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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 1/30/2026 has been entered.
Election/Restrictions
Applicant’s election without traverse of the species of inhibits CD300a activity in a macrophage, antibody, 10-100mg/kg and administration before an ischemic event in the reply filed on 3/4/2025 acknowledged. Upon further consideration, the species requirements are withdrawn.
Claims 1 and 7-15 are under consideration in the instant Office Action.
Modified Rejections Necessitated by Amendment
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1 and 7-15 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. Written Description.
Claim 1 is directed to a method of treating symptoms caused by ischemia or reperfusion after the ischemia by the administration of an CD300a neutralizing antibody effective to promote CD300b-dependent phagocytosis signals in a macrophage. The CD300a binding substance inhibits the activity of CD300b in macrophage (see claim 1), is a CD300a antibody and the antibody is monoclonal and a neutralizing antibody (see claims 1 and 7). Claims 8 and 9 are the towards the method of using the claimed product. As such, the claim is directed to an antibody or peptide defined entirely by function (binding).
See MPEP §2163(I)(A) which states:
"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. 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 a sufficient identifying characteristic for written description purposes, even when accompanied by a method of obtaining the claimed sequence.”
Independent claim 1 requires an “an CD300a neutralizing antibody that inhibits or suppresses the binding of CD300a to phosphatidylserine (PS) effective to promote CD300b-dependent phagocytosis signals in a macrophage” with the intended use of treating symptoms of ischemic damage. There is no structural requirement for the CD300a neutralizing antibody in claim 1 beyond function. Claims 1 and 7 claim generic species of CD300a-binding substances that encompass any antibody that meet the function by the claimed method. The claimed activity can be achieved in any form as long as the neutralizing antibody provides the specifically claimed function treating or preventing an ischemic injury. The instant specification fails to disclose any specific CD300a neutralizing antibody that has the required function. The claims do not require that the CD300a neutralizing antibody possess any particular conserved structure or other disclosed distinguishing feature expect generic antibody that binds CD300a. Therefore, the genera are merely defined by function and the instant specification fails to describe the full genera of molecules that are encompassed by these claims that require an CD300a neutralizing antibody. The instant specification fails to teach any CD300a neutralizing antibodies.
Claim 1 requires an “an CD300a neutralizing antibody that inhibits the binding of CD300A to PS effective to promote CD300b-dependent phagocytosis signals in a macrophage.” There is no structural requirement for a generic antibody substance beyond function. This can be achieved in any form as long as the an CD300a neutralizing antibody acts upon CD300a and somehow promotes CD3000b-dependent phagocytosis signals in a macrophage. Therefore, the genus is merely defined by function and the instant specification fails to describe the full genus of molecules that are encompassed by these claims..
Further, in this case, antibodies generally share certain characteristics such as Fc regions or hinge regions. However, these structures are not correlated with the binding function of the antibody. The hyper variable regions (HVRs), i.e., complementarity determining regions (CDRs) of an antibody, are well established in the art as the portion of the binding region which imparts the specificity of an antibody. However, there is no way to a priori look at an antigen sequence (CD3000a) and envisage the combination of six CDRs that will bind that antigen. First, even highly related CDRs may not bind the same target. See for example Kussie (IDS 8/9/2022) who demonstrates that a single amino acid change in the heavy chain of an antibody which binds p-axophenylarsonate (Ars) completely abrogates the ability of the antibody to bind Ars but adds the functionality of binding the structurally related p-azophenylsulfonate (e.g., abstract). Second, even when provided with several related antibodies that bind the desired target, this does not represent the astronomical and potentially unknowable breadth of all possible amino acid sequences which will result in the desired binding properties. This is exemplified by the Court decision in Abbvie (Abbvie v Janssen 759 F.3d 1285 (Fed. Cir. 2014)), where Abbvie developed over 200 antibodies that shared 99.5% identity in the variable regions (p.7) and which bound the target, but in no way allowed one to envisage the unique structure of Centocor’s antibodies which bound the same target but shared only 50% sequence similarity (see table on page 11).
