DETAILED ACTION
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 filed 02/20/2024 is a National Stage entry of PCT/AU2022/050932 , International Filing Date: 08/19/2022 claims foreign priority to 2021902626, filed 08/20/2021.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 05/31/2024 is in compliance with the
provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the
examiner.
Claim Status
The claim listing filed 09/26/2024 is pending. Claims 1-16 are currently amended. Claims 1-16 are pending and under examination.
Claim Objections
Claims 1, 12, 14, 15 and 16 are objected to because of the following informalities: Examiner respectfully requests capitalizing sequences: Claim 1, lines 6 and 7; claim 12, lines 5 and 6; claim 14, lines 5 and 6; claim 15, line 6; claim 16, line 6. Appropriate correction is required.
Claim 6 is objected to because of the following informalities: Examiner respectfully requests spelling out GVHD in the first use of this acronym. Appropriate correction is required.
Claim Rejections - 35 USC § 112
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 1-16 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, does not reasonably provide enablement for preventing an autoimmune disorder. 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. This is a scope of enablement rejection.
Claim 1 is directed to a method of treating or preventing an autoimmune disorder in a subject.
Claim 6 is directed to the method wherein the autoimmune disorder is allergic asthma, RA, MS, SLE, IDDM, psoriasis, scleroderma, glomerular nephritis, ankylosing spondylitis and GVHD as claimed.
Embodiments of the specification disclose "treating" includes therapeutic treatment [0051] -a therapeutic result in this context includes eradication or lessening of symptom. A therapeutic result need not be a complete amelioration of the condition (i.e. a cure) ([0055], last 3 lines). The instant specification is enabling for a method of treatment as disclosed, comprising administering the peptide, and quantifying experimental changes as demonstrated in a representative example for IL-2, in Fig 2g. The specification is not enabling for preventing an autoimmune disorder in claim 1, and the dependent claims, wherein “preventing" as disclosed, includes either preventing the onset of a disorder or a symptom of a disorder altogether or delaying the onset of disorder or a symptom of a disorder [0052].
As stated in § MPEP 2164.01(a), “there are many factors to consider when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any experimentation is ‘undue’. These factors include, but are not limited to:
1. The breadth of the claims;
2. The nature of the invention;
3. The state of the prior art;
4. The level of skill in the art;
5. The level of predictability in the art;
6. The amount of direction provided by the inventor;
7. The presence or absence of working examples;
8. The quantity of experimentation needed to make or use the invention based on the
disclosure.
See in re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988). The eight Wands
factors are applied to claims 1-16 as follows:
The breadth of the claims and the nature of the invention
Claims 1-16 are directed to a method of treating or preventing an autoimmune disorder in a subject comprising administering to the subject a therapeutically effective amount of peptide.
In Fig 2g, for example, the specification discloses a method of treatment, comprising administering the peptide, and quantifying significantly enhanced IL-2 production by isolated, anti CD3+ T cells [0181]. The specification does not provide evidence of a method of preventing an autoimmune disorder in a subject, preventing onset of an autoimmune disorder [0052]. Therefore, the claims are unduly broad with respect to preventing an autoimmune disorder.
The State of the Prior Art
It is noted that there is no prior art that teaches a method of preventing an autoimmune disorder wherein the disorder consists of allergic asthma, RA, MS, SLE, IDDM, psoriasis, scleroderma, glomerular nephritis, ankylosing spondylitis and GVHD as claimed.
The Level of Skill in the Art
Practitioners in this art (physicians/immunologists) would presumably be highly skilled in the art for providing a method of prevention for the disorders as claimed.
The Level of Predictability in the Art
It is noted that the therapeutic art is unpredictable, requiring each embodiment to be
individually assessed for physiological activity. The amount of guidance or direction needed to enable
the invention is inversely related to the amount of knowledge in the state of the art as well as the
predictability in the art. In re Fisher, 427 F.2d 833, 839, 166 USPQ 18, 24 (CCPA 1970). This is because it
is not obvious from the disclosure, of a specific method of preventing an autoimmune disorder. In the instant case, the specification discloses IL-2 production for isolated monocyte and anti-CD-stimulated PBMC cultures and inhibition of IL-12p40 upon treatment with peptide (Fig 3e-h). The specification does not demonstrate preventing an autoimmune disorder in a subject. Without any experimentation demonstrating the claimed method, the level of unpredictability remains high. Therefore, it is unpredictable that the peptide composition will function in the treatment method as claimed.
