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 .
DETAILED ACTION
Claims 1-42 are pending and under consideration.
It is noted that the prior art does not teach or suggest anti-IL-1β antibodies which comprise the HC CDRs 1-3 and LC CDRs 1-3 as recited by instant claims 4-7. However, claims 1-3 and 8-42 encompass a broad genus of anti-IL-1β antibodies which lacks written description and/or enablement support (see 112(a) rejection below).
Priority
It is acknowledged that this application is a 371 application of International Patent Appl. No. PCT/2021/037390 filed June 15, 2021, which claims the benefit of priority to U.S. Provisional Patent Appl. No. 63/039,680 filed June 16, 2020. The priority date has been established as June 16, 2020.
Information Disclosure Statement
The Information Disclosure Statement filed on 12/15/2022 has been considered and entered by examiner.
Specification
Tables should be numbered in a simple, consecutive sequence using Arabic numerals (e.g., Table 1, Table 2). The disclosure is objected to because of the following informalities: the specification has two Table 1, on pages 16 and 51 of Specification filed 05/15/2026.
Appropriate correction is required.
Claim Objections
Claim 1 is objected to because of the following informalities: “wherein the antibody” (at line 2) should be amended to “wherein the isolated antibody”. Appropriate correction is required.
Claim 4 is objected to because of the following informalities: “wherein the antibody” (at line 1) should be amended to “wherein the isolated antibody”. Appropriate correction is required.
Claim 5 is objected to because of the following informalities: “wherein the antibody” (at line 1) should be amended to “wherein the isolated antibody”. Appropriate correction is required.
Claim 6 is objected to because of the following informalities: “wherein the antibody” (at line 1) should be amended to “wherein the isolated antibody”. Appropriate correction is required.
Claim 7 is objected to because of the following informalities: “wherein the antibody” (at line 1) should be amended to “wherein the isolated antibody”. Appropriate correction is required.
Claim 8 is objected to because of the following informalities: “wherein the antibody” (at line 1) should be amended to “wherein the isolated antibody”. Appropriate correction is required.
Claim 10 is objected to because of the following informalities: “wherein the antibody” (at line 1) should be amended to “wherein the isolated antibody”. Appropriate correction is required.
Claim 12 is objected to because of the following informalities: “wherein the antibody” (at line 1) should be amended to “wherein the isolated antibody”. Appropriate correction is required.
Claim 13 is objected to because of the following informalities: “wherein the antibody” (at line 1) should be amended to “wherein the isolated antibody”. Appropriate correction is required.
Claim 14 is objected to because of the following informalities: “wherein the antibody” (at line 1) should be amended to “wherein the isolated antibody”. Appropriate correction is required.
Claim 15 is objected to because of the following informalities: “wherein the antibody” (at line 1) should be amended to “wherein the isolated antibody”. Appropriate correction is required.
Claim 16 is objected to because of the following informalities: “wherein the antibody” (at line 1) should be amended to “wherein the isolated antibody”. Appropriate correction is required.
Claim 31 is objected to because of the following informalities: “the antibody of claim 1” (at lines 2-3) should be amended to “the isolated antibody of claim 1”. Appropriate correction is required.
Claim 34 is objected to because of the following informalities: “wherein the disease” (at line 1) should be amended to “wherein the IL-1β mediated disease”. Appropriate correction is required.
Claim 40 is objected to because of the following informalities: “the antibody” of claim 40(ii) should be amended to “the isolated antibody of claim 1”. Appropriate correction is required.
Claim 42 is objected to because of the following informalities: “theanti-IL-1β antibody” should be amended to “the isolated antibody of claim 1”. Appropriate correction is required.
Claim Rejections - 35 USC § 112(b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 4-7, and 12 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Regarding claim 4, the phrase "(IgG26)" renders the claim indefinite because it is unclear whether the limitation(s) in the parenthesis is part of the claimed invention. See MPEP § 2173.05(d).
Regarding claim 5, the phrase "(IgGF4)" renders the claim indefinite because it is unclear whether the limitation(s) in the parenthesis is part of the claimed invention. See MPEP § 2173.05(d).
