DETAILED ACTION
1. The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
2 Applicant's amendment, filed on 8/27/2026, is acknowledged.
3. Claims 56-69 are pending.
4. While Applicant’s election of upper airway disorders as species is considered non-responsive since the specification at ¶[0957] defined all the recited in the claims as upper airway diseases, the Examiner has extended the search to cover all the claimed species.
5. Applicant’s election without traverse of Group II, claims 56-64 (now claims 56-69), directed to a method of protecting against, treating, or managing an eosinophil related disorder in a subject comprising administering to a subject in need thereof a therapeutically effective amount of an antibody which specifically binds to a human KIT receptor comprising SEQ ID NO: 1, or an antigen binding fragment thereof, and the species of an upper airway disease, filed on 03/20/2026 and 08/27/2026, is acknowledged.
6. Claims 56-69 are under examination as they read on a method of protecting against, treating, or managing an eosinophil related disorder in a subject comprising administering to a subject in need thereof a therapeutically effective amount of an antibody which specifically binds to a human KIT receptor comprising SEQ ID NO: 1, or an antigen binding fragment thereof.
7. Applicant’s IDS, filed 08/13/2024 and 03/20/2026, is acknowledged.
8. The following is a quotation of 35 U.S.C. 112(a) (Pre-AIA 35 U.S.C. 112, first paragraph):
(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.
4. Claims 65-67 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), as containing 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(s), at the time the application was filed, had possession of the claimed invention. This is a New Matter rejection.
The phrases “method is for treating an upper airway disease” claimed in claim 65, “the method is for treating allergic rhinitis, allergic sinusitis, foreign body aspiration, glottic stenosis, tracheal stenosis, laryngotracheomalacia, vascular rings, chronic obstructive pulmonary disease (COPD), congestive heart failure, eosinophilic bronchitis, polychondritis, sarcoidosis, papillomatosis, arthritis, or Wegener's granulomatosis” as claimed in claim 66 and “the method is for treating rheumatoid arthritis” as claimed in claim 67 represent a departure from the specification and the claims as originally filed.
Applicant’s amendment filed 03/20/2026 points to the specification at [0055] for support for the newly added limitations “method is for treating an upper airway disease” claimed in claim 65, “the method is for treating allergic rhinitis, allergic sinusitis, foreign body aspiration, glottic stenosis, tracheal stenosis, laryngotracheomalacia, vascular rings, chronic obstructive pulmonary disease (COPD), congestive heart failure, eosinophilic bronchitis, polychondritis, sarcoidosis, papillomatosis, arthritis, or Wegener's granulomatosis” and “the method is for treating rheumatoid arthritis”. However, the specification does not provide a clear support for such limitations. The specification at [0055] discloses:
Non-limiting examples of eosinophil or mast cell related indications include upper
airway diseases such as allergic rhinitis and sinusitis, foreign body aspiration, glottic stenosis, tracheal stenosis, laryngotracheomalacia, vascular rings, chronic obstructive pulmonary disease (COPD), and congestive heart failure, eosinophilic bronchitis, polychondritis, sarcoidosis, papillomatosis, arthritis (e.g., rheumatoid arthritis) and Wegener's granulomatosis.
Accordingly, the claimed disorders/indications encompass both eosinophil related indication as well as mast cell related indications. The specification fails to disclose which of these indications are eosinophil related and which of these indications are mast cell related indications. The specification under sections 6.4 and 6.4.3 discloses that treatment of a feline asthma model with anti-KIT antibody reduces eosinophil cell population (Example 4, page 117) and that the treatment of asthmatic cats with anti-KIT antibody decreases airway eosinophil cell numbers [00251]. No other indications recited in the claims discloses to be related to eosinophil disorders. The instant claims now recite limitations which were not clearly disclosed in the specification and recited in the claims as originally filed.
Novozymes A/S v. DuPont Nutrition Biosciences (Fed. Cir. 2013), the claimed invention is considered "as an integrated whole" rather than merely element by element. The instant specification does not particularly identify this combination of limitations.
A subgenus is not necessarily implicitly described by a genus encompassing it and a species upon which it reads, see In re Smith, 458 F.2d 1389, 1395, 173 USPQ 679, 683 (CCPA 1972).
Limitation of a class, generically disclosed, to a subgenus without any teaching of the subgenus is new matter unsupported by the specification. Ex parte Batchelder, 131 USPQ 38, 39 (1960).
In re Ruschig, 371 F.2d 990, 154 USPQ 118 (CCPA 1967), stating that [i]t is an old custom in the woods to mark trails by making blaze marks on the trees. It is of no help in finding a trail or in finding one’s way through the woods where the trails have disappeared or have not yet been made, which is more like the case hereto be confronted simply by a large number of unmarked trees. We are looking for blaze marks which single out particular trees. We see none.
The court in In re Ruschig said that a generic or a sub-generic disclosure cannot support a species unless the species is specifically described. In referring to the Ruchig case, the court in Purdue Pharma L.P. v. Faulding Inc., 230 F.3d 1320, 1326, 56 USPQ2d 1481, 1486 (Fed. Cir. 2000), said that “Ruschig makes clear that one cannot disclose a forest in the original application, and then later pick a tree out of the forest and say “here is my invention”. In order to satisfy the written description requirement, the blaze marks directing the skilled artisan to that tree must be in the originally filed disclosure. ("It is `not a question of whether one skilled in the art might be able to construct the patenteeís device from the teachings of the disclosure. . . . Rather, it is a question whether the application necessarily discloses that particular device") (quoting Jepson v. Coleman, 314 F.2d 533, 536, 136 USPQ 647, 649-50 (CCPA 1963)).