Thus, the art recognizes that the CDRs define the binding properties of an antibody and that even single amino acid changes to this region can completely abrogate the binding specificity of an antibody. As a further example, see Chen et al., 1995 (IDS 8/9/2022) which demonstrates single amino acid changes in the VH CDR2 sequence can increase binding, decrease binding, destroy binding, or have no effect on binding when compared to the wild-type antibody.
See also Koenig 2017 (IDS 8/9/2022), which provides a large mutation analysis study where every amino acid in both variable regions are substituted with every other amino acid. Looking at figure 1 of Koenig, the bottom half of each section (labeled VEGF) relates to the ability of the mutant to bind the original target, with blue meaning a reduced affinity and black meaning a complete loss of binding ability. In VH-CDR2, for example, mutating any given residue to cysteine, which is encompassed by the instant claims, resulted in reduced binding at 12 residues and a complete loss of binding at 5 residues. That is, at 100% of the positions, mutation to cysteine reduced or ablated the antibody’s ability to bind the target. Looking at a specific position, in 100% of the mutations of residue 55, binding was reduced (15/19) or eliminated (4/19). While residues 56-65 appear more tolerant of change, residues 50-55 are generally intolerant of change.
It is appreciated that Koenig is studying one specific antibody and there is no evidence that the instant antibodies would react in the same way. However, this is part of the problem. It is entirely unclear from the specification which residues of Applicant’s CDRs are tolerant or intolerant to change, and whether those tolerant positions are only tolerant to conservative mutations. The fact that some residues might tolerate mutation does not convey to the skilled artisan that Applicant knew which of the claimed residues were tolerant of such, i.e., does not convey that Applicant was in possession of those sequences which are mutated yet preserve the claimed function. In other words, the specification fails to convey possession of an invention commensurate in scope with what is now claimed and therefore fails to meet the written description requirement. Looking at Koenig figure 2A, ~200 mutations in the CDR region of the VH chain completely abrogates any binding. While 2B appears to indicate that the CDRs of VL are more tolerant of change than the heavy chain CDRs, still over half of the mutations reduce binding compared to the parent.
Thus, making changes to the CDR sequence of an antibody is a highly unpredictable process and the skilled artisan could not a priori make any predictions regarding such mutations with any reasonable expectation of success nor envisage the breadth of structurally unrelated CDR combinations that would still possess the required functions.
The specification fails to disclose any antibodies. Applicant fails to show possession of any antibodies with claimed functions. However, as discussed above, without any way to determine how broad the genus of such antibodies are, there is no way to determine the full breadth of what is claimed. There is no disclosure of any antibodies and it uncertain if any one disclosure of an antibody would not convey to the artisan that Applicant was in possession of the full genus of all antibodies which possess the required functions nor does it allow the skilled artisan to envisage the specific structure of such antibodies.
Further note the decision in Amgen v. Sanofi 2017, where the Court supported previous decisions (Centocor 2011; Abbvie 2014) that defining an antibody solely by what it binds does not satisfy the written description requirement, stating that this would allow patentees to “claim antibodies by describing something that is not the invention, i.e., the antigen”. This decision has precipitated guidance to the Office instructing that the portion of MPEP 2163 regarding the “newly characterized antigen test” (indicating a well-characterized antigen is sufficient to satisfy written description for antibodies which bind that antigen) should no longer be used and that contrary materials should not be relied upon as reflecting the current state of the law.
There is no structure for the claimed product beyond that is a monoclonal antibody. There is no structure-function correlation set forth in the instant specification. The instant specification discloses that the neutralizing CD3000a antibody comprises a CD300a binding substance that promotes CD300b-dependent phagocytosis signals in a macrophage wherein the activity modulator promotes CD300b dependent phagocytosis by binding the CD300a and inhibiting (neutralizing the binding of CD300a to PS (see paragraphs 22-24 of instant specification). Therefore, the function of the activity modulator is to block the binding of CD300a to PS to achieve its required function. Therefore, failing to meet the structure function correlation for both species of antibodies encompassed by the activity.
