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 .
Claim Status
Applicant’s preliminary amendments and remarks, filed 04/04/2024, are acknowledged.
Claims 1-19 are pending.
As such, claims 1-19 are pending examination and currently under consideration for patentability under 37 CFR 1.104.
DETAILED ACTION
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 07/02/2024 are acknowledged. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Notably, the disclosure statement filed lists a Search Report. The listing of the references cited in a Search Report itself is not considered to be an information disclosure statement (IDS) complying with 37 CFR 1.98. 37 CFR 1.98(a)(2) requires a legible copy of: (1) each foreign patent; (2) each publication or that portion which caused it to be listed; (3) for each cited pending U.S. application, the application specification including claims, and any drawing of the application, or that portion of the application which caused it to be listed including any claims directed to that portion, unless the cited pending U.S. application is stored in the Image File Wrapper (IFW) system; and (4) all other information, or that portion which caused it to be listed. In addition, each IDS must include a list of all patents, publications, applications, or other information submitted for consideration by the Office (see 37 CFR 1.98(a)(1) and (b)), and MPEP § 609.04(a), subsection I. states, "the list ... must be submitted on a separate paper." Therefore, the references cited in the Search Report have not been considered. Applicant is advised that the date of submission of any item of information or any missing element(s) will be the date of submission for purposes of determining compliance with the requirements based on the time of filing the IDS, including all "statement" requirements of 37 CFR 1.97(e). See MPEP § 609.05(a).
Note: If copies of the individual references cited on the Search Report are also cited separately on the IDS (and these references have not been lined-through) they have been considered.
Specification
The abstract of the disclosure is objected to because the abstract is missing a period after “periodontitis”. A corrected abstract of the disclosure is required and must be presented on a separate sheet, apart from any other text. See MPEP § 608.01(b).
The disclosure is objected to because of the following informalities:
[0051]: “significant higher” should read “significantly higher”.
[0051]: “This implicate” should read “This implicates”.
[0051]: “similar with in healthy” should read “within the healthy group”.
[0051]: “among the health” should read “among the healthy group”.
[0051]: “as comparing with health and gingivitis group” should read “as compared to the healthy and gingivitis groups”.
[0051]: “This implicated” should read “This implies”.
[0052]: “could protective” should read “could protect”.
[0052]: “All sample” should read “All samples”.
[0052]: “at the different position” should read “at the different positions”.
[0052]: “represent different of periodontitis progression from severity to normal” should read “represent different periodontitis progression from severe to normal”.
[0052]: “comparing with low does treatment or ligation only” should read “compared to low dose treatment or ligation only”.
[0079]: “Elisa” should read “ELISA”.
Appropriate correction is required.
The use of the term GraphPad Prism, Abcam, and Themo Scientific, which is a trade name or a mark used in commerce, has been noted in this application. The term should be accompanied by the generic terminology; furthermore the term should be capitalized wherever it appears or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the term.
Although the use of trade names and marks used in commerce (i.e., trademarks, service marks, certification marks, and collective marks) are permissible in patent applications, the proprietary nature of the marks should be respected and every effort made to prevent their use in any manner which might adversely affect their validity as commercial marks.
Claim Objections
Claims 4 and 6 are objected to because of the following informalities:
Claim 4: The term “domain” is repeated consecutively. Applicant should remove one of them.
Claim 6: “and IgD domain” should read “an IgD domain”.
Appropriate correction is required.
Claim Interpretation
Examiner acknowledges that the terms “comprises” and/or “comprising”, or “includes” and/or “including” or “has” and/or “having” when used in this specification, specify the presence of stated features, regions, integers, steps, operations, elements, and/or components, but do not preclude the presence or addition of one or more other features, regions, integers, steps, operations, elements, components, and/or groups thereof (see [0038]).
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 3, 5, 12, 14-17, and 19 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.
A broad range or limitation together with a narrow range or limitation that falls within the broad range or limitation (in the same claim) may be considered indefinite if the resulting claim does not clearly set forth the metes and bounds of the patent protection desired. See MPEP § 2173.05(c). In the present instance, claim 3 recites the broad recitation “the DAA domain comprises SEQ ID NO: 1”, and the claim also recites “a sequence having at least 90% amino acid sequence identity to SEQ ID NO: 1” which is the narrower statement of the range/limitation. The claim(s) are considered indefinite because there is a question or doubt as to whether the feature introduced by such narrower language is (a) merely exemplary of the remainder of the claim, and therefore not required, or (b) a required feature of the claims.
A broad range or limitation together with a narrow range or limitation that falls within the broad range or limitation (in the same claim) may be considered indefinite if the resulting claim does not clearly set forth the metes and bounds of the patent protection desired. See MPEP § 2173.05(c). In the present instance, claim 5 recites the broad recitation “the CA domain comprises SEQ ID NO: 2”, and the claim also recites “a sequence having at least 90% amino acid sequence identity to SEQ ID NO: 2” which is the narrower statement of the range/limitation. The claim(s) are considered indefinite because there is a question or doubt as to whether the feature introduced by such narrower language is (a) merely exemplary of the remainder of the claim, and therefore not required, or (b) a required feature of the claims.
Claim 12 is drawn to the bi-functional fusion protein of claim 11, wherein the bi-functional fusion protein is SEQ ID NO: 6 or SEQ ID NO: 7. This renders the claim indefinite because the claim fails to provide a transitional phrase (e.g., “comprising”, “consisting of”, etc.). The term “is” in the claim fails to indicate whether the scope is limited or not. As such, claim 12 is rejected.
