DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claim Status
Claims 1-18, 21, 23, 28, 30-34, 41, 47, and 51 have been cancelled and claims 19, 22, 24-25, and 29 have been amended, as requested in the amendment filed on 10/29/2025. Following the amendment, claims 19-20, 22, 24-27, 29, 35-40, 42-46, and 48-50 are pending in the instant application.
Claims 19-20, 22, 24-27, 29, 35-40, 42-46, and 48-50 are under examination in the instant office action.
Specification - Objections Withdrawn
Applicant has submitted an amended abstract and has amended pages 47 and 54 of the specification to remove embedded hyperlinks and/or other forms of browser executable code. As such, the objections to the specification are withdrawn.
Claim Objections - Withdrawn
Claims 35, 37, 39, and 40 were objected to for minor informalities. Applicant has amended the claims to correct the minor informalities such that the claims now recite “SEQ ID NO: 3” and “SEQ ID NO: 7”. As such, the objection to claims 35, 37, 39, and 40 are withdrawn.
Claim Rejections - 35 USC § 112 - Withdrawn
Claim 51 was rejected under 35 USC § 112(b) as being indefinite. Applicant has cancelled claim 51, rendering the rejection moot. As such, the rejection of claim 51 under 35 USC § 112(b) as being indefinite is withdrawn.
Claims 22 and 25 were rejected under 35 USC § 112(d) as being of improper dependent form. Applicant has amended claim 22 such that it now depends from claim 19 and has amended claim 25 to further recite a pharmaceutically acceptable carrier. As such, the rejection of claims 22 and 25 under 35 USC § 112(d) as being of improper dependent form is withdrawn.
Claim Rejections - 35 USC § 103 - Updated
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 text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
It is noted that the claim rejections presented below all rely on the same art references and teachings previously cited. However, the claim rejections have been updated as necessary to address the instantly amended claims.
Claim(s) 19-20, 22, 24-27, 29, 35-40, 42-46, and 48-50 is/are rejected under 35 U.S.C. 103 as being unpatentable over WO 2018/071576 A1 (06/03/2022 IDS; previously cited; herein after referred to as "Coligan") in view of WO 2018/094460 A1 (06/03/2022 IDS; previously cited; herein after referred to as "Hart").
With regard to claims 19-20 and 22, Coligan teaches methods for treating a subject with a solid tumor wherein said methods can include administering to the subject a therapeutically effective amount of (l) a CD300f inhibitor, (2) dendritic cells comprising an inactivated gene encoding CD300f, (3) T cells activated by the dendritic cells comprising an inactivated gene encoding CD300f, or combinations thereof, thereby treating the solid tumor in the subject (Abstract). A CD300f inhibitor of the invention can be, for example, a soluble protein, an antibody or aptamer that specifically binds CD300f, or an inhibitory nucleic acid molecule (RNAi), such as, but not limited to, a ribozyme, a siRNA or a shRNA wherein the CD300f antagonist can result in the induction of an immune response to the tumor (Page 20, Lines 21-24; emphasis added). Without being bound by theory, administration of one or more CD300f inhibitors increases antigen presentation by dendritic cells (i.e., antigen presenting cell), and results in the production of activated T cells (i.e., increases T cell responses), such as CD8+ cytotoxic cells, specific for the tumor (Page 35, Lines 5-7; emphasis added). Furthermore, methods of the invention can include administering additional therapeutic agents, such as, but not limited to, a chemotherapeutic agent, a biologic, a PD-1 antagonist, or a CTLA-4 antagonist wherein such agents can be administered before, after, or concurrently with the CD300f inhibitor (Page 41, Lines 5-10; emphasis added). Coligan also teaches that, in one example, the additional therapeutic agent can be a biologic agent (e.g., monoclonal antibody) or a small molecule such as those presented in Table 1 (Pages 42-43). Dendritic cells deficient for expression of CD300f are used to induce activated T cells, such as activated cytotoxic CD8+ T cells, specific for the tumor; a therapeutically effective amount of the activated T cells can be administered to subject with the tumor and, in