With respect to product in the method claims 1 and 7-15, it is recognized that information which is well known in the art need not be described in detail in the specification (MPEP §2163(II)(A)(2)). See, e.g., Hybritech, Inc. v. Monoclonal Antibodies, Inc., 802 F.2d 1367, 1379-80, 231 USPQ 81, 90 (Fed. Cir. 1986). However, sufficient information must be provided to show that the inventor had possession of the invention as claimed. MPEP §2163(II)(A)(3)(a) also discusses Univ. of Rochester v. G.D. Searle & Co., 358 F.3d 916, 927, 69 USPQ2d 1886, 1894-95 (Fed. Cir. 2004), where a method of using a PGHS-2 inhibitor did not meet the written description as the inhibitor itself was not sufficiently described, clearly indicating that written description of the compound is still required in a method of using that compound. In this case, it is clear from the specification that the invention is in an antibody. Thus, the prior art cannot provide sufficient written description of this genus of compounds and the specification as filed, and does not sufficiently describe the genus either as there is an unknown amount of structurally distinct antibodies in this genus (see Amgen and Centocor decisions discussed above) with a specific function only.
To satisfy the written description requirement, a patent specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. See, e.g., Vas-Cath, Inc., v. Mahurkar, 935 F.2d at 1563, 19 U.S.P.Q.2d at 1116. 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. An activity modulator that encompasses an antibody described only by functional characteristic, such as antibody neutralized the CD300a activity and inhibits the binding of the CD300a to PS, without any known or disclosed correlation between that function and the structure of the sequence, is not a sufficient identifying characteristic for written description purposes, even when accompanied by a method of obtaining the biomolecule of interest. In re Bell, 991 F.2d 781, 26 U.S.P.Q.2d 1529 (Fed. Cir. 1993). In re Deuel, 51 F.3d 1552, 34 U.S.P.Q.2d 1210 (Fed. Cir. 1995). In the instant case, the specification provides insufficient direction or guidance concerning the relationship between the structure of the possible peptide and antibody to demonstrate possession of the breadth of the genus antibodies encompassed by the instant claims, especially in view of the unpredictability of such an endeavor. The prior art as evidenced by Edwards et al., 2003 (IDS 8/9/2022) teaches there is a substantially huge antibody diversity produced to one single antigen target. Edwards provides evidence that over 1000 antibodies, all different amino acid sequences, were generated towards one single protein antigen target (see abstract). Without a correlation between structure and function, the claims do little more than define the claimed invention by function. That is not sufficient to satisfy the written description requirement. See Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406 (“definition by function … does not suffice to define the genus because it is only an indication of what the gene does, rather than what it is”).
Without this guidance or direction, the skilled artisan would not consider applicant to be in possession of the claimed genus of antibodies because the skilled artisan recognizes that even seemingly minor changes made without guidance or direction as to the relationship between the particular amino acid sequence of the instantly claimed antibody and its ability to bind antigen, can dramatically affect antigen-antibody binding. Applicant has not described the claimed invention sufficiently to show they had possession of the claimed genus of antibodies that inhibit the activity of CD300a in macrophages or binding of CD300a to PS. 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 University of Rochester v. G.D. Searle & Co., 358 F.3d 916, 69 USPQ2d 1886 (Fed. Cir. 2004). The instant specification even fails to specifically teach what domain of CD3000a to target and accomplish the function inhibiting the activity of CD300a in macrophages or binding of CD300a to PS as required to achieve the function.
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 claimed genus. A “representative number of species” means that the species which are adequately described are representative of the entire genus. Thus, when there is substantial variation within the genus, one must describe a sufficient variety of species to reflect the variation within the genus.
What constitutes a "representative number" is an inverse function of the skill and knowledge in the art. Satisfactory disclosure of a "representative number" depends on whether one of skill in the art would recognize that the applicant was in possession of the necessary common attributes or features of the elements possessed by the members of the genus in view of the species disclosed. For inventions in an unpredictable art, adequate written description of a genus which embraces widely variant species cannot be achieved by disclosing only one species within the genus.