In the instant case such blaze marks for the claimed indications as eosinophil related disorders do not appear.
10. Claims 56-58 and 61-69 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention.
Claims 56-58 and 61-69 encompass a broad genus of anti-human KIT receptor antibodies in the treatment of eosinophil related disorders
However, there does not appear to be an adequate written description in the specification as-filed of the essential structural feature that provides the recited function of protecting against, treating or managing an eosinophil related disorder. The Guidelines for the Examination of Patent Applications Under the 35 U.S.C. 112, ¶ 1 "Written Description" Requirement make clear that 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, reduction to drawings, or by disclosure of relevant, identifying characteristics, i.e., 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 applicant was in possession of the genus.
The specification at [1064] discloses methods for producing and screening for specific antibodies using hybridoma technology are routine and well known in the art. For example, in the hybridoma method, a mouse or other appropriate host animal, such as a sheep, goat, rabbit, rat, hamster or macaque monkey, is immunized to elicit lymphocytes that produce or are capable of producing antibodies that will specifically bind to the protein (e.g., extracellular domain of human KIT) used for immunization. Alternatively, lymphocytes may be immunized in vitro. Lymphocytes then are fused with myeloma cells using a suitable fusing agent, such as polyethylene glycol, to form a hybridoma cell (Goding, Monoclonal Antibodies: Principles and Practice, pp. 59-103 (Academic Press, 1986)). Additionally, a RIMMS (repetitive immunization multiple sites) technique can be used to immunize an animal (Kilptrack et al., 1997 Hybridoma 16:381-9, which is incorporated herein by reference).
[1066] Antibodies described herein include antibody fragments which recognize specific KIT antigens and can be generated by any technique known to those of skill in the art.
The Sequence Listing indicates that SEQ ID NO: 1 is 972 amino acid long sequence.
The specification at ¶ [0016] disclose that the anti-KIT antibody for use in the methods provided herein is a bivalent monospecific antibody. In certain aspects, the anti-KIT antibody for use in the methods provided herein is a humanized antibody. In particular aspects, the anti-KIT antibody for use in the methods provided herein is a naked antibody. In one aspect, the anti-KIT antibody for use in the methods provided herein is not a bispecific antibody.
[0923] FIG. 2A, FIG. 2B, and FIG. 2C demonstrate that an antibody comprising the CDRs depicted in Table 1, below (herein referred to as “anti-KIT-1”), inhibits ligand-induced phosphorylation of KIT in mast cells. (A) Fluorescence-activated cell sorting (“FACS”) analysis demonstrating the expression of KIT on LAD2. (B) FACS analysis demonstrating the expression of FcεR1 on LAD2 cells. (C) ELISA assay with an anti-phosphorylated tyrosine antibody to detect the level of ligand-induced phosphorylation of KIT in the presence of anti-KIT-1 antibody.
[0924] FIG. 3A, FIG. 3B, and FIG. 3C demonstrate that anti-KIT-1 antibody inhibits mast cell degranulation and cytokine release. (A) The percent of 0-hexosaminidase (“B-hex”) released by LAD2 cells is analyzed in the presence and absence of anti-KIT-1 in the presence and absence of ligand stimulation.
[0926] FIG. 5A and FIG. 5B demonstrate that anti-KIT-1 administration decreases the airway eosinophil population.
[1132] This example demonstrates that administration of anti-KIT-1 antibody to healthy dogs significantly reduces the population of mast cells.
[1137] Anti-KIT-1 antibody was administered to healthy dogs as described above. Preliminary evaluations indicated that anti-KIT-1 antibody in dogs is well-tolerated with minimal clinical toxicity.
6.4 Example 4: Treatment of a feline asthma model with anti-KIT antibody reduces eosinophil cell populations. [1149] Treatment of Asthmatic Cats with Anti-KIT Antibody Decreases Airway Eosinophil cell numbers. [1151] These data indicate that administration of anti-KIT-1 antibody significantly reduces eosinophil accumulation during an allergic asthma response.
Claim 1 requires a broad genus of "antibody which specifically binds to a human KIT receptor comprising SEQ ID NO:1” recited in claim 1. While the amino acid sequence of KIT was known, immunizing an animal with human KIT receptor will generate antibodies directed to a number of different epitopes within the amino acid residues at positions 1-972 of SEQ ID NO: 1 and not necessarily to the same epitope which is bound by the claimed anti-KIT1 antibody comprising the CDRs of SEQ ID NO: 2-7. The knowledge of the amino acid sequence of human KIT receptor of SEQ ID NO: 1, by itself, did not put Applicants in possession of anti-KITantibodies that protect against, treat or manage an eosinophil related disorder.
The USPTO has released a Memo on the Clarification of Written Description Guidance For Claims Drawn to Antibodies and Status of 2008 Training Materials, 02/22/2018.
See https://www.uspto.gov/sites/default/files/documents/amgen_22feb2018.pdf.
The Memo clarifies the applicability of USPTO guidance regarding the written description requirement of 35 U.S.C. § 112(a) concerning the written description requirement for claims drawn to antibodies, including the following.
“In view of the Amgen decision, adequate written description of a newly characterized antigen alone should not be considered adequate written description of a claimed antibody to that newly characterized antigen, even when preparation of such an antibody is routine and conventional”.
In contrast to applicant’s reliance of describe the epitope of the human KIT of SEQ ID NO: 1 in providing a fully characterized antigen / specific epitope as well as claiming structural elements of the antigen in the protection, treatment and management of eosinophil related disorder, there is insufficient written description of the required kind of structure-identifying information about the corresponding makeup of the claimed anti-human KIT antibodies to demonstrate possession.