The term “complement related disease” in claims 14-17 is a relative term which renders the claim indefinite. The term “complement related disease” is not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention. The claims nor specification fail to define what the term means or embodies; thus one would not be apprised as to the scope of the invention. For example, does the invention encompass diseases that are indirectly impacted by the complement system, or is the invention only claiming diseases directly resulting from the complement system. Further, while claims 15 and 17 indicate “bone loss”, it is unclear whether the bone loss is the complemented related disease or is a symptom of the complement related disease. As such, claims 14-17, and dependent claim 19, are rejected.
Claim Rejections - 35 USC § 112(a) 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 1-11 and 13-19 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.
The MPEP states that the purpose of the written description requirement is to ensure that the inventor had possession, as of the filing date of the application, of the specific subject matter later claimed. The MPEP lists factors that can be used to determine if sufficient evidence of possession has been furnished in the disclosure of the application. These include “level of skill and knowledge in the art, partial structure, physical and/or chemical properties, functional characteristics alone or coupled with a known or disclosed correlation between structure and function, and the method of making the claimed invention.”
The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, disclosure of drawings, or by disclosure of relevant identifying characteristics, for example, structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the Applicants were in possession of the claimed genus. See Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406.
Claim 1 is drawn to a bi-functional fusion protein that inhibits a complement signaling pathway, wherein the bi-functional fusion protein comprises a complement C4b binding motif, a complement C3b binding motif, and an Fc region.
Claim 2 is drawn to the bi-functional fusion protein of claim 1, wherein the complement C4b binding motif comprises a decay-accelerating activity (DAA) domain derived from complement receptor I.
Claim 3 is drawn to the bi-functional fusion protein of claim 2, wherein the DAA domain comprises SEQ ID NO: 1, or a sequence having at least 90% amino acid sequence identity to SEQ ID NO: 1.
Claim 4 is drawn to the bi-functional fusion protein of claim 1, wherein the complement C3b binding motif comprises a cofactor domain (CA) domain derived from complement receptor I.
Claim 5 is drawn to the bi-functional fusion protein of claim 4, wherein the CA domain comprises SEQ ID NO: 2, or a sequence having at least 90% amino acid sequence identity to SEQ ID NO: 2.
Claim 6 is drawn to the bi-functional fusion protein of claim 1, wherein the Fc region comprises an IgG domain, an IgE domain, an IgM domain, and IgD domain, an IgA domain, or an IgY domain.
Claim 7 is drawn to the bi-functional fusion protein of claim 6, wherein the IgG domain is an IgG1 domain, an IgG2 domain, an IgG3 domain, or an IgG4 domain.
Claim 8 is drawn to the bi-functional fusion protein of claim 7, wherein the IgG1 domain is SEQ ID NO: 3.
Claim 9 is drawn to the bi-functional fusion protein of claim 1, wherein the complement C4b binding motif is at N-terminal of Fc region, and the complement C3b binding motif is at C-terminal of Fc region; or the complement C3b binding motif is at N-terminal of Fc region, and the complement C4b binding motif is at C-terminal of Fc region.
Claim 10 is drawn to the bi-functional fusion protein of claim 9, further comprising two linkers, one of the two linkers is placed between the complement C4b binding motif and the N-terminal of Fc region, the other one of the two linkers is placed between the complement C3b binding motif and the C-terminal of Fc region; or one of the two linkers is placed between the complement C3b binding motif and the N-terminal of Fc region, the other one of the two linkers is placed between the complement C4b binding motif and the C-terminal of Fc region.
Claim 11 is drawn to the bi-functional fusion protein of claim 10, wherein each one of the two linkers is SEQ ID NO: 4.
Claim 13 is drawn to the bi-functional fusion protein of claim 1, wherein orders of the bi-functional fusion protein comprises: the complement C4b binding motif, the complement C3b binding motif, and the Fc region; the complement C3b binding motif, the complement C4b binding motif, and the Fc region; the Fc region, the complement C4b binding motif, and the complement C3b binding motif; or the Fc region, the complement C3b binding motif, and the complement C4b binding motif.
Claim 14 is drawn to a pharmaceutical composition for the treatment of a complement related disease, comprising the bi-functional fusion protein of claim 1, and at least one pharmaceutically acceptable carrier.
Claim 15 is drawn to the pharmaceutical composition of claim 14, wherein the complement related disease comprises bone loss.
Claim 16 is drawn to a method of treating or preventing a complement related disease comprising administering to a patient in need thereof an effective amount of the bi-functional fusion protein of claim 1.
Claim 17 is drawn to the method of claim 16, wherein the complement related disease comprises bone loss characterized by a metabolic imbalance as a result of a net excess of bone resorption over bone formation.
Claim 18 is drawn to the method of claim 17, wherein a disease associated with the bone loss is periodontal disease.
Claim 19 is drawn to the method of claim 16, wherein the patient is human or non-human vertebrates.