To provide adequate written description and evidence of possession of the claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, methods of making the claimed product, or any combination thereof. In the instant case, the only factors present in the claims are a recitation of one generic, broad genus that encompassed a diverse and huge number of possible activity modulators that encompass peptides or antibodies that bind the CD300a while only disclosing one antibody. The specification does not provide a consistent structure for all of the possible antibodies and fails to provide a representative number of species for the claimed genus. Accordingly, in the absence of sufficient recitation of distinguishing identifying characteristics, the specification does not provide adequate written description of the claimed genus.
Vas-Cath Inc. v. Mahurkar, 19USPQ2d 1111, clearly states 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 they invented what is claimed.” (See Vas-Cath at page 1116).
With the exception of specifically disclosed peptides or antibodies with specific CDRs, the skilled artisan cannot envision the detailed chemical structure of all of the encompassed activity modular that encompass peptides and antibodies, and therefore conception is not achieved until reduction to practice has occurred, 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 of isolating it. The product itself is required. See Fiers v. Revel, 25 USPQ2d 1601 at 1606 (CAFC 1993) and Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016.
One cannot describe what one has not conceived. See Fiddes v. Baird, 30 USPQ2d 1481 at 1483. In Fiddes, claims directed to mammalian FGF's were found to be unpatentable due to lack of written description for that broad class. 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).
Therefore, claims 1 and 7-15 do not meet the written description requirement.
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 and 7-15 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 enablement requirement. 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.
The factors to be considered in determining whether a disclosure would require undue experimentation include (1) the quantity of experimentation necessary, (2) the amount of direction or guidance presented, (3) the presence or absence of working examples, (4) the nature of the invention, (5) the state of the prior art, (6) the relative skill of those in the art, (7) the predictability or unpredictability of the art and, (8) the breadth of the claims. In re Wands, 8 USPQ2d, 1400 (CAFC 1988).
The instant claims call for a method of treating symptoms of ischemia or reperfusion after ischemia in or at risk of experiencing an ischemic event in a patient by administering an CD300a neutralizing antibody that inhibits or suppresses the binding of CD3000a to PS effective to promote CD300b-dependent phagocytosis signals in a macrophage. Dependent claim 7 do claim generic species that encompass any antibody or peptide that meet the function by the claimed method. The claimed activity can be achieved in any form as long as an CD300a neutralizing antibody effective to promote CD300b-dependent phagocytosis signals in a macrophage provides the specifically claimed function treating or preventing an ischemic disease. The patient population includes anyone having an ischemic disease or has the potential of having an ischemic disease that affects their heart, lung, brain, spinal cord, retina, kidney or limbs. The methods of treating and/or preventing ischemic damage also encompass curing ischemia in view of the definitions set forth in the instant specification. The instant claims are broad and generic while what is disclosed in the instant specification is narrow and specific. The prior art only provides examples of blocking CD300a binding to PS and modulates the phagocytosis of dead cells, as evidenced by Simhadri et al., 2012 (IDS, 8/9/2022)but fails to show how any of all the possible treatments encompass by the instants can successfully promote CD300b-dependent phagocytosis signals in a macrophage in any ischemic injury in any of these areas that encompass the central nervous system or lungs, heart, kidneys and limbs or at risk of experiencing an ischemic event in a patient. Also, Shibuya et al., US2015/0047059 (IDS, 8/9/2022) teaches an activity modulator comprising a CD300a-binding substance that inhibits the binding of CD300a to phosphatidylserine (PS; see paragraphs 43, [1]-[3] and claim 25). Shibuya teaches an activity modulator that includes peptides and antibodies (see paragraph 43 [3] and [5]) 5. Shibuya teaches that the CD300a-binding substance include neutralizing antibodies against CD300a including monoclonal antibodies (see paragraph 155). The prior art teach methods or activity modulators of CD300a, but fail to teach how this treatment would promote CD300b-dependent phagocytosis signals in a macrophage or successfully treat a subject at risk of experiencing an ischemic event.
The instant specification does not provide any examples or evidence that this type of treatment would promote CD300b-dependent phagocytosis signals in a macrophage and treat ischemic injury in any of the target organs (brain, retina, lungs, heart, kidney, etc.) suffering from ischemic injury or at risk of experiencing an ischemic event. Further, the instant specification fails to teach any other possible agents that have the instantly claimed function, as discussed above in the written description rejection, and able to treat symptoms in an ischemic injury/damage in the patient population. There is no support provided in the instant specification or in the prior or instant art that teaches or supports the ability to prevent or cure an ischemic disease in the patient population.