Also, see Amgen Inc. v. Sanofi, 124 USPQ2d 1354 (Fed. Cir. 2017).
There is no evidence that knowledge of the chemical structure of an antigen gives the required kind of structure identifying information about the corresponding antibodies Applicants attempt to describe the invention by describing something that is not the invention: viz., the antigens to which the antibodies may bind. There nothing in the disclosure that describes the antibodies as required by the test set forth in Ariad.
However, the anti-human KIT antibodies are required to practice the invention. The specification also fails to provide any specific structural or physical information so as to define a genus of antibodies having the desired therapeutic properties. Applicant is merely relying on the identification of integrin αvß6 as the antigen and the well-known structure of antibodies in general. However, the claims do not recite a general antibody, but an antibody having a specific desired activity. However, Federal Circuit clarification of the law of written description as it applies to antibodies. Amgen v. Sanofi, 872 F.3d 1367 (Fed. Cir. 2017).
The claims are directed to a genus of anti-human KIT antibodies. However, Federal Circuit clarification of the law of written description as it applies to antibodies. The U.S. Court of Appeals for the Federal Circuit (Federal Circuit) decided Amgen v. Sanofi, 872 F.3d 1367 (Fed. Cir. 2017), which concerned adequate written description for claims drawn to antibodies. The Federal Circuit explained in Amgen that when an antibody is claimed, 35 U.S.C. § 112(a) requires adequate written description of the antibody itself. Amgen, 872 F.3d at 1378-79. The Amgen court expressly stated that the so-called "newly characterized antigen" test, which had been based on an example in USPTO-issued training materials and was noted in dicta in several earlier Federal Circuit decisions, should not be used in determining whether there is adequate written description under 35 U.S.C. § 112(a) for a claim drawn to an antibody. Citing its decision in Ariad Pharmaceuticals, Inc. v. Eli Lilly & Co., the court also stressed that the "newly characterized antigen" test could not stand because it contradicted the quid pro quo of the patent system whereby one must describe an invention in order to obtain a patent. Amgen, 872 F.3d at 1378-79, quoting Ariad Pharmaceuticals, Inc. v. Eli Lilly & Co., 598 F.3d 1336, 1345 (Fed. Cir. 2010). In view of the Amgen decision, adequate written description of a newly characterized antigen alone should not be considered adequate written description of a claimed antibody to that newly characterized antigen, even when preparation of such an antibody is routine and conventional.
Moreover, there is insufficient written description of the required kind of structure-identifying information about the corresponding makeup of the claimed anti-human KIT antibodies to demonstrate possession. Also, see Amgen Inc. v. Sanofi, Aventisub LLC, No. 2017-1480 (Fed. Cir. 2017). The Court reiterated that adequate written description must “contain enough information about the actual makeup of the claimed products . . . .” The Court simultaneously suggested that the “newly characterized antigen” test “flouts” section 112 because it “allows patentees to claim antibodies by describing something that is not the invention, i.e. the antigen.” The Court concluded that for written description of an antibody to be adequate when presented with “functional” terminology, there must be an established correlation in the art between structure and function.
For instance, citing to Centocor, the Court analogized an antigen and antibody to a lock and a key. For an antigen where there is only a finite number of binding antibodies, discovering those antibodies may be routine and conventional, and description of the antigen alone may be sufficient. By contrast, for antigens with millions of keys, or millions of potentially binding antibodies, description of the antigen and even a couple of examples may be far from sufficient.
Artisans are well aware that knowledge of a given antigen (for instance human KIT) provides no information concerning the sequence/structure of antibodies that bind the given antigen. For example, Edwards et al (J Mol Biol. 2003 Nov 14;334(1): 103-18) teach that over 1,000 different antibodies to a single protein can be generated, all with different sequences spanning almost the entire heavy and light chain germline repertoire (42/49 functional heavy chain germlines and 33 of 70 V-lambda and V-kappa light chain germlines, and with extensive diversity in the FICDR3 region sequences (that are generated by VDJ germline segment recombination) as well, see entire document). Similarly, Lloyd et al (Protein Eng Des Sel. 2009 Mar;22(3):159-68) teach that a large majority of VH/VL germline gene segments are used in the antibody response to an antigen, even when the antibodies were selected by antigen binding, as their sequencing studies revealed that out of 841 unselected and 5,044 selected antibodies, all but one of the 49 functional VH gene segments was observed (see entire document). Goel et al (J Immunol. 2004 Dec 15; 173(12):7358-67) disclose the synthesis of three mAbs that bind to the same short (12-mer) peptide and found that the sequences of these antibodies which bound the same epitope exhibited diverse V gene usage indicating their independent germline origin (see entire document). As such, it does not seem possible to predict the sequence/structure of an antibody that binds a given antigen as there does not appear to be any common or core structure present within all antibodies that gives rise to the function of antigen binding. Further, given data such as that of Edwards et al. indicating the diversity of sequence bound in a population of antibodies that bind to a given antigen no number of species appears to reasonably representative of the breadth of the genus of antibodies that bind the given antigen. Indeed, Kanyavuz et al (Nat Rev Immunol. 2019 Jun; 19(6):355-368) teach that “Theoretically, under physiological conditions, the human immune system can generate BCRs with 1026 distinct sequences, an astronomical number that is far greater than the calculated number of all B cell clones that can be generated during the lifespan of a healthy human (estimated to be 4 x 1014).