The specification discloses the expression and purification of bi-functional complement pathways inhibitory proteins (see Example 1). Functional DAA and CA domains for C3b/C4b binding in human complementary receptor (CR1) were used to construct the Fc fusion proteins (i.e., CA-Fc-DAA (SB001) and DAA-Fc-CA (SB002)). As shown in Fig. 3, the molecular weight of the purified CA-Fc-DAA or DAA-Fc-CA fusion protein is about 130kDa. Example 2 discloses in vitro binding activity of complement inhibitors against C3b and C4b. Example 3 discloses inhibition of classic complement and alternative pathways by the bi-functional inhibitor. Example 4 discloses the expression of C3b/C4b in human periodontal biopsies. Example 5 discloses the correlation between the expression of C3b/C4b in gum tissues and human periodontitis progression. The specimens were divided into four grades (0 is unstained, 1 is weak, 22 is moderate, and 3 is strong) and the relative area were divided into five grades (0 is unstained, 1 is 1-10%, 2 is 11-50%, 3 is 51-80%, and 4 is 81-100%).
Example 6 discloses the prevention of ligature-induced periodontitis in rat with administration of bi-functional complement inhibitor. For micro-computerized tomography (micro-CT) analysis, reconstructed three-dimensional images were used to assess the distance between the cementoenamel junction (CEJ) and the coronal level of the alveolar bone crest (ABC) in all dimensions wherein the alveolar bone loss is defined as the measurement of the distance from CEJ to ABC (CEJ-ABC, mm). There was a severe bone resorption evidenced by a marked increase of CEJ-ABC distances in the ligature group when compared to the non-ligature (control) group at day 5 (D5) and day 7 (D7) (see Figs. 10B to 10E). The results showed that there was no significant difference between the ligation group (L group) and ligation low group (D group) on D7 (see Fig. 11B). However, administration of high dose bi-functional inhibitor significantly diminished alveolar bone destruction at D7 (see Fig. 11C), indicating that the bi-functional inhibitor exerts a protective effect to alleviate ligature-induced periodontitis in rats. Example 7 discloses the efficacy study of bi-functional complement inhibitor in an animal model. Lastly, Example 8 discloses the pharmacokinetic assessment of complement inhibitor in mice and monkeys.
However, the specification fails to disclose that Applicant was in possession of the large genus of bi-functional fusion proteins as claimed. Further, the claims are drawn to structures comprising at least 90% amino acid sequence identity to SEQ ID Nos: 1 and 2, but the claims nor specification disclose which amino acid residues must be maintained in order to maintain its function. Additionally, the specification fails to disclose that Applicant was in possession of a bi-functional fusion protein wherein the order is as recited in claim 13. The specification also fails to disclose of the large genus of bi-functional fusion proteins preventing any complement related disease, or treating or preventing a complement related disease in a patient.
Although the specification discloses bi-functional complement inhibitors SB001 and SB002, and the disease periodontitis, the claims are not limited to these inhibitors or disease, and are inclusive of any bi-functional fusion protein that inhibits a complement signaling pathway, wherein the bi-functional fusion protein comprises a complement C4b binding motif, a complement C3b binding motif, and an Fc region that also treats or prevents any complement related disease. This indicates that there are hundreds, if not thousands, of possible bi-functional fusion proteins-complement related disease encompassed by the claims. Thus, the claims encompass a vast genus of disease-inhibitor treatments that have the claimed functions. However, the specification provides limited guidance on the structure and steps required for maintaining the claimed function(s). Therefore, the specification does not provide adequate written description to identify the broad and variable genus of bi-functional fusion proteins because, inter alia, the specification does not disclose a correlation between the necessary structure of the inhibitor and the function(s) recited in the claims; and thus, the specification does not distinguish the claimed genus from others, except by function. Further, the specification fails to provide method steps that result in treating complement related disease patients. Although the term protein does impart some structure, the structure that is common to proteins is generally unrelated to its specific binding function; therefore, correlation is less likely for proteins than for other molecules. Accordingly, the specification does not define any structural features commonly possessed by the members of the genus, because while the description of an ability of the claimed substance may generically describe the molecule’s function, it does not describe the substance itself. A definition by function does not suffice to define the genus because it is only an indication of what the substance does, rather than what it is; therefore, it is only a definition of a useful result rather than a definition of what achieves the result. In addition, because the genus of substances is highly variable (i.e. each substance would necessarily have a unique structure, See MPEP 2434), the generic description of the substance is insufficient to describe the genus. Further, given the highly diverse nature of proteins, even one of skill in the art cannot envision the structure of a protein by only knowing its inhibitory characteristics. Thus, the specification does not provide substantive evidence for possession of this large and variable genus, encompassing a potentially massive number of fusion proteins and variants thereof claimed only be a functional characteristic(s) and/or partial structure.
A biomolecule sequence described only by a functional characteristic, without any known or disclosed correlation between that function and the structure of the sequence, normally is not sufficient identifying characteristics for written description purposes, even when accompanied by a method of obtaining the agent. The specification does not adequately describe the correlation between the chemical structure and function of the genus, such as structural domains or motifs that are essential and distinguish members of the genus from those excluded. Thus, the genus of bi-functional fusion proteins has no correlation between their structure and function.
MPEP § 2163.03(V) states:
While there is a presumption that an adequate written description of the claimed invention is present in the specification as filed, In re Wertheim, 541 F.2d 257, 262, 191 USPQ 90, 96 (CCPA 1976), a question as to whether a specification provides an adequate written description may arise in the context of an original claim. An original claim may lack written description support when (1) the claim defines the invention in functional language specifying a desired result but the disclosure fails to sufficiently identify how the function is performed or the result is achieved or (2) a broad genus claim is presented but the disclosure only describes a narrow species with no evidence that the genus is contemplated. See Ariad Pharms., Inc. v. Eli Lilly & Co., 598 F.3d 1336, 1349-50 (Fed. Cir. 2010) (en banc). The written description requirement is not necessarily met when the claim language appears in ipsis verbis in the specification. "Even if a claim is supported by the specification, the language of the specification, to the extent possible, must describe the claimed invention so that one skilled in the art can recognize what is claimed. The appearance of mere indistinct words in a specification or a claim, even an original claim, does not necessarily satisfy that requirement. “Enzo Biochem, Inc. v. Gen-Probe, Inc., 323 F.3d 956, 968, 63 USPQ2d 1609, 1616 (Fed. Cir. 2002).