The instant claims call for a method of treating symptoms in any ischemic injury including any neuronal injury in a patient using any antibody as claimed in the instant claims that just require an antibody or peptide that only requires an intended function of binding to CD300a but does not set forth any specific structure beyond a generic CD300a antibody. The instant claims are broad and generic while what is enabled is narrow and specific. The instant specification only provides one example of CD300a antibody administration reducing injury in brain ischemia, see instant [0083]-[0098]. The instant specification only showed amelioration of symptoms of ischemic but not how it is effective to promote CD300b-dependent phagocytosis signals in a macrophage. Further, the instant specification fails to teach any other possible antibodies that have the instantly claimed function and treat any symptoms in any ischemic disease in a patient population.
Claims 1 and 7 encompasses any of the claimed antibodies to treat symptoms of ischemic injury. The nature of the invention is clinical medicine comprising physiological modulation with an agent for a disorder of the central nervous system (CNS), and is therefore of the highest complexity due to the complex nature of the nervous system. The claim is equally unfettered by any limitation drawn to any means by which the physiological process step may be accomplished. Independent claims 1 and 7 are a “single means” claim in that it recites any antibody from these claims treat the injury in a subject. The instant fact pattern is similar to that in In re Hyatt, 798 F.2d 712, 218 USPQ 195 (Fed. Cir. 1983), wherein a single means claim which covered every conceivable means for achieving the stated purpose was held nonenabling for the scope of the claim because the specification at most disclosed only those means known to the inventors. In the instant case, the specification provides only a few examples that meet the function requirements of the antibodies in the instant claim but fails to show how these antibodies are capable of promoting CD300b-dependent phagocytosis signals in a macrophage to treat ischemic injury. Therefore, the specification fails to provide enough guidance for one skilled in the art on how to practice the instant method, thereby requiring trial and error experimentation to identify compounds meeting the functional limitations of the claims.
The art does not provide compensatory teachings of what antibodies would block PS binding and promote CD300b-dependent phagocytosis signals in a macrophage. One of ordinary skill would also have perform unknown number of experiments to determine if the claimed antibodies are able to provide the specific effect in a patient population that has not yet to date been shown to be capable of stopping the injury from occurring. This would require undue experimentation. The scope of the claims must bear a reasonable correlation with the scope of enablement (In re Fisher, 166 USPQ 19 24 (CCPA 1970)). Without such guidance, the changes which can be made and still maintain activity/utility is unpredictable and the experimentation left to those skilled in the art is unnecessarily, and improperly, extensive and undue. See Ex parte Forman, 230 USPQ 546 (Bd. Pat. App. & Int. 1986).
As set forth above, inadequate guidance is presented in the specification to overcome the obstacles in practicing the claimed invention in its full scope. The test of enablement is not whether any experimentation is necessary, but whether, if experimentation is necessary, it is undue. Given the tremendous breath of scope involving the instant claims, it would require undue experimentation for one of skill in the art to practice the claimed invention in its full scope. Therefore, the specification fails to provide enough guidance for one skilled in the art on how to practice the full scope of the instantly claimed method, thereby requiring trial and error experimentation to identify compounds meeting the functional limitations of the claims. The general knowledge and level of skill in the art do not supplement the omitted description because specific, not general, guidance is what is needed. One of skill in the art would neither expect nor predict the appropriate methods of treating all neurodegenerative conditions in the manner claimed. Therefore, in view of the lack of guidance in the specification and in view of the discussion above, undue experimentation would indeed be required to make and use the invention commensurate with the scope of the claims.
The scope of the claims must bear a reasonable correlation with the scope of enablement. In re Fisher, 166 USPQ 18(CCPA 1970) indicates that the more unpredictable an area is, the more specific enablement is necessary in order to satisfy the statute.