Regarding claim 6, the phrase "(IgG26A)" renders the claim indefinite because it is unclear whether the limitation(s) in the parenthesis is part of the claimed invention. See MPEP § 2173.05(d).
Regarding claim 7, the phrase "(IgG26AW)" renders the claim indefinite because it is unclear whether the limitation(s) in the parenthesis is part of the claimed invention. See MPEP § 2173.05(d).
Regarding claim 12, the phrases "preferably" and “more preferably” render the claim indefinite because it is unclear whether the limitations following the phrases are part of the claimed invention. See MPEP § 2173.05(d).
Claim Rejections - 35 USC § 112(d)
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claim 12 is rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Claim 12, which depends on claim 8, recites: “a VH that is at least 80%, preferably 85%, more preferably 90%, identical to the heavy chain variable domain VH of antibody IgG26, IgGF4, IgG26A or IgG26AW, and a VL that is at least 80%, preferably 85%, more preferably 90%, identical to the VL of antibody IgG26, IgGF4, IgG26A or IgG26AW”. However, the antibody of claim 8 comprises a VH comprising SEQ ID NO: 21 and/or a VL comprising SEQ ID NO: 22. SEQ ID NO: 21 and SEQ ID NO: 22 are the VH and VL of antibody IgG26AW, respectively (as evidenced by SEQENCE LISTING of the instant specification). Thus, claim 12 fails to include all the limitations of claim 8 and broaden the scope of claim 8.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
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 1-3, and 8-42 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 applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention. This is a WRITTEN DESCRIPTION rejection.
Claim 1 is drawn to an antibody which binds to interleukin-1β (IL-1β). The claim recites HC CDR2 comprising more than 8000 variants, HC CDR3 comprising 6 variants, LC CDR1 comprising about 400 variants, and a specific LC CDR3. The claim encompasses even more combinations (millions possible combinations) of these recited CDRs. In addition, claim 1 does not define HC CDR1 or LC CDR2. Thus, the claims encompass unlimited possible combinations for HC CDRs 1-3 and LC CDRs 1-3. These antibodies varies significantly, have different structures and properties.
The specification discloses only a few anti-IL-β antibodies: IgG26, IgGF4, IgG26A, IgG26AW, and variants described in Table 3 of the instant publication US 2023/0220065 A1, all of the antibodies comprise a complete set of HC CDRs 1-3 and LC CDRs 103. The specification does not disclose any other antibodies encompassed by claim 1 with claimed properties (e.g. bind to IL-1β). Thus, the specification fails to provide adequate written description to demonstrate that Applicant was in possession of the claimed genus.
MPEP 2163 II A 3(a) states: Disclosure of an antigen fully characterized by its structure, formula, chemical name, physical properties, or deposit in a public depository does not, without more, provide an adequate written description of an antibody claimed by its binding affinity to that antigen, even when preparation of such an antibody is routine and conventional. See Amgen Inc. v. Sanofi, 872 F.3d 1367, 1378, 124 USPQ2d 1354, 1361 (Fed. Cir. 2017)("knowledge of the chemical structure of an antigen [does not give] the required kind of structure-identifying information about the corresponding antibodies"); see also Centocor Ortho Biotech, Inc. v. Abbott Labs., 636 F.3d 1341, 1351-52, 97 USPQ2d 1870, 1877 (Fed. Cir. 2011)(patent disclosed the antigen the claimed antibody was supposed to bind, but did not disclose any antibodies with the specific claimed properties).
By the time the invention was made, it is well established in the art that the formation of an intact antigen-binding site in an antibody usually required the association of the complete heavy and light chain variable regions of a given antibody, each of which consists of three "complementarity determining regions" ("CDRs") which provide the majority of the contact residues for the binding of the antibody to its target epitope. Even a single point mutation in HCDR1 region could lead to antibody lose its binding activity (Ni et al., The Protein Journal, 43, pp. 683-696, July 2024, see Abstract). Wong (Wong et al., MABS, 2021, Vol. 13, No. 1, e1873478, Publication Year: 2021) teaches that sequence-distant antibodies can target the same epitope (Abstract). Thus, one ordinary skill in the art would not be able to visualize other antibody encompassed by the claims, which binds to IL-1β, based on the disclosed antibodies in the specification.