The amount of Direction Provided by the Inventor and The Presence or Absence of
Working Examples
The instant specification does not provide adequate guidance with regard to preventing an autoimmune disorder in a subject. Applicant’s limited disclosure is noted but is not sufficient to justify claiming the method broadly. Absent a reasonable a priori expectation of success for preventing, one skilled in the art would have to extensively test the peptide composition, determine an effective dose on a subject, ascertain prevention of onset of an autoimmune disorder, etc. Since each prospective
embodiment, and indeed future embodiments as the art progresses, would have to be empirically
tested, and those which initially failed tested further, an undue amount of experimentation would be required to practice the invention as it is claimed in its current scope, because the specification provides
inadequate guidance to do otherwise. The amount of direction or guidance presented in the
specification is very limited. As discussed in “[t]he Level of Predictability in the Art” section supra, the
specification teaches working examples of inhibition of IL-12p40 upon treatment with peptide (Fig 3e-h).
There is no prior art that teaches prevention of autoimmunity using the peptide composition, in a subject. Also, as noted in the “Breadth of the Claims and Nature of Invention” section, the specification does not provide evidence that a subject is administered a therapeutically effective amount for prevention of an autoimmune disorder.
As such, the examples used in the specification are not indicative broadly of a method of
preventing with the desired result of preventing onset of an autoimmune disorder [0052]. It is further noted that Applicant provides no data, examples, figures, etc. demonstrating a subject or an effective amount of peptide for prevention. In the absence of such information, a person of ordinary skill in the art would reasonably require undue quantity of experimentation.
Conclusion of Enablement Analysis 35 USC § 112(a)
MPEP § 2164.01(a), 4th paragraph states that “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).
After applying the Wands factors and analysis to claims 1-16, in view of the Applicant’s
entire disclosure, it is concluded that the practice of the invention as claimed in claims 1-16
would not be enabled by the written disclosure for treatment of a disorder. Therefore claims 1-16 are rejected under 35 U.S.C. §112(a) for failing to disclose sufficient information to enable a person of
skill in the art to prevent autoimmunity in a subject as claimed.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1-8, 12-16 are rejected under 35 U.S.C. 102 (a)(1) and 35 U.S.C. 102 (a)(2) as being anticipated by Agrez, Michael, Valentine, hereinafter Agrez (Agrez, Michael, Valentine; WO2019/218015A1; published 21 Nov 2019).
The applied reference has a common Applicant and inventor with the instant application. Based upon the earlier effectively filed date of the reference, it constitutes prior art under 35 U.S.C. 102(a)(2). This rejection under 35 U.S.C. 102(a)(2) might be overcome by: (1) a showing under 37 CFR 1.130(a) that the subject matter disclosed in the reference was obtained directly or indirectly from the inventor or a joint inventor of this application and is thus not prior art in accordance with 35 U.S.C. 102(b)(2)(A); (2) a showing under 37 CFR 1.130(b) of a prior public disclosure under 35 U.S.C. 102(b)(2)(B) if the same invention is not being claimed; or (3) a statement pursuant to 35 U.S.C. 102(b)(2)(C) establishing that, not later than the effective filing date of the claimed invention, the subject matter disclosed in the reference and the claimed invention were either owned by the same person or subject to an obligation of assignment to the same person or subject to a joint research agreement.