Undue experimentation would be required to produce the invention commensurate with the breadth of the claims based on the disclosure of the instant specification and the knowledge in the art. Reasonable correlation must exist between the scope of the claims and scope of enablement set forth. In view of the quantity of experimentation necessary, the limited working examples, the unpredictability of the art, the lack of sufficient guidance in the specification, and the breadth of the claims, it would take undue trial and error to practice full scope of the claimed invention.
In conclusion, the instant claims encompass an invention of tremendous breadth, and essentially call for trial and error by the skilled artisan to begin discovering how to make the claimed invention without assisting the skilled artisan in such an endeavor, which amounts to undue experimentation and is therefore insufficient to constitute adequate enablement.
Response to Amendment
The declaration under 37 CFR 1.132 filed 1/13/2026 is insufficient to overcome the rejection of claims 1 and 7-15 based upon 112 written description and enablement as set forth in the last Office action because: they do not address the same scope as the instant claims. Please note that the declaration is hard to read and interpret since the text and figures are very pixelated and the resolution does not allow one to be able to read the figure legends. The instant claims call for a very specific effect to be produced: any CD300a antibody type that would inhibit PS binding and the treatment would promote CD300b-dependent phagocytosis signals in a macrophage and treat ischemic injury in any of the target organs (brain, retina, lungs, heart, kidney, etc.) suffering from ischemic injury or at risk of experiencing an ischemic event. The declaration only shows that different CD300a antibody clones prevent PS binding. There is no evidence provided that these antibodies are capable of promote CD300b-dependent phagocytosis signals in a macrophage and treat ischemic injury in any of the target organs (brain, retina, lungs, heart, kidney, etc.) suffering from ischemic injury or at risk of experiencing an ischemic event. The declaration fails to demonstrate how CD300a is linked to CD300b phagocytosis. Therefore, the declaration is not found persuasive since what is demonstrated in very narrow in scope and the claims rea on much broader and unenabled scope.
Response to Arguments
Applicant's arguments filed 1/13/2026 have been fully considered but they are not persuasive. Applicant argues that they do not need to disclose an CD300a neutralizing antibodies since they are known in the prior art. This is not found persuasive because the instant claims are towards a method requiring a specific antibody with a specific function. While the prior art does disclose CD300a neutralizing antibodies there is no support for the fact any known or unknown generic CD300a neutralizing antibody would be actually be capable of producing the required effect of promoting CD300b-dependent phagocytosis signals in a macrophage and treat ischemic injury in any of the target organs (brain, retina, lungs, heart, kidney, etc.) suffering from ischemic injury or treating a subject at risk of experiencing an ischemic event as required in the instant claims. The written description issue for the non-specific antibody is due to the fact that this specifically claimed antibody has to produce a very specific function, such as promoting CD300b-dependent phagocytosis signals in a macrophage and treat ischemic injury in any of the target organs (brain, retina, lungs, heart, kidney, etc.) suffering from ischemic injury or treating a subject at risk of experiencing an ischemic event. Therefore, there is a need for a specific disclosure of what specific antibodies are capable of doing this without undue experimentation. This is the other reason why the enablement rejection is also maintained. The reasonable interpretation of the instant claims read on promoting CD300b-dependent phagocytosis signals in a macrophage and treat ischemic injury in any of the target organs (brain, retina, lungs, heart, kidney, etc.) suffering from ischemic injury or treating a subject at risk of experiencing an ischemic event which are very specific and high function results and would require undue experimentation to determine exactly which antibodies under the genus of CD300a neutralizing antibodies are actually capable of producing these results. While the applicant presents data to indicate one of the possible CD300a neutralizing antibodies prevent PS binding, it does not show how they are capable of promoting CD300b-dependent phagocytosis signals in a macrophage and treat ischemic injury in any of the target organs (brain, retina, lungs, heart, kidney, etc.) suffering from ischemic injury or treating a subject at risk of experiencing an ischemic event. Examiner notes that there is no evidence provided that supports the full scope of the instant claims. Finally, as set forth above, the instant specification or instant claims do not provide evidence or support for the full scope of the claimed invention and the rejections of record are maintained.
Conclusion
No claims are allowed.
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/AURORA M FONTAINHAS/Primary Examiner, Art Unit 1675