In the instant case, the specification discloses only a few antibodies IgG26, IgGF4, IgG26A, IgG26AW, and variants described in Table 3 of the instant publication US 2023/0220065 A1 which can bind to IL-1β. Fig. 11 and [0049] of the instant publication US 2023/0220065 A1 show that antibodies IgG26, IgGF4, IgG26A, and IgG26AW have very different therapeutic activities (inhibitory effect on IL-1β signaling). Only IgG26AW shows required therapeutic activity for lung cancer and breast cancer (Examples 7 and 8).
In view of above, these disclosed antibodies would not tell the structure and properties of other antibodies, variants or antibody fragments encompassed by the claims with different combinations of HC CDRs 1-3 and LC CDRs 1-3.
In addition, the claims identify the antibodies by function only, where the function is to:
binding to IL-1β (claim 1);
specifically binding to human IL-1β (claims 9);
cross-reacting with human IL-1β and a non-human IL-1β (claim 10)
treating IL-1β mediated disease including inflammatory disease, an autoimmune disease, or a cancer (claims 31-39).
The specification and prior art have not established the relationship between the claimed functions and the structure of the antibody. One of ordinary skilled in the art would not be able to readily recognize/visualize an antibody with required properties. Taken together, applicant has not provided sufficient evidence to show that the inventors possess a genus of antibodies to IL-1β which have the claimed functions and can be used in the claimed methods.
Although Applicants may argue that it is possible to screen for antibodies with claimed properties/functions, the court found in (Rochester v. Searle, 358 F.3d 916, Fed Cir., 2004) that screening assays are not sufficient to provide adequate written description for an invention because they are merely a wish or plan for obtaining the claimed chemical invention. "As we held in Lilly, "[a]n adequate written description of a DNA ... 'requires a precise definition, such as by structure, formula, chemical name, or physical properties,' not a mere wish or plan for obtaining the claimed chemical invention." 119 F.3d at 1566 (quoting Fiers, 984 F.2d at 1171 ). For reasons stated above, that requirement applies just as well to non-DNA (or RNA) chemical inventions." Knowledge of screening methods provides no information about the structure of any future antibodies or antibody fragments yet to be discovered that may function as claimed.
Claim 2 recites 7 possible HC CDR1 sequences. As set forth above, the claim does not define a complete HC CDRs 1-3 and LC CDRs 1-3 which is required for antigen-binding. In addition, the claim still encompasses large number of variants of CDRs and combinations of CDRs of claim 1.
Claim 3 recites 3 possible LC CDR2 sequences. As set forth above, the claim does not define a complete HC CDRs 1-3 and LC CDRs 1-3 (still lacking HC CDR1) which is required for antigen-binding. In addition, the claim still encompasses large number of variants of CDRs and combinations of CDRs of claim 1.
Claim 8 recites a VH of SEQ ID NO: 21 and/or a VL of SEQ ID NO: 22. By reciting “or”, the claim still encompasses antibodies without complete CDRs of VH or VL. In addition, the claim still encompasses large number of variants of CDRs and combinations of CDRs of VH or VL recited by claim 1.
Claim 12 by reciting at “least 80% identical to VH and VL of antibodies IgG26, IgGF4, IgG26A and IgG26AW”, the claim encompass large number of VH and VL variants ore recited antibodies and the variations can occur at the CDR regions.
Thus, similar to claim 1, claims 2, 3, 8 and 12 also lack written description support.
Claims 9-11, and 13-30 encompass the antibodies of claim 1. Given that the specification lacking written description of the claimed antibodies, logically, the specification also lacks written description to antibody conjugates comprising the antibody, a pharmaceutical composition comprising the antibody, a nucleic acid or a nucleic acid set encoding the antibody; or a host cell comprising the nucleic acid or a nucleic acid set thereof, or a method of using the host cell to produce antibodies.