Applicant has not shown possession of a representative number of species of bi-functional fusion proteins. The disclosure of only one or two species encompassed within a genus adequately describes a claim directed to that genus only if the disclosure "indicates that the patentee has invented species sufficient to constitute the gen[us]." See Enzo Biochem, 323 F.3d at 966, 63 USPQ2d at 1615; Noelle v. Lederman, 355 F.3d 1343, 1350, 69 USPQ2d 1508, 1514 (Fed. Cir. 2004) (Fed. Cir. 2004) ("[A] patentee of a biotechnological invention cannot necessarily claim a genus after only describing a limited number of species because there may be unpredictability in the results obtained from species other than those specifically enumerated.") (MPEP 2163).
The instant claims do not fully describe the structure of the complement C4b motif and a complement C3b binding motif to achieve the required function. Accordingly, the specification also does not provide adequate written description to identify the broad genus of bi-functional fusion proteins, claimed only by a function characteristic(s) and not structures per se, because inter alia, it does not describe a sufficient number and/or a sufficient variety of representative species to reflect the breadth and variation within the claimed genus. Consequently, based on the lack of information within the specification, there is evidence that a representative number and a representative variety of the numerous bi-functional fusion proteins had not yet been identified and thus, the specification represents little more than a wish for possession. Therefore, one of skill in the art would not conclude that Applicant was in possession of the broad and highly variable genus of bi-functional fusion proteins claimed only by a partial structure and functional characteristic(s). Thus the bi-functional fusion proteins described by the instant claims encompasses an overly broad genus, the structure of the complement C4b motif and the complement C3b binding motif, and the functional outcome.
In Amgen Inc. v. Sanofi, 124 USPQ2d 1354 (Fed. Cir. 2017), relying upon Ariad Pharms., Inc. v. Eli Lily & Co., 94 USPQ2d 1161 (Fed Cir. 2010), it is noted that to show invention, a patentee must convey in its disclosure that is “had possession of the claimed subject matter as of the filing date. Demonstrating possession “requires a precise definition” of the invention. To provide this precise definition” for a claim to a genus, a patentee must disclose “a representative number of species within the scope of the genus of structural features common to the members of the genus so that one of skill in the art can visualize or recognize the member of the genus” (see Amgen at page 1358). Also, it is not enough for the specification to show how to make and use the invention, i.e., to enable it (see Amgen at page 1361). An adequate written description must contain enough information about the actual makeup of the claimed products — “a precise definition, such as structure, formula, chemic name, physical properties of other properties, of species falling with the genus sufficient to distinguish the gene from other materials”, which may be present in “functional terminology when the art has established a correlation between structure and function” (Amgen page 1361). Most significant to the present case, the Court held that "knowledge of the chemical structure of an antigen [does not give] the required kind of structure-identifying information about the corresponding antibodies" (Amgen at 1361). The idea that written description of an antibody can be satisfied by the disclosure of a newly-characterized antigen “flouts basic legal principles of the written description requirement” as it “allows patentees to claim antibodies by describing something that is not the invention, i.e., the antigen... And Congress has not created a special written description requirement for antibodies” (Amgen at page 1362).
Abbvie v. Centocor (Fed. Cir. 2014) is also relevant to the instant claims. In Abbvie, the Court held that a disclosure of many different antibodies was not enough to support the genus of all neutralizing antibodies because the disclosed antibodies were very closely related to each other in structure and were not representative of the full diversity of the genus. The Court further noted that functionally defined genus claims can be inherently vulnerable to invalidity challenge for lack of written description support especially in technology fields that are highly unpredictable where it is difficult to establish a correlation between structure and function for the whole genus or to predict what would be covered by the functionally claimed genus.
The instant case has many similarities to AbbVie above. First, the claims clearly attempt to define the genus of bi-functional fusion proteins by the functions of inhibiting a complement signaling pathway comprising a complement C4b binding motif and a complement C3b binding motif. Additionally, the claims attempt to define the genus of bi-functional fusion proteins by the vast functions of treating or preventing any complement related disease. As noted by AbbVie above, functionally defined genus claims can be inherently vulnerable to invalidity challenge for lack of written description. Second, there is no information in the specification based upon which one of skill in the art would conclude that the disclosed species for which applicant has identified as having the recited functions would be representative of the entire genus. The specification discloses no structure to correlate with the function. Therefore, the specification provides insufficient written description to support the genus encompassed by the claim.
Furthermore, regardless whether a compound is claimed per se or a method is claimed that entails the use of the compound, the inventor cannot lay claim to that subject matter unless he can provide a description of the compound sufficient to distinguish infringing compounds from non-infringing compounds, or infringing methods from non-infringing methods. Univ. of Rochester v. G.D. Searle & Co., 358 F.3d 916, 920-23, 69 USPQ2d 1886, 1890-93 (Fed. Cir. 2004).
Vas-Cath Inc. v. Mahurkar, 19 USPQ2d 1111, 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.)