Regarding claim 1, Examiner interprets ‘comprising an amino acid sequence’ as inclusive or open-ended (MPEP§ 2111.03 (I)), therefore, SEQ ID NO: 1 and SEQ ID NO: 2 as recited, is with any N/C terminal additions. The claim limitation ‘group consisting of’ is interpreted as a Markush group presenting a closed set of alternatives. Accordingly, Agrez teaches a method of treating age-related immune dysfunction (i.e. autoimmunity disorder) in a subject, the method comprising administering to the subject a composition comprising a peptide for activating Lck (See page 11, line 34). Agrez teaches Lck activating polyarginine polypeptides (see Fig 6, Fig 37, Fig 38; SEQ ID NO: 65; Example 5; RSKAKNPLY-RRRRRRRRR-(2Adod)4-NH2 ("IK14804")). Specifically, Agrez teaches RSKAKNPLYR-(2Adod)4-NH2 (i.e. SEQ ID NO: 1) which is 100 % identical to the SEQ ID NO: 1 peptide as claimed.
Regarding claim 2, Agrez teaches Interleukin -2 (IL-2) is a growth-promoting cytokine that is produced primarily by helper T cells and regulates growth and function of various cells that are involved in cellular and humoral immunity. The expression of IL-2 decreases with age (i.e. dysregulated IL-2 homeostasis) and this decline has been shown to parallel the age-related decrease in immunologic function (see page 87, line 29).
Regarding claim 3, the rejection is noted above in the teachings in Agrez (see page 87, line 29).
Regarding claim 4, the rejection is noted above in the teachings in Agrez (see page 87, line 29).
Regarding claim 5, Agrez teaches a method of treating age-related immune dysfunction (i.e. autoimmunity disorder) in a subject (see page 11, line 34); the expression of IL-2 decreases with age (i.e. deficient) (see page 87, line 29). Agrez teaches that Lck activating peptides increase IL-2Ra (CD25) expression on a T cell line (Figure 10), CD4+ T cells (Figure 11 ), CD4+ and CDS+ cells within PBMCs (Figure 13), and increase the proliferation of CDS+ T cells (Figure 20, Figure 21, Figure 27), and the proliferation of NK cells (Example 20). Accordingly, the Lck activating peptides in Agrez, increase the physiological effects of IL-2Ra (see page 88, line 4). Notably, Agrez teaches a method of reducing T cell exhaustion (page 72, line 20), wherein IL-2 production and cytokine polyfunctionality, is lost early (See page 73, line 17)
Regarding claim 6, Agrez teaches immune dysfunction (i.e. autoimmunity disorder) in a subject, the method comprising administering to the subject a composition comprising a peptide for activating Lck (See page 11, line 34). Although Agrez does not specifically list allergic asthma,…GVHD, immune dysfunction as disclosed in Agrez, encompasses the recited claim limitation.
Regarding claim 7, Agrez teaches a method of treating age-related immune dysfunction (i.e. autoimmunity disorder) in a subject (see page 11, line 34); the expression of IL-2 decreases with age (i.e. deficient) (see page 87, line 29).
Regarding claim 8, in addition to the rejection noted above for claim 7, Agrez discloses that compromised IFN gamma production in the elderly contributes to the immune risk phenotype and the reduced capacity to produce this cytokine in the elderly disease susceptibility with aging (see page 84, line 25).
Regarding claim 12, Agrez teaches that IK14804 increases Lck activity above control by 468 % (see Figure 1, page 178) (i.e. modulates activity of Lck). The claim limitation ‘modulates the …subject’ is interpreted as intended result as the body of the claim fully and intrinsically sets forth all limitations of the claimed invention, and the preamble merely states, for example, the purpose or intended use of the invention, rather than any distinct definition of any of the claimed invention's limitations (See § MPEP 2111.02 (II)).
Regarding claim 13, Agrez teaches in Figure 37 that IK14804 increases IL-2 secretion in a human T lymphocyte (Jurkat) cell line (i.e. T cells). Cells are seeded at 1 million cells per well (12 well plate, 2 mL volume) and stimulated with Biotin-CD3, CD28, and 15 avidin (5 : 5 : 1.25μg) (See page 23, line 11). See Fig 38; see page 165, line 5.
Regarding claim 14, the claim limitation ‘does not..IL-12p40’ is interpreted as intended result as the body of the claim fully and intrinsically sets forth all limitations of the claimed invention.
Regarding claim 15, Agrez teaches oral or topical administration (see page 129, line 33).
