is a CDK4 inhibitor for SCLC (non-small cell lung cancer) whereas Lerociclib is a CDK4 inhibitor for non-small cell lung cancer.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Patent ‘840 and Alvarez-Fernandez et al. and administer a CDK4 inhibitor in combination with the CT20p peptide. One skilled in the art would have been motivated to administer both as both are taught as treating lung cancer. As a general principle it is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose, the idea of combining them flows logically from their having been individually taught in the prior art. See In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) MPEP 2144.06.
Regarding claim 15, since CDK4 inhibitors are taught as being associated with treating lung cancer as taught by Alvarez-Fernandez et al., it would be expected that CDK4 would have increased level in lung cancer cells.
Claims 1-2, 4-6, 11 and 22 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-18 of U.S. Patent No. 9040662 as evidenced by Showalter et al. (Scientific Reports, January 21 2020). Although the conflicting claims are not identical, they are not patentably distinct from each other because both sets of claims overlap in scope.
The instant claims are set forth above.
Patent ‘662 claims a method of permeabilizing membranes of cells comprising administering to the cell an effective amount of a CT20p peptide wherein SEQ ID NO: 2-4 or a combination of two or more of SEQ ID NO: 1-4. The cell is a cancer cell wherein the cancer cell is a breast cancer cell, colorectal cancer cell or lung cancer cell or wherein the cancer cell is a drug resistant cancer cell.
Instant SEQ ID NO: 1 has 100% identity to SEQ ID No: 1 of Patent ‘662. It is noted that the instant claims do not exclude the inclusion of additional CT20p peptides.
Therefore, Patent ‘662 claims administration to the same subject (e.g. someone with cancer) an effective amount of the same CT20 peptide.
Regarding the claimed CCT2, as evidenced by Showalter et al., CT20p directly interacts with CCT2 (page 2, 2nd complete paragraph).
Regarding claim 22, this claim merely recites the drug-resistant cancer and does not actually require the subject to have a drug-resistant cancer. Therefore, this claim does not distinguish the instant claims from the subjects taught in Patent ‘662.
Claims 7-8, 10 and 15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-18 of U.S. Patent No. 9040662 as evidenced by Showalter et al. (Scientific Reports, January 21 2020) as applied to claims 1-2, 4-6, 11 and 22 above and in view of Alvarez-Fernandez et al. Although the conflicting claims are not identical, they are not patentably distinct from each other because both sets of claims overlap in scope.
The instant claims are set forth above.
While Patent ‘662 claims treating breast cancer with a CT20p peptide, Patent ‘662 does not claim further administering a cell cycle inhibitor or that the cells have a higher level of CDK4 biomarker. However, this deficiency is cured by Alvarez-Fernandez et al.
Alvarez-Fernandez et al. is directed to mechanism of sensitivity and resistance to CDK4/6 inhibition. Table 1 teaches CDK4/6 inhibitors in active clinical trials. These include Palbociclib which is approved for metastatic breast cancer, among others. In breast cancers, amplification or overexpression of CCNE1 is correlated (Table 2).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Patent ‘662 and Alvarez-Fernandez et al. and administer a CDK4 inhibitor in combination with the CT20p peptide. One skilled in the art would have been motivated to administer both as both are taught as treating breast cancer. As a general principle it is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose, the idea of combining them flows logically from their having been individually taught in the prior art. See In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) MPEP 2144.06.
Regarding claim 10, Alvarez-Fernandez et al. teaches administration to metastatic breast cancer.
Regarding claim 15, Alvarez-Fernandez et al. teaches that overexpression of CCNE1 is correlated to breast cancer. Thus, in breast cancer subjects one would expect overexpression of this biomarker.
Claims 1-2, 4-6, 11 and 22 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-11 of U.S. Patent No. 11179436 as evidenced by Showalter et al. (Scientific Reports, January 21 2020). Although the conflicting claims are not identical, they are not patentably distinct from each other because both sets of claims overlap in scope.
The instant claims are set forth above.
Patent ‘436 claims a method for treating cancer in a subject in need thereof comprising administering to the subject a therapeutically effective amount of a CT20p peptide consisting of SEQ ID No: 1 wherein the cancer is a breast cancer cell, colorectal cancer cell, lung cancer or liver cancer. Administration an additional anti-cancer drug is claimed.
Instant SEQ ID NO: 1 has 100% identity to SEQ ID No: 1 of Patent ‘436.
Therefore, Patent ‘436 claims administration to the same subject (e.g. someone with cancer) an effective amount of the same CT20 peptide.
Regarding the claimed CCT2, as evidenced by Showalter et al., CT20p directly interacts with CCT2 (page 2, 2nd complete paragraph).
Regarding claim 22, this claim merely recites the drug-resistant cancer and does not actually require the subject to have a drug-resistant cancer. Therefore, this claim does not distinguish the instant claims from the subjects taught in Patent ‘436.
Claims 7-8, 10 and 15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-11 of U.S. Patent No. 11179436 as evidenced by Showalter et al. (Scientific Reports, January 21 2020) as applied to claims 1-2, 4-6, 11 and 22 above and in view of Alvarez-Fernandez et al. Although the conflicting claims are not identical, they are not patentably distinct from each other because both sets of claims overlap in scope.