Further, the skilled artisan cannot envision the detailed chemical structure of the encompassed bi-functional fusion proteins, 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 nucleic acid and/or protein itself is required. See Fiers v. Revel, 25 USPQ2d 1601, 1606 (CAFC 1993) and Amgen Inc. V. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016. In Fiddes v. Baird, 30 USPQ2d 1481, 1483, 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 held that: ... To fulfill the written description requirement, a patent specification must describe an invention and does 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 (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 1966.
Regarding the encompassed proteins and peptides, protein chemistry is one of the most unpredictable areas of biotechnology. This unpredictability prevents prediction of the effects that a given number or location of mutation will have on a protein (such as TNF or a cytokine) as taught by Skolnick et al. (Trends Biotechnol. 2000 Jan;18(1):34-9), sequence-based methods for predicting protein function are inadequate because of the multifunctional nature of proteins (see e.g. abstract). Further, just knowing the structure of the protein is also insufficient for prediction of functional sites (see e.g. abstract). Sequence to function methods cannot specifically identify complexities for proteins, such as gain and loss of function during evolution, or multiple functions possible within a cell (see e.g. page 34, right column). Skolnick advocates determining the structure of the protein, then identifying the functionally important residues since using the chemical structure to identify functional sites is more in line with how a protein actually works (see e.g. page 34, right column).
The sensitivity of proteins to alterations of even a single amino acid in a sequence are exemplified by Burgess et al. (J. Cell Biol. 111:2129-2138, 1990) who teach that replacement of a single lysine reside at position 118 of acidic fibroblast growth factor by glutamic acid led to the substantial loss of heparin binding, receptor binding and biological activity of the protein and by Lazar et al. (Mol. Cell. Biol., 8:1247-1252, 1988) who teach that in transforming growth factor alpha, replacement of aspartic acid at position 47 with alanine or asparagine did not affect biological activity while replacement with serine or glutamic acid sharply reduced the biological activity of the mitogen. These references demonstrate that even a single amino acid substitution will often dramatically affect the biological activity and characteristics of a protein.
Further, Miosge (Proc Natl Acad Sci U S A. 2015 Sep 15;112(37):E5189-98) teach that Short of mutational studies of all possible amino acid substitutions for a protein, coupled with comprehensive
functional assays, the sheer number and diversity of missense mutations that are possible for proteins means that their functional importance must presently be addressed primarily by computational inference (see e.g. page E5189, left column). However, in a study examining some of these methods, Miosge shows that there is potential for incorrect calling of mutations (see e.g. page E5196, left column, top paragraph). The authors conclude that the discordance between predicted and actual effect of missense mutations creates the potential for many false conclusions in clinical settings where sequencing is performed to detect disease-causing mutations (see e.g. page E5195, right column, last paragraph). The findings in their study show underscore the importance of interpreting variation by direct experimental measurement of the consequences of a candidate mutation, using as sensitive and specific an assay as possible (see e.g. page E5197, left column, top paragraph). Additionally, Bork (Genome Research, 2000,10:398-400) clearly teaches the pitfalls associated with comparative sequence analysis for predicting protein function because of the known error margins for high-throughput computational methods. Bork specifically teaches that computational sequence analysis is far from perfect, despite the fact that sequencing itself is highly automated and accurate (p. 398, column 1). One of the reasons for the inaccuracy is that the quality of data in public sequence databases is still insufficient. This is particularly true for data on protein function. Protein function is context dependent, and both molecular and cellular aspects have to be considered (p. 398, column 2). Conclusions from the comparison analysis are often stretched with regard to protein products (p. 398, column 3). Further, although gene annotation via sequence database searches is already a routine job, even here the error rate is considerable (p. 399, column 2). Most features predicted with an accuracy of greater than 70% are of structural nature and, at best, only indirectly imply a certain functionality (see legend for table 1, page 399). As more sequences are added and as errors accumulate and propagate it becomes more difficult to infer correct function from the many possibilities revealed by database search (p. 399, paragraph bridging columns 2 and 3). The reference finally cautions that although the current methods seem to capture important features and explain general trends, 30% of those features are missing or predicted wrongly. This has to be kept in mind when processing the results further (p. 400, paragraph bridging cols 1 and 2).
One key issue is the prediction of protein function based on sequence similarity, which could be one way to identify the functional proteins that are useful in the instant claims. Kulmanov et al (Bioinformatics, 34(4), 2018, 660–668), teach that there are key challenges for protein function prediction methods (see e.g. page 661, left column). These challenges arise from the difficulty identifying and accounting for the complex relationship between protein sequence structure and function (see e.g. page 661, left column). Despite significant progress in the past years in protein structure prediction, it still requires large efforts to predict protein structure with sufficient quality to be useful in function prediction (see e.g. page 661, left column). Another challenge is that proteins do not function in isolation. In particular higher level physiological functions that go beyond simple molecular interactions will require other proteins and cannot usually be predicted by considering a single protein in isolation (see e.g. page 661, left column). Due to these challenges it is not obvious what kinds of features should be used to predict the functions of a protein and whether they can be generated efficiently for a large number of proteins, such as the vast genus of proteins and peptides that may be encompassed by the instant claims (see e.g. page 661, left column).