Regarding claim 16, Agrez teaches RSKAKNPLYR-(2Adod)4-NH2 (i.e. SEQ ID NO: 1) which is 100 % identical to the SEQ ID NO: 1 peptide as claimed.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries 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.
Claim(s) 1-16 are rejected under 35 U.S.C. 103 as being unpatentable over Agrez, Michael, Valentine, hereinafter Agrez (Agrez, Michael, Valentine; WO2019/218015A1; published 21 Nov 2019).
Regarding claim 9, the teachings in Agrez has been set forth above, for treatment of autoimmune disorder in a subject.
Agrez does not teach treatment of autoimmune disorder in a subject having cancer.
Agrez teaches administration of polypeptides to Lewis Lung Cancer mice (metastatic model) (i.e. subject has cancer) (see page 158, Example 34). See Example 33 and Example 35. Although Agrez teaches IK14800 peptide lacking the fatty acid (i.e. 2Adod), in the cancer model, it would have been prima facie obvious to one of ordinary skill in the art to use peptide IK14804, which Agrez teaches as having Lck activating activity (see Example 40, page 161). One motivated to do so would have a reasonable expectation of success as Agrez discloses in Fig. 1, that IK14804 has a 468% increase in Lck activation above control, versus IK14800 (lacking 2Adod) that demonstrates 377% Lck activation above control.
Regarding a method of treatment of autoimmune disorder in a subject having cancer, obviousness can be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so. In re Kahn, 441 F.3d 977, 986, 78 USPQ2d 1329, 1335 (Fed. Cir. 2006) (discussing rationale underlying the motivation suggestion-teaching test as a guard against using hindsight in an obviousness analysis).
Consequently, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to treat a subject having autoimmune disorder and cancer, as Agrez teaches administration of Lck activating peptides, to a subject, presenting the two conditions individually. One motivated to do so would have a reasonable expectation of success, as the peptides accomplish Lck activation and that Lck activation is demonstrated in the teachings in Agrez for immune dysfunction (i.e. autoimmune disorder) and cancer. Thus, one would have recognized that modifying the teaching of Agrez, would have yielded predictable results and improved the clinical outcome in a subject having autoimmune disorder and cancer (See MPEP § 2143 l(A)(D)).
Regarding claim 10, the rationale for the rejection has been noted above. Agrez teaches suitable drugs conventionally used for the treatment of the particular disease or condition may be utilized with therapeutic agent(s) as described herein in the combination therapy, such as checkpoint blockers (i.e. cancer therapy) (page 126, line 28). Specifically, Agrez teaches Jurkat cells activated by means of exposure to culture dish adhered anti-CD3 antibody to induce cell surface expression of programmed cell death receptor 1 (PD-1 ), and cultured for 48 hours in the absence of additives or with the peptide RSKAKNPLY-RRRRRRRRR-NH2 (IK14800 at 2.5 μM) alone, 5 μg/ml recombinant PD-L 1 (the ligand for PD-1) alone to induce checkpoint blockade in the cells, or with the IK14800 peptide plus recombinant PD-L 1. IL-2R alpha (CD25) is measured in cell lysates by means of a standard commercially available ELISA kit (page 145, lines 1-5).
Regarding claim 11, the rationale for the rejection is noted above.
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.
1. Claims 1-16 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 20 and 21 of U.S. Patent No. 11912789 in view of Agrez, Michael, Valentine, hereinafter Agrez (Agrez, Michael, Valentine; WO2019/218015A1; published 21 Nov 2019). Although the claims at issue are not identical, they are not patentably distinct from each other.
Regarding claim 1, reference patent ‘789 teaches a method of inducing an immune response in a subject, comprising administering to the subject a composition comprising an Lck activating peptide. ‘Comprising’ is open-ended and is interpreted as the sequence in the reference patent with any N/C terminal additions. Accordingly, the peptide sequence in the reference patent (see SEQ ID NO: 12 and SEQ ID NO: 17; is a 100 % match to the instant sequences as claimed. Reference patent ‘789, discloses subject as presenting age-related immune dysfunction (see Col 43, paragraph 9, line 2) (see claim 20).