Given the claimed broadly class of antibodies and in the absence of sufficient disclosure of relevant identifying characteristics for the broadly claimed class of antibodies to human KIT receptor of SEQ ID NO: 1 in the protecting against, treating or managing an eosinophil related disorder, the patentee must establish “a reasonable structure-function correlation” either within the specification or by reference to the knowledge of one skilled in the art with functional claims
AbbVie Deutschland GmbH & Co. v. Janssen Biotech, Inc. (Fed. Cir. 2014), MPEP 2163.
The specification at best describes plan for making antibodies that bind human KIT receptor of SEQ ID NO: 1 and then identifying those that satisfy claim limitations, but mere “wish or plan” for obtaining claimed invention is not sufficient.
Centocor Ortho Biotech Inc. v. Abbott Laboratories, 97 USPQ2d 1870 (Fed. Cir. 2011).
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.). Consequently, Applicant was not in possession of the instant claimed invention. See University of California v. Eli Lilly and Co. 43 USPQ2d 1398.
Applicant is invited to point to clear support or specific examples of the claimed invention in the specification as-filed.
11. Claims 56-69 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 of treating asthma with anti-KIT-1 antibody comprising the CDRs of SEQ ID NO: 2-7 by decreasing airway eosinophil cell number, does not reasonably provide enablement for treating each and every eosinophil related disorder. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the invention commensurate in scope with these claims.
The claims are directed at a broad genus of anti-KIT antibodies and a broad genus of eosinophil related disorder including but not limited to indications include upper airway diseases such as allergic rhinitis and sinusitis, foreign body aspiration, glottic stenosis, tracheal stenosis, laryngotracheomalacia, vascular rings, chronic obstructive pulmonary disease (COPD), and congestive heart failure, eosinophilic bronchitis, polychondritis, sarcoidosis, papillomatosis, arthritis (e.g., rheumatoid arthritis) and Wegener's granulomatosis [0957].
Factors to be considered in determining whether undue experimentation is required to practice the claimed invention are summarized In re Wands (858 F2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988)). The factors most relevant to this rejection are the scope of the claim, the amount of direction or guidance provided, the lack of sufficient working examples, the unpredictability in the art and the amount of experimentation required to enable one of skill in the art to practice the claimed invention.
The claims are directed to a broad class of antibodies was that the class was defined by its function—the ability to bind to human KIT receptor of SEQ ID NO: 1 and preventing against, treating and managing each and eosinophil related disorder such as allergic rhinitis, allergic sinusitis, foreign body aspiration, glottic stenosis, tracheal stenosis, laryngotracheomalacia, vascular rings, chronic obstructive pulmonary disease (COPD), congestive heart failure, eosinophilic bronchitis, polychondritis, sarcoidosis,papillomatosis, arthritis, or Wegener's granulomatosis. However, the specification did not give the skilled in the art enough information to choose candidate antibodies from the millions of options and therefore required scientists to engage in a great deal of experimentation and failure. “That is not enablement”—it is a “hunting license.”
The specification discloses only one species of anti-KIT antibodies, KIT-1 comprising SEQ ID NO: 2-7; while the claims are directed to a genus of millions of anti-hKIT antibodies.
In Sanofi-Aventisub, the Federal Circuit relied on its prior precedential opinions when determining whether the full scope of a genus was enabled. These decisions included McRO, Inc. v. Bandai Namco Games Am. Inc., 959 F.3d 1091 (Fed. Cir. 2020) (hereafter McRO); Wyeth & Cordis Corp. v. Abbott Laboratories, 720 F.3d 1380 (Fed. Cir. 2013) (hereafter Wyeth); Enzo Life Sciences, Inc. v. Roche Molecular Systems, Inc., 928 F.3d 1340 (Fed. Cir. 2019) (hereafter Enzo); and Idenix Pharmaceuticals LLC v. Gilead Sciences Inc., 941 F.3d 1149 (Fed. Cir. 2019) (hereafter Idenix).
The Federal Circuit, citing McRO, provided guidance on the application of enablement to genus claims, holding that “[a]lthough a specification does not need to describe how to make and use every possible variant of the claimed invention, when a range is claimed, there must be reasonable enablement of the scope of the range.” Sanofi-Aventisub, 987 F.3d at 1085 (internal quotations omitted). Additionally, the Federal Circuit characterized Wyeth as holding “that due to the large number of possible candidates within the scope of the claims and the specification's corresponding lack of structural guidance, it would have required undue experimentation to synthesize and screen each candidate to determine which compounds in the claimed class exhibited the claimed functionality.” Id. at 1086. Similarly, the Federal Circuit characterized Enzo as holding “that the specification failed to teach one of skill in the art whether the many embodiments of the broad claims would exhibit that required functionality.” Id. Finally, the Federal Circuit characterized Idenix as affirming “the district court's determination that the claims had both structural and functional limitations, and that undue experimentation would have been required to synthesize and screen the billions of possible compounds because, given a lack of guidance across that full scope, finding functional compounds would be akin to finding a `needle in a haystack.' ” Id.
This case is akin to the issue in Sanofi-Aventisub, the court relied on evidence showing that the scope of the claims encompassed millions of antibodies and that it was necessary to screen each candidate antibody in order to determine whether it met the functional limitations of the claim. Id. at 1088. Consequently, the Federal Circuit concluded that there was a lack of enablement. While the specification in Amgen identified 26 exemplary antibodies that performed the claimed function by their amino acid sequences, the claims at issue were directed to a class that included “a `vast' number of additional antibodies” that Amgen had not described by their amino acid sequences. Id. at 1256. The Supreme Court found that Amgen sought to monopolize an entire class of antibodies by their function, which was much broader than the 26 exemplary antibodies disclosed by their amino acid structure. In the instant case, the specification discloses only two species that performed the claimed function by their amino acid sequences, with the claimed genus of 9,905 different anti-hANGPTL3 antibodies. The instant claims are directed to a class of anti-hANGPTL3 antibodies that included “a `vast' number of additional antibodies” that the instant specification fails to describe their amino acid sequences.