The state of the art regarding the structure-function correlation cannot be relied upon because functional characteristics of any peptide/protein are determined by its structure as evidenced by Greenspan et al. 1999 (Defining epitopes: It's not as easy as it seems; Nature Biotechnology, 17:936-937). Greenspan et al. teach that as little as one substitution of an amino acid (e.g. alanine) in a sequence results in unpredictable changes in the 3-dimenstional structure of the new peptide sequence which, in turn, results in changes in the functional activity such as binding affinity of the peptide sequence (page 936, 1st column). Greenspan et al. teach that contribution of each residue (i.e. each amino acid) cannot be estimated with any confidence if the replacement affects the properties of the free form of the molecule (page 936, 3rd column).
Given not only the teachings of Skolnick et al., Lazar et al., Burgess et al., and Greenspan et al., but also the limitations and pitfalls of using computational sequence analysis and the unknown effects of alternative splicing, post translational modification and cellular context on protein function as taught by Bork, the claimed bi-functional fusion proteins could not be predicted based on sequence identity. Clearly, it could not be predicted that a polypeptide or a variant that shares only partial homology with a disclosed protein or that is a fragment of a given SEQ ID NO. will function in a given manner.
The claimed invention as a whole may not be adequately described where an invention is described solely in terms of a method of its making coupled with its function and there is no described or art-recognized correlation or relationship between the structure of the invention and its function (see MPEP 2163). A patent specification must set forth enough detail to allow a person of ordinary skill in the art to understand what is claimed and to recognize that the inventor invented what is claimed. In the case of proteins, an adequate written description 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 (see Lilly, 119 F.3d at 1566 (quoting Fiers, 984 F.2d 15 1171 ). Because the specification does not describe the amino acid sequences nor any core structures for potentially numerous different amino acid sequences which would have the recited dissociation constant, one of skill in the art would reasonably conclude that applicant was not in possession of the claimed genus of all bi-functional fusion proteins.
A key role played by the written description requirement is to prevent “attempt[s] to preempt the future before it has arrived.” Ariad at 1353, (quoting Fiers v. Revel, 984 F.2d at 1171). Upholding a patent drawn to a genus of antibodies that includes members not previously characterized or described could negatively impact the future development of species within the claimed genus of antibodies.
While "examples explicitly covering the full scope of the claim language" typically will not be required, a sufficient number of representative species must be included to "demonstrate that the patentee possessed the full scope of the [claimed] invention." Lizard tech v. Earth Resource Mapping, Inc., 424 F.3d 1336, 1345, 76 USPQ2d 1724,1732 (Fed. Cir. 2005).
In the absence of sufficient recitation of distinguishing characteristics, the specification does not provide adequate written description of the claimed genus. One of skill in the art would not recognize from the disclosure that the applicant was in possession of the claimed bi-functional fusion proteins. Possession may not be shown by merely describing how to obtain possession of members of the claimed genus or how to identify their common structural features (see, Univ. of Rochester v. G.D. Searle & Co., 358 F.3d 916,927, 69 USPQ2d 1886, 1895 (Fed. Cir. 2004); accord Ex Parte Kubin, 2007-0819, BPAI 31 May 2007, opinion at p. 16, paragraph 1). 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).
Without an adequate structural description of the claimed components and descriptive support on how to put them together, one of ordinary skill in the art would not be reasonably apprised that Applicant was in possession of the genus of bi-functional fusion proteins as claimed. Applicant is reminded that Vas-Cath makes clear that the written description provision of 35 U.S.C. 112 is severable from its enablement provision (see page 1115).
Claim Rejections - 35 USC § 112(a) Scope of 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 16-19 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 periodontitis (alveolar bone destruction) comprising administering inhibitor SB002 in rat models, does not reasonably provide enablement for treating or preventing any complement related disease comprising administering to a patient in need thereof an effective amount of any bi-functional fusion protein. 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.
The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
MPEP § 2164.01 states:
The standard for determining whether the specification meets the enablement
requirement was cast in the Supreme Court decision of Minerals Separation Ltd. v. Hyde, 242 U.S.
261, 270 (1916) which postured the question: is the experimentation needed to practice the
invention undue or unreasonable? That standard is still the one to be applied. In re Wands, 858
F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988). Accordingly, even though the statute does
not use the term "undue experimentation," it has been interpreted to require that the claimed
invention be enabled so that any person skilled in the art can make and use the invention without
undue experimentation. In re Wands, 858 F.2d at 737, 8 USPQ2d at 1404 (Fed. Cir. 1988).
There are many factors to be considered when determining whether there is sufficient evidence
to support a determination that a disclosure does not satisfy the enablement requirement and whether
any necessary experimentation is "undue." These factors include, but are not limited to:
(A) The breadth of the claims;
(B) The nature of the invention;
(C) The state of the prior art;
(D) The level of one of ordinary skill;
(E) The level of predictability in the art;
(F) The amount of direction provided by the inventor;
(G) The existence of working examples; and
(H) The quantity of experimentation needed to make or use the invention based on the content
of the disclosure.
In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988). The factors most relevant for this rejection are: (A) the breadth of the claims; (B) the nature of the invention; (E) the level of predictability in the art; (F) the amount of direction provided by the inventor; (G) the existence of working examples; and (H) the quantity of experimentation needed to make or use the invention based on the content of the disclosure.
In regard to Wands factors (A) and (B), the breadth of the claims needed to enable the invention
is determined by whether the scope of enablement provided to one skilled in the art by the disclosure is
commensurate with the scope of protection sought in the claims. AK Steel Corp. v. Sollac, 344 F.3d 1234, 1244, 68 USPQ2d 1280, 1287 (Fed. Cir. 2003); In re Moore, 439 F.2d 1232, 1236, 169 USPQ 236, 239 (CCPA 1971). The propriety of a rejection based upon the scope of a claim relative to the scope of the enablement concerns (1) how broad the claim is with respect to the disclosure and (2) whether one
skilled in the art could make and use the entire scope of the claimed invention without undue
experimentation.