While Patent ‘436 claims treating breast cancer with a CT20p peptide, Patent ‘848 does not claim further administering a cell cycle inhibitor or that the cells have a higher level of CDK4 biomarker. However, this deficiency is cured by Alvarez-Fernandez et al.
Alvarez-Fernandez et al. is directed to mechanism of sensitivity and resistance to CDK4/6 inhibition. Table 1 teaches CDK4/6 inhibitors in active clinical trials. These include Palbociclib which is approved for metastatic breast cancer, among others. In breast cancers, amplification or overexpression of CCNE1 is correlated (Table 2).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Patent ‘436 and Alvarez-Fernandez et al. and administer a CDK4 inhibitor in combination with the CT20p peptide. One skilled in the art would have been motivated to administer both as both are taught as treating breast cancer. As a general principle it is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose, the idea of combining them flows logically from their having been individually taught in the prior art. See In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) MPEP 2144.06.
Regarding claim 10, Alvarez-Fernandez et al. teaches administration to metastatic breast cancer.
Regarding claim 15, Alvarez-Fernandez et al. teaches that overexpression of CCNE1 is correlated to breast cancer. Thus, in breast cancer subjects one would expect overexpression of this biomarker.
Claims 1-2, 4-6, 10-11, 15 and 22 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-9 of U.S. Patent No. 10159706 in view of Khaled et al. as evidenced by Showalter et al. (Scientific Reports, January 21 2020). Although the conflicting claims are not identical, they are not patentably distinct from each other because both sets of claims overlap in scope.
The instant claims are set forth above.
Patent ‘706 claims a composition comprising a C-terminal B cell lymphoma-2 (Bcl-2)-associated X protein (Bax) peptide (CT20p peptide) and a pharmaceutically acceptable carrier, wherein the CT20p peptide consists of the amino acid sequence of SEQ ID NO: 1 or comprises the amino acid sequence of SEQ ID NO: 2, 3, or 4. Instant SEQ ID NO: 1 has 100% identity to SEQ ID No: 1 of Patent ‘706.
Patent ‘706 does not claim a method of treating cancer. However, this deficiency is cured by Khaled et al.
Khaled et al. is directed to method and compositions comprising a CT20 peptide.
Claimed is a method of treating a subject suspected of having a cancer. A therapeutic regimen is initiated if the CCT level in the sample is above a pre-determined threshold level (i.e. there is an elevated CCT level). The therapeutic regimen comprises administering to a subject an effective amount of a composition comprising a CT20 peptide (claim 1). The CT20 peptide comprises an amino acid sequencing having at least 60% identity to SEQ ID NO: 1-6 (claim 2). Cancers include breast cancer (claim 10). SEQ ID NO: 1 of Khaled et al. has 100% identity to instantly claimed SEQ ID No: 1.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Patent ‘706 and Haled et al. and utilize the composition of Patent ’706 in a method of treating cancer. One skilled in the art would have been motivated to utilize the composition in this manner as Patent ‘706 and Khaled et al. both teach SEQ ID NO: 1 and Khaled et al. teaches this peptide can be used to treat cancer.
Regarding the claimed CCT2, as evidenced by Showalter et al., CT20p directly interacts with CCT2 (page 2, 2nd complete paragraph).
Regarding claim 10, Khaled et al. claims that the pre-determined range of CCT amounts can be obtained from subject having been diagnosed with metastatic cancer, not having metastatic cancer, or any combination thereof (claim 18). It is taught targeting CCT in cells comprising a CT20 peptide wherein the cells include metastatic cancer cells (paragraph 0084; 0100; 0117; 0124; 0137; 0212; 0243).
Regarding claim 15, Khaled et al. expressly claims the cancer is breast cancer. As evidenced by Showalter et al., CDK2 and CDK4 are increased in breast cancer cells (page 6, last paragraph).
Regarding claim 22, this claim merely recites the drug-resistant cancer and does not actually require the subject to have a drug-resistant cancer. Therefore, this claim does not distinguish the instant claims from the subjects taught in Patent ‘706.
Claims 7-8 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-9 of U.S. Patent No. 10159706 in view of Khaled et al. as evidenced by Showalter et al. (Scientific Reports, January 21 2020) as applied to claims 1-2, 4-6, 10-11, 15 and 22 above and in further view of Alvarez-Fernandez et al. Although the conflicting claims are not identical, they are not patentably distinct from each other because both sets of claims overlap in scope.
The instant claims are set forth above.
The teachings of Patent ‘706 and Khaled et al. are set forth above.
While treating breast cancer is obvious, administration with a cell cycle inhibitor is not expressly claimed. However, this deficiency is cured by Alvarez-Fernandez et al.
The teachings of Alvarez-Fernandez et al. are set forth above.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Patent ‘706, Khaled et al. and Alvarez-Fernandez et al. and administer a CDK4 inhibitor in combination with the CT20p peptide. One skilled in the art would have been motivated to administer both as both are taught as treating breast cancer. As a general principle it is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose, the idea of combining them flows logically from their having been individually taught in the prior art. See In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) MPEP 2144.06.
Conclusion
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/ABIGAIL VANHORN/Primary Examiner, Art Unit 1636
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