Claims 31-42 recite different methods of using the antibodies of claim 1. Given that the specification lacking written description of the claimed antibodies, logically, the specification also lacks written description to the methods of using the antibodies. In addition, regarding methods of treating IL-1β mediated diseases, as evidenced by Rébé (Rébé et al., Cancers, 2020, 12, 1791, Publication Date: 07/04/2020), IL-1β is produced and secreted by various cell types, such as immune cells, fibroblasts, or cancer cells. In cancer, IL-1β has pleiotropic effects on immune cells, angiogenesis, cancer cell proliferation, migration, and metastasis. Moreover, anti-cancer treatments are able to promote IL-1β production by cancer or immune cells, with opposite effects on cancer progression (§ Abstract; and Table 1). IL-1β has different effects on immune cells. Thus, its pro- or anti-tumor effect may rely on the type and frequency of immune cells in the tumor (page 13, para. 3). Depending on the cancer type or stage, the main type of immune cells present in the tumor microenvironment, and the anti-cancer treatment used, inhibiting IL-1β may or may not be beneficial for patients (the first paragraph of § 4. Therapeutic Perspective, on page 16). The exact explanation for pro- or anti-tumor effects of IL-1β are not yet known. The level of IL-1β produced, the type of producing cells, the microenvironment, the stage of the cancer, and the anti-cancer-treatment used may all participate in the divergent effects of IL-1β. Similarly, for autoimmune disease such as Rheumatoid arthritis (RA), some of RA patients do not respond to anti-IL-1β antibody (canakinumab) therapy, because the extent of the involvement of IL-1β in the RA disease process, though definitely existent, is not as marked as other cytokines such as tumor necrosis factor-α and IL-6 (see page 7, col. 1, para. 2 of Ait-Oudhia et al., CPT: Pharmacometrics & Systems Pharmacology, (2012) 1, e5, Publication Date: 09/26/2012). In view of above, one of ordinary skill in the art would not recognize that applicant has the possession of the claimed treating methods for all IL-1β mediated diseases and all the claimed antibodies, based on the data disclosed in the specification.
Taken together, the instant specification has not provided a sufficient description showing the necessary functional characteristics coupled with a known or disclosed correlation between functions and the structure. Thus, the specification is not sufficient to show the applicant was in possession of the claimed inventions.
Claims 31-38 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:
a method for treating IL-13 mediated disease in a subject, the method comprising administering to a subject in need thereof an effective amount of the antibody of claim 1, wherein the antibody is IgG26AW, wherein IL-13 mediated disease is a lung cancer or a breast cancer, wherein the subject having a lung cancer or having a breast cancer.
does not reasonably provide enablement for:
a method for treating IL-13 mediated disease in a subject, the method comprising administering to a subject in need thereof an effective amount of the antibody of claim 1.
The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the invention commensurate in scope with these claims. This is a SCOPE OF ENABLEMENT rejection.
To be enabling, the specification 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 that:
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 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 wherein, citing Ex parte Forman, 230 USPQ 546 (Bd. Apls. 1986) at 547, the court recited eight factors to consider when assessing whether or not a disclosure would require undue experimentation. These factors are:
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 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
Nature of invention and breadth of the claims:
The claims are drawn to a method for treating IL-13 mediated disease in a subject, the method comprising administering to a subject in need thereof an effective amount of the antibody of claim 1.
Based on paragraph [0136] of the instant publication US 2023/0220065 A1: IL-1β mediated diseases refers to any medical condition associated with increased levels of IL-1β or increased sensitivity to IL-1β. Thus, the claims encompass a broad genus of diseases, at least including diseases listed in claims 34-38.
Based on paragraph [0153], the term “treating: refers to the term "treating" refers to the application or administration of a composition including one or more active agents to a subject, who has a target disease or disorder, a symptom of the disease/disorder, or a predisposition toward the disease/disorder, with the purpose to cure, heal, alleviate, relieve, alter, remedy, ameliorate, improve, or affect the disorder, the symptom of the disease, or the predisposition toward the disease or disorder. In addition, the subject to be treated is a subject having, suspected of having, or at risk for the IL-1β mediated disease. Given Broadest Reasonable Interpretation (BRI), the claims encompass subjects do not have an IL-1β mediated disease.