The nature of the invention is a method of treating or preventing a complement related disease comprising administering to a patient in need thereof an effective amount of the bi-functional fusion protein of claim 1. Therefore, the nature of the invention is a biochemical case, where there is natural unpredictability in performance of certain species other than those specifically enumerated; see MPEP § 2163. Accordingly, it is the Office’s position that undue experimentation would be required to practice the functionality of the claimed method, with a reasonable expectation of success, because it would not be predictable from the disclosure of any one particular species may or may not work; see MPEP § 2164.03.
In regard to Wands factors (C), (D), and (E), the state of the prior art is what one skilled in the art would have known, at the time the application was filed, about the subject matter to which the claimed invention pertains and provides evidence for the degree of predictability in the art; see MPEP § 2164.05(a). The claims encompass treating any complement-mediated disease or disorder with a bi-functional fusion protein that inhibits a complement signaling pathway, wherein the bi-functional fusion protein comprises a complement C4b binding motif, a complement C3b binding motif, and an Fc region.
The art confirms the intricate complexity of the complement system. Morgan et al (Nat Rev Drug Discov 14, 857–877 (2015)) indicates that there will be a no ‘one size fits all’ solution to complement therapies because agents that are effective in one disease might do nothing in, or even exacerbate, another due to the inevitability that a drug that blocks any of the complement pathways will increase the risk of infections (see pg. 859, left col; pg. 861, left col). The merits of anti-complement therapy in preclinical models of disease have been explored in hundreds of papers; however, only a few drugs have entered clinical trials and fewer still have progressed beyond Phase I (see pg. 859, left col). Any drug that stops activation of the classical pathway will affect the clearance of immune complexes and apoptotic cells; and, inhibition of the activation pathways may disrupt an individual’s capacity to mount an adaptive immune response (see pg. 861, left col). Specifically, when activation fragments such as C3a, C5a, C4d, Bb and terminal complement complex (TCC) are present in the disease their levels can be monitored to demonstrate response to therapy and confirm target engagement; however, for diseases restricted to specific sites, for example, the retina, central nervous system or kidney glomerulus, plasma complement biomarkers may not reflect the response to therapy and are poor tools for assessing target engagement (see pg. 874). This is supported by Nilsson et al (Front. Immunol. 14:1334050 (2023)) who discuss the challenges encountered when accurately determining the complement status, particularly within the constraints of routine clinical practice including: pathway complexity, heterogeneity of complement-mediated diseases, patient heterogeneity, lack of sensitivity, sample sensitivity, and lack of standardization (see entire document). Specifically, Nilsson et al discuss that patients with complement disorders exhibit substantial clinical diversity and variations in complement profiles, and complement activation is highly dynamic and can change rapidly in response to stimuli (see pg. 2, left col).
As such, the art indicates complement diseases can affect the efficacy of therapeutics used to treat it. Therefore, the art is unpredictable regarding treatment of all complement diseases with a single compound or class of compounds.
In regard to Wands factors (F), (G) and (H), 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). The "amount of guidance or direction" refers to that information in the application, as originally filed, that teaches exactly how to make or use the invention. The more that is known in the prior art about the nature of the invention, how to make, and how to use the invention, and the more predictable the art is, the less information needs to be explicitly stated in the specification. In contrast, if little is known in the prior art about the nature of the invention and the art is unpredictable, the specification would need more detail as to how to make and use the invention in order to be enabling. See, e.g., Chiron Corp. v. Genentech
Inc., 363 F.3d 1247, 1254, 70 USPQ2d 1321, 1326 (Fed. Cir. 2004).
The claims are drawn to a method of treating or preventing a complement related disease comprising administering to a patient in need thereof an effective amount of the bi-functional fusion protein of claim 1.
The working examples provided by Applicant do not demonstrate a method of treating or preventing any complement-related disease in a patient comprising administering a bi-functional fusion protein of claim 1, excluding SB002 with periodontitis (alveolar bone destruction). Applicant discloses that there was no significant difference between the ligation group (L group) and ligation low group (D group) on D7 (see Fig. 11B). However, administration of high dose bi-functional inhibitor significantly diminished alveolar bone destruction at D7 (see Fig. 11C), indicating that the bi-functional inhibitor exerts a protective effect to alleviate ligature-induced periodontitis in rats. The working examples do not support that the claimed bi-functional fusion proteins would treat or prevent the vast genus of complement related diseases. Because the specification only studied in rat models of one complement pathway activity with one bi-functional fusion protein, one cannot assume that the method of treating or preventing a vast variety of diseases will work similarly to the rat models provided in the specification. In the absence of empirical determination, one skilled in the art would be subjected to undue experimentation to determine if the claimed method of treating or preventing any complement related disease would result in therapeutic response as recited in the claims.
Applicant is reminded that “a patent is not a hunting license. It is not a reward for search, but compensation for its successful conclusion” and “[p]atent 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”. See Genentech, 108 F.3d 1361, 1366 (Fed. Cir. 1997).
In view of all of the above, one of skill in the art would be forced into undue experimentation to practice the claimed invention, and thus, the claimed invention does not satisfy the requirements of 35 U.S.C. 112 first paragraph.