The scope of the instant claims encompassed millions of antibodies and that it was necessary to first generate and then screen each candidate to determine whether it met the functional limitations. The Federal Circuit concluded that there was a lack of enablement, which was affirmed by the Supreme Court in Amgen.
The claims simply direct skilled artisans to engage in the same iterative, trial-and-error process the inventors followed to discover the two antibodies they elected to disclose and that “[u]nder Amgen, such random trial-and-error discovery, without more, constitutes unreasonable experimentation that falls outside the bounds required by § 112(a).” Id. at *8, *10.
Also, the claims are directed at a broad genus of eosinophil related disorder including upper airway diseases such as allergic rhinitis and sinusitis, foreign body aspiration, glottic stenosis, tracheal stenosis, laryngotracheomalacia, vascular rings, chronic obstructive pulmonary disease (COPD), and congestive heart failure, eosinophilic bronchitis, polychondritis, sarcoidosis, papillomatosis, arthritis (e.g., rheumatoid arthritis) and Wegener's granulomatosis [0957] and instant claim 66.
At issue whether the claimed eosinophil disorder in claims 65-68 are eosinophil related disorder. The specification at [0957] discloses that such diseases are eosinophil OR mast cell related indications. The specification fails to indicate which disorder is eosinophil related and which disorder is mast cell related disorder.
The specification under section 6.4 Example 4 discloses that treatment of a feline asthma model with anti-KIT antibody reduces eosinophil cell populations.
The specification at [1149] discloses that treatment of asthmatic cats with anti-KIT antibody decreases airway eosinophil cell numbers.
[1150] Anti-KIT-1 antibody was evaluated in an established feline model of BGA-induced asthma, with each cat acting as its own control after a wash-out period. Ten cats were dosed at 20 mg/kg anti-KIT-1 antibody on days −1 and 14 of each 28-day treatment phase. For analysis of the acute phase of asthma, airway eosinophilia were assessed one day after the first 20 mg/kg infusion of anti-KIT-1. Airway eosinophilia were significantly reduced in the acute model (FIG. 5A, p=0.009). To analyze the chronic phase of asthma, airway eosinophilia were assessed one week after the second anti-KIT-1 antibody administration during phase II. Sustained reductions in the airway eosinophilia were observed in the chronic phase as compared to placebo-treated cats (FIG. 5B, p=0.032). Effects of airway reactivity were not observed in either the acute or chronic phase.
[1151] These data indicate that administration of anti-KIT-1 antibody significantly reduces eosinophil accumulation during an allergic asthma response.
The specification discloses only treating asthma with anti-KIT-1 antibody by reducing the airway eosinophilia.
The scope of the claims encompasses the treatment and prevention of each and every eosinophil related disorder, each and every upper airway disease and allergic rhinitis, allergic sinusitis, foreign body aspiration, glottic stenosis, tracheal stenosis, laryngotracheomalacia, vascular rings, chronic obstructive pulmonary disease (COPD), congestive heart failure, eosinophilic bronchitis, polychondritis, sarcoidosis, papillomatosis, arthritis, or Wegener's granulomatosis with the claimed anti-KIT-1 antibody comprising the CDRs of SEQ ID NO: 2-7.
The specification does not provide exemplification of animal model to treat and prevent eosinophil related disorder, each and every upper airway disease and allergic rhinitis, allergic sinusitis, foreign body aspiration, glottic stenosis, tracheal stenosis, laryngotracheomalacia, vascular rings, chronic obstructive pulmonary disease (COPD), congestive heart failure, eosinophilic bronchitis, polychondritis, sarcoidosis, papillomatosis, arthritis, or Wegener's granulomatosis with the claimed anti-KIT-1 antibody comprising the CDRs of SEQ ID NO: 2-7. Besides asthma, no effect of any therapy was administered to treat or protect against or manage each and every eosinophil related disorder, each and every upper airway disease and allergic rhinitis, allergic sinusitis, foreign body aspiration, glottic stenosis, tracheal stenosis, laryngotracheomalacia, vascular rings, chronic obstructive pulmonary disease (COPD), congestive heart failure, eosinophilic bronchitis, polychondritis, sarcoidosis, papillomatosis, arthritis, or Wegener's granulomatosis with the claimed anti-KIT-1 antibody comprising the CDRs of SEQ ID NO: 2-7.
Besides the treating asthma, the specification fails to provide enablement for protect against, treat or manage each and every eosinophil related disorder, each and every upper airway disease and allergic rhinitis, allergic sinusitis, foreign body aspiration, glottic stenosis, tracheal stenosis, laryngotracheomalacia, vascular rings, chronic obstructive pulmonary (COPD), congestive heart failure, eosinophilic bronchitis, polychondritis, sarcoidosis, papillomatosis, arthritis, or Wegener's granulomatosis with the claimed anti-KIT-1 antibody comprising the CDRs of SEQ ID NO: 2-7.