Furthermore, as set forth above, claim 1 recites HC CDR2 comprising more than 8000 variants, HC CDR3 comprising 6 variants, LC CDR1 comprising about 400 variants, and a specific LC CDR3. The claim encompasses even more combinations (millions possible combinations) of these recited CDRs. Claim 1 does not define HC CDR1 or LC CDR2. Thus, the claims encompass unlimited possible combinations for HC CDRs 1-3 and LC CDRs 1-3. These antibodies varies significantly, have different antigen-binding structures and therapeutic properties.
Relative skill in the art:
The relative skill of those in the art is high with an MD or a PhD.
Level of unpredictability in the art and State of the prior art:
How an antibody works generally depends on the unique microenvironment and biology of that specific disease. As evidenced by Rébé (Rébé et al., Cancers, 2020, 12, 1791, Publication Date: 07/04/2020), IL-1β is produced and secreted by various cell types, such as immune cells, fibroblasts, or cancer cells. In cancer, IL-1β has pleiotropic effects on immune cells, angiogenesis, cancer cell proliferation, migration, and metastasis. Moreover, anti-cancer treatments are able to promote IL-1β production by cancer or immune cells, with opposite effects on cancer progression (§ Abstract; and Table 1). IL-1β has different effects on immune cells. Thus, its pro- or anti-tumor effect may rely on the type and frequency of immune cells in the tumor (page 13, para. 3). Depending on the cancer type or stage, the main type of immune cells present in the tumor microenvironment, and the anti-cancer treatment used, inhibiting IL-1β may or may not be beneficial for patients (the first paragraph of § 4. Therapeutic Perspective, on page 16). The exact explanation for pro- or anti-tumor effects of IL-1β are not yet known. The level of IL-1β produced, the type of producing cells, the microenvironment, the stage of the cancer, and the anti-cancer-treatment used may all participate in the divergent effects of IL-1β. Similarly, for autoimmune disease such as Rheumatoid arthritis (RA), some of RA patients do not respond to anti-IL-1β antibody (canakinumab) therapy, because the extent of the involvement of IL-1β in the RA disease process, though definitely existent, is not as marked as other cytokines such as tumor necrosis factor-α and IL-6 (see page 7, col. 1, para. 2 of Ait-Oudhia et al., CPT: Pharmacometrics & Systems Pharmacology, (2012) 1, e5, Publication Date: 09/26/2012).
Taken together, it is unpredictable whether an antibody encompassed by claim 1 would be effective to treat an IL-1β mediated disease (e.g. cancer, autoimmune disease) in a subject.
Regarding treating subject at a risk for the IL-1β mediated disease, given Broadest Reasonable Interpretation (BRI), all subjects are at a risk for the IL-1β mediated disease. For example, Brennan (Brennan et al., JNCI J Natl Cancer Inst (2022), 114 (3):djab204, Publication Year: 2022), it is still unclear about the proportion of the cancers which is preventable, both in practice and in theory; for example, what portion is attributable to the environment or lifestyle or genetic inheritance or bad luck. There are important causes that remain to be detected (page 354, col. 2, para. 1). Thus, one of ordinary skill in the art could not predict the claimed antibodies would be able to reduce the risk for an IL-1β mediate disease (including cancer) encompassed by the claims.
Regarding the broadly claimed antibodies, the state of the prior art is such that it involves screening both in vitro and in vivo a large number of antibodies to determine which antibody exhibits the desired therapeutic activities, because even minor changes in the amino acid sequences of the heavy and light variable regions, particularly in the CDRs, may dramatically affect antigen-binding function as evidenced by Ni (Ni et al., The Protein Journal, 43, pp. 683-696, July 2024, see Abstract). Riemer (Riemer et al. Mol Immunol, 2005 42(9): 1121-1124, Publication Date: 2005-01-08) teaches that antibodies binding the same antigens have been shown to both ameliorate and aggravate disease symptoms (entire document, particular page 1123, column 1), indicating unpredictability of therapeutic outcomes. Consistent with prior art, Fig. 11 and [0049] of the instant publication US 2023/0220065 A1 show that antibodies IgG26, IgGF4, IgG26A, and IgG26AW have very different therapeutic activities (inhibitory effect on IL-1β signaling). Only IgG26AW shows required therapeutic activity (Example 6).