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.
US 2015/0079084 A1
Claims 1-4, 6-8, 14-17, and 19 are rejected under 35 U.S.C. 102(a)(1) and 35 U.S.C. 102(a)(2) as being anticipated by Her et al (US 2015/0079084 A1, publication date: 03/19/2015).
The applied reference has a common 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).
With respect to instant claims 1-4, Her et al teach of a fusion protein that inhibits complement activation and VEGF activity comprising a complement inhibiting domain (CID), a VEGF inhibiting domain (VID), and a half-life prolonging domain (see claim 1). Her et al teach that the half-life prolonging domain comprises an immunoglobulin Fc region (see claim 7). Her et al teach that the CID can comprise a portion of a complement regulating protein that binds to a complement component and inhibits complement activation; for example, human CR1 (allotype A) is a large glycoprotein (200 kD) consisting of an extracellular domain comprising 30 repeating homologous short consensus repeats (SCR) each ranging from 60 to 70 amino acids… wherein the first 3 SCRs (SCRs8-10) of the second LHR (LHR-B) and the first 3 SCRs (SCR15-17) of the third LHR (LHR-C) are nearly identical (see [0051]). These SCRs both bind C3b with a high affinity and C4b with an intermediate affinity (see [0051]).
Her et al disclose that the human CR1 is the only complement regulator that has DAA (see para. [0006]). Further, Her et al disclose of a CID comprising SEQ ID NO: 4 which shares 100% identity with instant SEQ ID NO: 1 (see alignment).
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With respect to instant claims 6-8, Her et al disclose that the Fc region comprises an IgG domain , IgA domain, IgD domain, IgM, or IgE domain (see [0063]). Further, Her et al disclose that the IgG domain is a human Fc of IgG1, IgG2, IgG3, or IgG4 (see [0063]). Her et al disclose that the Fc region comprises SEQ ID NO: 39 which shares 100% identity with instant SEQ ID NO: 3 (see alignment).
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With respect to instant claims 14-17 and 19, Her et al disclose of unit dosage forms for the treatment and/or prevention of complement-related disease, the dosage forms comprising any one of the fusion proteins or formulations (see [0181]; claims 26). Her et al disclose of administering to the individual an effective amount of the fusion protein to treat and/or prevent a complement-related disease wherein the individual is a human (see [0177]). Her et al disclose that the disease includes rheumatoid arthritis (see [0154] and [0156]; claims 35 and 36).
As such, the teachings of Her et al anticipates the present invention.
EP 3586860 A1
Claims 1-2, 4, 6-7, 13-14, 16, and 19 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Schmidt et al (EP 3586860 A1, publication date: 01/01/2020).
With respect to instant claims 1-2, 4, and 13, Schmidt et al disclose of a multi-module polypeptide comprising (i) an Fc receptor binding module; (ii) a first complement control protein repeat (CCP) module; and (iii) a second CCP module binding to at least one host cell surface marker, to complement factor C3b, to complement factor C4b, to a degradation product of complement factor C3b, and/or to a degradation product of complement factor C4b; wherein said second CCP module is C-terminal of said Fc receptor binding module and of said first CCP module (see Abstract). Schmidt et al disclose that CCP domains are peptide sequences comprising approx. 60 to 70 amino acids and besides binding to complement proteins C3b and/or C4b, CCP domains were found to mediate further activities including decay accelerating activity and Factor I cofactor activity (see [0016]-[0020]).
With respect to instant claims 6 and 7, Schmidt et al disclose that the Fc receptor binding module is an Fc module of an IgG, preferably of an IgG1 (see [0015] and [0074]; claim 8).
With respect to instant claim 14, Schmidt et al disclose that the claimed multi-module polypeptide can be formulated into a pharmaceutical composition further comprising a pharmaceutical acceptable carrier (see [0057]-[0059] and [0066]).
Lastly, with respect to instant claims 16 and 19, Schmidt et al disclose of a method for treating and/or preventing inappropriate complement activation and/or a disease having inappropriate complement activation as a symptom in a subject comprising administering an effective dose of a multi-module polypeptide according to the present invention (see [0068]). Schmidt et al disclose that the subject is preferably a mammal and most preferably a human (see [0070]).
As such, the teachings of Schmidt et al anticipates the present invention.
Allowable Subject Matter
The sequences in claim 12 appear to be free of the art. The closest prior art is Her et al (US 2015/0079084 A1, publication date: 03/19/2015) which teach of a fusion protein that inhibits complement activation and VEGF activity comprising a complement inhibiting domain (CID), a VEGF inhibiting domain (VID), and a half-life prolonging domain (see claim 1). Her et al teach that the half-life prolonging domain comprises an immunoglobulin Fc region (see claim 7). Her et al teach that the CID can comprise a portion of a complement regulating protein that binds to a complement component and inhibits complement activation. While the art teaches of instant SEQ ID NO: 1 (see above), the art fails to disclose of a construct comprising SEQ ID Nos: 6 and 7 (see alignments).
SEQ ID NO: 6 Alignment
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SEQ ID NO: 7 Alignment
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Conclusion
Claims 1-19 are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to DANAYA L MIDDLETON whose telephone number is (571)270-5479. The examiner can normally be reached M-F 9:30AM - 6PM with flex.
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/DANAYA L MIDDLETON/Examiner, Art Unit 1674
/VANESSA L. FORD/Supervisory Patent Examiner, Art Unit 1674
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