Given the relatively incomplete understanding in correlating between the KIT-1 antibody and in vivo animal models to clinical protecting against, treating and managing each and every eosinophil related disorder, each and every upper airway disease and allergic rhinitis, allergic sinusitis, foreign body aspiration, glottic stenosis, tracheal stenosis, laryngotracheomalacia, vascular rings, chronic obstructive pulmonary disease (COPD), congestive heart failure, eosinophilic bronchitis, polychondritis, sarcoidosis, papillomatosis, arthritis, or Wegener's granulomatosis involved, and the lack of a reasonable correlation between the narrow disclosure in the specification and the broad scope of protection sought in the claims, the claims are not enabled. See MPEP 2164.08.
In re Fisher, 166 USPQ 18 indicates that the more unpredictable an area is, the more specific enablement is necessary in order to satisfy the statute. One cannot extrapolate the teachings of the specification to the scope of the claims because the claims are drawn to the methods of protecting against, treating or managing each and every eosinophil related disorder, each and every upper airway disease and allergic rhinitis, allergic sinusitis, foreign body aspiration, glottic stenosis, tracheal stenosis, laryngotracheomalacia, vascular rings, chronic obstructive pulmonary disease (COPD), congestive heart failure, eosinophilic bronchitis, polychondritis, sarcoidosis, papillomatosis, arthritis, or Wegener's granulomatosis with anti-KIT-1 antibody comprising the CDRs of SEQ ID NO: 2-7. No working empirical data demonstrated that the anti-KIT antibody KIT-1 would be use for the claimed treatments. The specification lacks empirical data on the in vivo efficacy of the anti-KIT-1 antibody on subjects suffering from each and every eosinophil related disorder, each and every upper airway disease and allergic rhinitis, allergic sinusitis, foreign body aspiration, glottic stenosis, tracheal stenosis, laryngotracheomalacia, vascular rings, chronic obstructive pulmonary disease (COPD), congestive heart failure, eosinophilic bronchitis, polychondritis, sarcoidosis, papillomatosis, arthritis, or Wegener's granulomatosis. The experiments in the specification never successfully used the anti-human KIT antibody KIT-1 to treat and protect against or manage each and every eosinophil related disorder, each and every upper airway disease and allergic rhinitis, allergic sinusitis, foreign body aspiration, glottic stenosis, tracheal stenosis, laryngotracheomalacia, vascular rings, chronic obstructive pulmonary disease (COPD), congestive heart failure, eosinophilic bronchitis, polychondritis, sarcoidosis, papillomatosis, arthritis, or Wegener's granulomatosis.
The MPEP states that the issue of "correlation" is also dependent on the state of the prior art. In other words, if the art is such that a particular model is recognized as correlating to a specific condition, then it should be accepted as correlating unless the examiner has evidence that the model does not correlate. Even with such evidence, the examiner must weigh the evidence for and against correlation and decide whether one skilled in the art would accept the model as reasonably correlating to the condition. See MPEP 2164.02.
Further, in Rasmusson v. SmithKline Beecham Corp., 75 USPQ2d 1297-1303 (CAFC 2005), the court states “If mere plausibility were the test for enablement under section 112, applicants could obtain patent rights to “inventions” consisting of little more than respectable guesses as to the likelihood of their success. When one of the guesses later proved true, the 'inventor' would be rewarded the spoils instead of the party who demonstrated that the method actually worked. That scenario is not consistent with the statutory requirement that the inventor enable an invention rather than merely proposing an unproved hypothesis.”
Reasonable correlation must exist between the scope of the claims and scope of the enablement set forth. In view on the quantity of experimentation necessary the limited working examples, the nature of the invention, the state of the prior art, the unpredictability of the art and the breadth of the claims, it would take undue trials and errors to practice the claimed invention.
12. 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.
13. Claims 56-59 and 61-69 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by WO2012103165 (IDS B25).
The `165 publication teaches method for treating or managing rheumatoid arthritis, inflammatory bowel disease, asthma, allergic inflammation, a gastrointestinal disorder or mastocytosis, the method comprising administering to a subject in need thereof a therapeutically effective amount of an antibody or antigen-binding fragment thereof, which immunospecifically binds to human KIT and comprises: (i) a variable light (“VL”) chain region comprising a VL CDR1, VL CDR2, and VL CDR3 comprising the amino acid sequences of SEQ ID NO: 20, SEQ ID NO: 21, and SEQ ID NO: 22 (identical to claimed SEQ ID NO: 2-4), respectively; and (ii) a variable heavy (“VH”) chain region comprising a VH CDR1, VH CDR2, and VH CDR3 comprising the amino acid sequences of SEQ ID NO: 23, SEQ ID NO: 24, and SEQ ID NO: 25 (identical to claim SEQ ID NO: 5-7), respectively, wherein the antibody is a monoclonal antibody, wherein the antibody is a humanized antibody(see [0010], [0017], [00410], [00411], [0014]. Claims 62-63 are included because the reference provides no age limit to the subject. The subject is human [0065].
While the `001 publication does not teach that the refenced disorders are “eosinophil related disorder” in claims 56-57 and “reducing airway eosinophilia” in claim 69, the mechanism of action does not have a bearing on the patentability of the invention if the invention was already known or obvious. Even though applicant has proposed or claimed the mechanism by which anti-KIT antibody alleviates symptoms of allergic airway disease, asthma, inflammatory bowel disease, Crohn's disease, ulcerative colitis, cancer, autoimmune disease, type I diabetes, rheumatoid arthritis, and autoimmune encephalitis does not appear to distinguish the prior art teaching the same or nearly the same methods to achieve the same end result. Mere recognition of latent properties in the prior art does not render nonobvious an otherwise known invention. In re Wiseman, 201 USPQ 658 (CCPA 1979). Granting a patent on the discovery of an unknown but inherent function would remove from the public that which is in the public domain by virtue of its inclusion in, or obviousness from, the prior art. In re Baxter Travenol Labs, 21 USPQ2d 1281 (Fed. Cir. 1991). See M.P.E.P. 2145.