Regarding claim 2, reference patent ‘789 provides a method of inducing an immune response in a subject (see claim 20). Embodiments of the specification in the reference patent ‘789, disclose that the expression of IL-2 decreases with age and this decline has been shown to parallel the age-related decrease in immunologic function (see Col 46, line 49).
Regarding claim 3, reference patent ‘789 teaches a method of inducing an immune response in a subject (see claim 20); Reference patent ‘789, discloses subject as presenting age-related immune dysfunction (see Col 43, paragraph 9, line 2).
Reference patent does not teach IL-2 mediated.
Agrez teaches Interleukin -2 (IL-2) is a growth-promoting cytokine that is produced primarily by helper T cells and regulates growth and function of various cells that are involved in cellular and humoral immunity. The expression of IL-2 decreases with age (i.e. dysregulated IL-2 homeostasis) and this decline has been shown to parallel the age-related decrease in immunologic function (see page 87, line 29).
Consequently, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to treat a subject presenting age-related immune dysfunction, as disclosed in the reference patent ‘789, with the teachings in Agrez, demonstrating decrease in IL-2 expression with age. One motivated to do so would have a reasonable expectation of success, as the peptides accomplish treating IL-2 mediated autoimmune disorder. Thus, one would have recognized that modifying the teaching of Agrez, would have yielded predictable results and improved the clinical outcome in a subject having autoimmune disorder mediated by IL-2(See MPEP § 2143 l(A)(D)).
Regarding claim 4, the obviousness rationale has been noted above.
Regarding claim 5, reference patent ‘789 teaches that the expression of IL-2 decreases with age and this decline has been shown to parallel the age-related decrease in immunologic function (see Col 46, line 49). See claim 20.
Regarding claim 6, reference patent ‘789 teaches a method of inducing an immune response in a subject (see claim 20); Reference patent ‘789, discloses subject as presenting age-related immune dysfunction (see Col 43, paragraph 9, line 2).
Reference patent does not teach autoimmunity.
Agrez teaches immune dysfunction (i.e. autoimmunity disorder) in a subject, the method comprising administering to the subject a composition comprising a peptide for activating Lck (See page 11, line 34). Although Agrez does not specifically list allergic asthma.…GVHD, immune dysfunction as disclosed in Agrez, encompasses the recited claim limitation.
Consequently, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to treat a subject with immune dysfunction as disclosed in the reference patent ‘789, with the teachings in Agrez,, as the list of autoimmune disorders encompass immune dysfunction. Thus, one would have recognized that modifying the teaching of Agrez, with the teachings in the reference patent ‘789 would have yielded predictable results and improved the recited list of conditions (See MPEP § 2143 l(A)(D)).
Regarding claim 7, the reference patent ‘789 teaches a method inducing an immune response in a subject (see Col 46, line 49). See claim 20.
Regarding claim 8, reference patent ‘789 does not teach determining the levels of IFNg.
Agrez discloses that compromised IFN gamma production in the elderly contributes to the immune risk phenotype and the reduced capacity to produce this cytokine in the elderly disease susceptibility with aging (see page 84, line 25).
Consequently, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to treat a subject with immune dysfunction as disclosed in the reference patent ‘789, wherein IFN gamma production is compromised as disclosed in the teachings in Agrez. Thus, one would have recognized that modifying the teaching of Agrez, with the teachings in the reference patent ‘789 would have yielded predictable results as the subject population is the same in both references for the method of treatment (See MPEP § 2143 l(A)(D)).
Regarding claim 9, reference patent ‘789 teaches a method of a method of inducing an immune response in a subject (see claim 20). Reference patent teaches a method of treating cancer (see claim 21).
Reference patent does not teach treating autoimmune disorder and cancer.