As such, one of ordinary skill in the art could not immediately predict, recognize, or distinguish those antibodies that bind an antigen (e.g. IL-1β) with desired therapeutic effect from antibodies that bind the antigen but lack desired therapeutic effect. Thus the prior art teaches the therapeutic effectiveness of an IL-1β antibody of claim 1 for treating an IL-1β mediated disease is not a certainty, and is determined empirically.
Direction or guidance and working examples:
The working example of the specification discloses only one antibody IgG26AW which has anti-cancer activity in vivo for lung cancer and breast cancer (Examples 7 and 8). However, no working example has been demonstrated that administering to a subject with an IL-1β antibody of claim 1 is effective in treating other cancers, or any inflammatory disease, or an autoimmune disease.
The quantity of experimentation needed:
The factors outlined in In Re Wands' mentioned above apply here, and in particular as per the MPEP 2164.01 (a): "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)." It is very clear that one could not make/use this very broad invention that has no working examples in this unpredictable art without undue experimentation. Genetech Inc vs Nova Nordisk 42 USPQ 2d 1001 "A patent is not a hunting license. It is not a reward for search but compensation for its successful conclusion and patent protection is granted in return for an enabling disclosure of an invention, not for vague intimations of general ideas that may or may not be workable.”
Given the unlimited number of IL-1β antibodies encompassed by claim 1 and/or unlimited IL-1β mediated diseases encompassed by claim 31, the lack of specific guidance and the insufficient working examples, undue experimentation would be required of one of skilled in the art to produce the invention commensurate with the scope of the method as claimed.
Related Prior Art
Gram (Gram et al., US 2004/0063913 A1, Publication Date: 04/01/2004) teaches an anti-IL-1β antibody and the use of such antibodies for the treatment of IL-1 mediated diseases and disorders ([0001], [0014]-[0015]). Gram teaches that the specific IL-1β antibody: ACZ885 ([0100]). Gram teaches DNA construct encoding the antibodies (claim 6), an expression vector comprising the DNA construct (claim 8), a process for generating the antibody comprising (i) culturing an organism which is transformed with the expression vector (claim 9). Gram teaches that ACZ885 can neutralize the action of human IL-1β induced IL-6 release (Example 3, [0128]). Gram teaches the IL-1 mediated diseases, including inflammatory conditions, autoimmune diseases ([0088]). However, Gram does not teach the IL-1β antibodies comprising the CDRs as instantly claimed. Given the unpredictability in the art, one of ordinary skill in the art would not be able to reach the claimed antibodies, such as IgG26, IgGF4, IgG26A or IgG26AW.
Masat (Masat et al., US 2008/0044414 A1, Publication Date: 02/21/2008) teaches an IL-1β antibody (claims 1, 2, 8, 9, 35 and 36). Masat teaches a nucleic acid encoding the antibody or antibody fragment of claim 1 (claim 37), a vector comprising the nucleic acid of claim 37 (claim 43), a cell comprising the nucleic acid of claim 37 or the vector of claim 43 (claim 44), a hybridoma that produces the antibody or antibody fragment of claim 1 (claim 47). Masat teaches a method of treating or preventing an IL-1 related disease or condition in a mammal comprising administering an effective amount of the antibody or antibody fragment of claim 1, to a mammal in need thereof, whereby a disease is treated or prevented in the mammal (claim 53), wherein the IL-1 related disease or condition is an inflammatory disease, autoimmune disease, or a cancer (claim 54). However, Masat does not teach the IL-1β antibodies comprising the CDRs as instantly claimed. Given the unpredictability in the art, one of ordinary skill in the art would not be able to reach the claimed antibodies, such as IgG26, IgGF4, IgG26A or IgG26AW.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to CHENG LU whose telephone number is (571)272-0334. The examiner can normally be reached Monday-Friday 8-5.
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/CHENG LU/ Examiner, Art Unit 1642
/SAMIRA J JEAN-LOUIS/ Supervisory Patent Examiner, Art Unit 1642
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