The reference teachings anticipate the instant claims
14. Claims 56 and 69 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Yamada et al. Gunma Childrens Med Ctr, Gunma, Japan SOURCE: Blood, (NOV 16 2008) Vol. 112, No. 11, pp. 179.
Yamada et al teaches that chronic eosinophilic leukemia (CEL) mice (eosinophilic related disorder) were treated with a blocking anti-c-kit antibody, ACK-2, or an isotype-matched control antibody. ACK-2 treatment suppressed the circulating eosinophil count and spleen weight significantly in CEL mice. These results suggest that SCF signaling is required for eosinophilic leukemia development induced by FIP1L1/PDGFRa. It is noted that ACK-2 binds both mouse and human cKIT (ThermoFisher Scientific Catalog # 14-1172-82).
The reference teachings anticipate the claimed invention.
15. Claims 56-58 and 61-69 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by WO2009135001A2(IDS B21) as is evidenced by ThermoFisher Scientific Catalog # 14-1172-82.
The `001 publication teaches and claims methods of modulating an immune response in a mammal, comprising inhibiting c- Kit activity in dendritic cells, wherein the immune response is associated with a disease, wherein the disease is selected from the group consisting of an allergic airway disease, asthma, inflammatory bowel disease, Crohn's disease, ulcerative colitis, cancer, autoimmune disease, type I diabetes, rheumatoid arthritis, and autoimmune encephalitis, wherein the c-Kit activity in dendritic cells is inhibited by administering a c-Kit binding reagent to the mammal, wherein the binding reagent is a stem cell factor decoy or an antibody, wherein, the antibody is selected from the group consisting of ACK-2; YB5.B8; and K44.2 (see published claims 1-10). The `001 publication further teaches that the "subject" refers to members of the animal kingdom including but not limited to human beings that are treated using the methods. The antibody includes humanized antibodies. It is noted that ACK-2 binds both mouse and human cKIT (ThermoFisher Scientific Catalog # 14-1172-82).
While the `001 publication does not teach that the refenced disorders are “eosinophil related disorder” in claims 56-57 and “reducing airway eosinophilia” in claim 69, the mechanism of action does not have a bearing on the patentability of the invention if the invention was already known or obvious. Even though applicant has proposed or claimed the mechanism by which anti-KIT antibody alleviates symptoms of allergic airway disease, asthma, inflammatory bowel disease, Crohn's disease, ulcerative colitis, cancer, autoimmune disease, type I diabetes, rheumatoid arthritis, and autoimmune encephalitis does not appear to distinguish the prior art teaching the same or nearly the same methods to achieve the same end result. Mere recognition of latent properties in the prior art does not render nonobvious an otherwise known invention. In re Wiseman, 201 USPQ 658 (CCPA 1979). Granting a patent on the discovery of an unknown but inherent function would remove from the public that which is in the public domain by virtue of its inclusion in, or obviousness from, the prior art. In re Baxter Travenol Labs, 21 USPQ2d 1281 (Fed. Cir. 1991). See M.P.E.P. 2145.
Claims 62-63 are included because the `001 publication did not limit the treatment to any subpopulation.
The reference teachings anticipate the claimed invention.
16. The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
17. Claims 56-69 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 11891452 (IDS A123).
Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the `452 patent are directed to method for treating or managing a KIT-associated disorder, wherein the KIT-associated disorder is rheumatoid arthritis, inflammatory bowel disease, asthma, allergic inflammation, a gastrointestinal disorder or mastocytosis, the method comprising administering to a subject in need thereof a therapeutically effective amount of an isolated antibody or antigen-binding fragment thereof, which immunospecifically binds to human KIT and comprises: (i) a light chain variable region (“VL”) comprising the amino acid sequence: DIVMTQSPSX.sub.K1LSASVGDRVTITCKASQNVRTNVAWYQQKPGKAPKX.sub.K2LIYSAS YRYSGVPDRFX.sub.K3GSGSGTDFTLTISSL.sub.QX4EDFAX.sub.K5YX.sub.K6CQQYNSYPRTEGGG TKVEIK (SEQ ID NO: 12), wherein X.sub.K1 is an amino acid with an aromatic or aliphatic hydroxyl side chain, X.sub.K2 is an amino acid with an aliphatic or aliphatic hydroxyl side chain, X.sub.K3 is an amino acid with an aliphatic hydroxyl side chain, X.sub.K4 is an amino acid with an aliphatic hydroxyl side chain or is P, X.sub.K5 is an amino acid with a charged or acidic side chain, and X.sub.K6 is an amino acid with an aromatic side chain; and (ii) a heavy chain variable region (“VH”) comprising the amino acid sequence: QVQLVQSGAEX.sub.H1KKPGASVKX.sub.H2SCKASGYTFTDYYINWVX.sub.H3QAPGKGLEWIA RIYPGSGNTYYNEKFKGRX.sub.H4TX.sub.H5TAX.sub.H6KSTSTAYMX.sub.H7LSSLRSEDX.sub.H8AVYFCA RGVYYFDYWGQGTTVTVSS (SEQ ID NO: 11), wherein X.sub.H1 is an amino acid with an aliphatic side chain, X.sub.H2 is an amino acid with an aliphatic side chain, X.sub.H3 is an amino acid with a polar or basic side chain, X.sub.H4 is an amino acid with an aliphatic side chain, X.sub.H5 is an amino acid with an aliphatic side chain, X.sub.H6 is an amino acid with an acidic side chain, X.sub.H7 is an amino acid with an acidic or amide derivative side chain, and X.sub.H8 is an amino acid with an aliphatic hydroxyl side chain, wherein :
(i) the VL comprises the amino acid sequence of SEQ ID NO: 8 (identical to SEQ ID NO: 14) and the VH comprises the amino acid sequence of SEQ ID NO: 4 (identical to claim SEQ ID NO: 10);