Agrez teaches administration of polypeptides to Lewis Lung Cancer mice (metastatic model) (i.e. subject has cancer) (see page 158, Example 34). See Example 33 and Example 35. Although Agrez teaches IK14800 peptide lacking the fatty acid (i.e. 2Adod), in the cancer model, it would have been prima facie obvious to one of ordinary skill in the art to use peptide IK14804, which Agrez teaches as having Lck activating activity (see Example 40, page 161). One motivated to do so would have a reasonable expectation of success as Agrez discloses in Fig. 1, that IK14804 has a 468% increase in Lck activation above control, versus IK14800 (lacking 2Adod) that demonstrates 377% Lck activation above control.
Regarding a method of treatment of autoimmune disorder in a subject having cancer, obviousness can be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so. In re Kahn, 441 F.3d 977, 986, 78 USPQ2d 1329, 1335 (Fed. Cir. 2006) (discussing rationale underlying the motivation suggestion-teaching test as a guard against using hindsight in an obviousness analysis).
Consequently, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to treat a subject having autoimmune disorder, as in the teachings in the reference patent ‘789, and cancer, as Agrez teaches administration of Lck activating peptides, to a subject, presenting the two conditions individually. One motivated to do so would have a reasonable expectation of success, as the peptides accomplish Lck activation and that Lck activation is demonstrated in the teachings in Agrez for immune dysfunction (i.e. autoimmune disorder) and cancer. Thus, one would have recognized that modifying the teaching of Agrez with the teachings in the reference patent ‘789, would have yielded predictable results and improved the clinical outcome in a subject having autoimmune disorder and cancer (See MPEP § 2143 l(A)(D)).
Regarding claim 10, reference patent teaches treating cancer (see claim 21).
Reference patent ‘789 does not teach subject receiving cancer therapy.
Rationale for the rejection has been noted above. Agrez teaches suitable drugs conventionally used for the treatment of the particular disease or condition may be utilized with therapeutic agent(s) as described herein in the combination therapy, such as checkpoint blockers (i.e. cancer therapy) (page 126, line 28). Specifically, Agrez teaches Jurkat cells activated by means of exposure to culture dish adhered anti-CD3 antibody to induce cell surface expression of programmed cell death receptor 1 (PD-1 ), and cultured for 48 hours in the absence of additives or with the peptide RSKAKNPLY-RRRRRRRRR-NH2 (IK14800 at 2.5 μM) alone, 5 μg/ml recombinant PD-L 1 (the ligand for PD-1) alone to induce checkpoint blockade in the cells, or with the IK14800 peptide plus recombinant PD-L 1. IL-2R alpha (CD25) is measured in cell lysates by means of a standard commercially available ELISA kit (page 145, lines 1-5).
Regarding claim 11, the rationale for the rejection is noted above.
Regarding claim 12, the claim limitation ‘modulates the …subject’ is interpreted as intended result as the body of the claim fully and intrinsically sets forth all limitations of the claimed invention, and the preamble merely states, for example, the purpose or intended use of the invention, rather than any distinct definition of any of the claimed invention's limitations (See § MPEP 2111.02 (II)). See claim 20 in reference patent ‘789.
Regarding claim 13, Agrez teaches in Figure 37 that IK14804 increases IL-2 secretion in a human T lymphocyte (Jurkat) cell line (i.e. T cells). Cells are seeded at 1 million cells per well (12 well plate, 2 mL volume) and stimulated with Biotin-CD3, CD28, and 15 avidin (5 : 5 : 1.25μg) (See page 23, line 11). See Fig 38; see page 165, line 5.
Regarding claim 14, the claim limitation ‘does not...IL-12p40’ is interpreted as intended result as the body of the claim fully and intrinsically sets forth all limitations of the claimed invention. See claim 20.
Regarding claim 15, Agrez teaches oral or topical administration (see page 129, line 33).
Regarding claim 16, reference patent ‘789 teaches SEQ ID NO: 12 and SEQ ID NO: 17. See claim 20.
Conclusion
No claim is allowed.
Correspondence
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ARCHANA VARADARAJ whose telephone number is (571)272-2366. The examiner can normally be reached Monday-Friday 10:00am-5:00pm.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Melissa Fisher can be reached at 5712707430. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/ARCHANA VARADARAJ/ Examiner, Art Unit 1658
/Melissa L Fisher/ Supervisory Patent Examiner, Art Unit 1658
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