(ii) the VL comprises the amino acid sequence of SEQ ID NO: 10 (comprising the claimed VL-CDRs) and the VH comprises the amino acid sequence of SEQ ID NO: 3 (comprising the claimed VH-CDRs and claimed SEQ ID NO:9)
(iii) the VL comprises the amino acid sequence of SEQ ID NO: 8 (identical to SEQ ID NO: 14) and the VH comprises the amino acid sequence of SEQ ID NO: 6 (identical to claimed SEQ ID NO: 12)
(iv) the VL comprises the amino acid sequence of SEQ ID NO: 7 (identical to SEQ ID NO: 13) and the VH comprises the amino acid sequence of SEQ ID NO: 5 (identical to claim 11)
(v) the VL comprises the amino acid sequence of SEQ ID NO: 7 identical to SEQ ID NO: 13) and the VH comprises the amino acid sequence of SEQ ID NO: 2 (identical to claim 8)
(iii) the VL comprises the amino acid sequence of SEQ ID NO: 8 (identical to SEQ ID NO: 14) and the VH comprises the amino acid sequence of SEQ ID NO: 6 (identical to SEQ ID NO:12)
18. Claims 56-69 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3-14, 16 and 19 of U.S. Patent No. US 10781267 B2 (IDS A114).
Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the `267 patent are directed to a method for treating or managing a KIT-associated disorder, wherein the KIT-associated disorder is associated with KIT expression and/or activity, the method comprising administering to a subject in need thereof a therapeutically effective amount of an isolated antibody, or an antigen-binding fragment thereof, which immunospecifically binds to human KIT and comprises comprising the claimed SEQ ID NOs.
19. Claims 56-64, 66 and 69 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-7 of U.S. Patent No. US 11987626 (IDS A124).
Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the `626 patent are directed to methods of protecting against, treating, or managing an eosinophil related disorder caused by eosinophils in the gastrointestinal tract (the issued subgenus of eosinophils in the gastrointestinal tract anticipated the claimed genus of eosinophil related disorder) in response to an allergen, comprising administering to a human subject having the disorder a therapeutically effective amount of a monoclonal antibody which specifically binds to a human KIT receptor comprising SEQ ID NO: 1, or an antigen binding fragment thereof, wherein the antibody or antigen binding fragment thereof each comprises a light chain variable region (“VL”) comprising VL CDRs 1-3 comprising SEQ ID NOs: 2-4, respectively, and a heavy chain variable region (“VH”) comprising VH CDRs 1-3 comprising SEQ ID NOs: 5-7, respectively, wherein the antibody comprises a VL comprising a VL sequence selected from the group consisting of SEQ ID NOs: 13, 14, 15, and 16; and a VH comprising a VH sequence selected from the group consisting of SEQ ID NOs: 8, 9, 10, 11, and 12. The claims of the `626 patent anticipate instant claims 56-64 and 69 and render claim 66 obvious.
20. Claims 56-59, 61- 69 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. US 11884699 (IDS A122).
Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the `699 patent are directed to methods for treating or managing rheumatoid arthritis, inflammatory bowel disease, asthma, allergic inflammation, a gastrointestinal disorder or mastocytosis, the method comprising administering to a subject in need thereof a therapeutically effective amount of an antibody or antigen-binding fragment thereof, which immunospecifically binds to human KIT and comprises: (i) a variable light (“VL”) chain region comprising a VL CDR1, VL CDR2, and VL CDR3 comprising the amino acid sequences of SEQ ID NO: 20, SEQ ID NO: 21, and SEQ ID NO: 22 (identical to claimed SEQ ID NOs: 2-4), respectively; and (ii) a variable heavy (“VH”) chain region comprising a VH CDR1, VH CDR2, and VH CDR3 comprising the amino acid sequences of SEQ ID NO: 23, SEQ ID NO: 24, and SEQ ID NO: 25 (identical to claims SEQ ID NOs: 5-7), respectively, wherein the antibody is a monoclonal antibody, wherein the antibody is a humanized antibody, wherein the antibody is a humanized monoclonal antibody, wherein the antibody comprises an Fc region of a human IgG1 or IgG4 antibody. The claims of the `699 anticipate the instant claims. The claimed mechanism of action are considered inherent property of the referenced antibody when administered to the same patient for the same end result.
21. Claims 56-69 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 17-18, 26-30 of copending Application No. 18/273680 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of `680 claims methods for protecting against, treating or managing a KIT-associated disorder, comprising administering to a subject in need thereof a therapeutically effective amount of the antibody claimed antibody, a conjugate or the pharmaceutical composition thereof, wherein the KIT-associated disorder is an eosinophil related disorder, asthma, an inflammatory condition, rheumatoid arthritis, an allergic inflammation, inflammatory bowel disease.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
22. No claim is allowed.
23. Any inquiry concerning this communication or earlier communications from the examiner should be directed to MAHER M HADDAD whose telephone number is (571)272-0845. The examiner can normally be reached on Monday-Friday from7:00AM to 4:30PM. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Misook Yu, can be reached at telephone number 571-272-0839. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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October 6, 2026
/MAHER M HADDAD/ Primary Examiner, Art Unit 1644
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