particular embodiments, the T cells and/or dendritic cells are amo1ogous and, in some non-limiting examples, the subject can be administered an additional therapeutic agent such as, but not limited to, a CD300f inhibitor, a chemotherapeutic agent, an anti-neoplastic agent, a PD-1 antagonist or a CTLA-4 antagonist (Page 51, Lines 14-22). Coligan further teaches that tumor cells, such as apoptotic or killed cells, may be used to deliver antigen to either immature or mature dendritic cells, either freshly isolated or obtained from in vitro culture, wherein expression of CD300f is decreased in the dendritic cells (Page 54, Lines 13-22). In one embodiment, tumor cells comprising an antigen (e.g., tumor/cancer antigen) are co-cultured with immature dendritic cells for a time sufficient to allow the antigen to be internalized by the immature dendritic cells wherein the immature dendritic cells are then caused to mature by the addition of a maturation factor to the culture medium; the matured dendritic cells expressing processed antigen on their surface are then exposed to T cells for potent cytotoxic T cell induction to the tumor or, alternatively, one or more specific tumor antigens can be used wherein exemplary tumor antigens that can be used include but are not limited to those shown in Table l (Id.). Thus, Coligan teaches methods for treating solid tumors comprising administering a CD300f inhibitor (e.g., a CD300f binding protein such as an antibody or aptamer) and further comprising administering an additional agent (e.g., a biologic) wherein the administration results in activation (i.e., increases activity) of T cells against a solid tumor. It is noted that while Coligan doesn’t explicitly teach the administration of a CD300f inhibitor with a target antigen (i.e., tumor or cancer antigen), it is noted that Coligan teaches co-incubating antigen-presenting cells with tumor/cancer antigen (see for example Table 1) to facilitate antigen presentation and Coligan also teaches that CD300f inhibitors increase antigen presentation which subsequently activates T cells (i.e., activates T cells against the antigen). However, it is noted that Coligan does not teach or suggest coupling a CD300f binding protein to a target antigen. This deficiency is remedied by Hart.
Hart teaches an antibody, or antigen binding fragment thereof, that specifically binds to a CD300f polypeptide, and the use of that antibody or antigen binding fragment thereof, in therapy (Page 1, Lines 3-5) and further teaches an immunoconjugate comprising an isolated antibody, or antigen binding fragment thereof, which specifically binds to an extracellular domain of CD300f, wherein the antibody, or antigen binding fragment thereof, is coupled to a moiety (Pages 4-5; see eighth aspect, for example). Examples of moieties include, for example, a radioisotope (e.g., iodine-131, yttrium-90 or indium-111), a detectable label (e.g., a fluorophore or a fluorescent nanocrystal), a therapeutic compound (e.g., a chemotherapeutic or an anti-inflammatory), a colloid (e.g., gold), a toxin (e.g., ricin), a nucleic acid, a peptide (e.g., a serum albumin binding peptide), a protein (e.g., a protein comprising an antigen binding domain of an antibody or serum albumin), a compound that increases the half-life of the antibody or antigen binding protein in a subject (e.g., polyethylene glycol or other water-soluble polymer having this activity) or mixtures thereof (Pages 28-29).
Coligan and Hart are considered to be analogous to the present invention as they are in the same field of CD300f and therapeutics. Thus, one of ordinary skill in the art could ascertain, from the teachings of Coligan, that administering a CD300f inhibitor (i.e., a CD300f binding protein) and target antigen (e.g., tumor or cancer antigen) would specifically increase the presentation of said target antigen and would subsequently result in the activation of T cells against said target antigen and thus treat a disease/condition associated with said target antigen. Furthermore, it would have been obvious to one of ordinary skill in the art to modify the method suggested by Coligan such that the CD300f inhibitor is coupled to a moiety, as suggested by Hart, wherein the moiety is the target antigen such as a cancer antigen (i.e., a protein) suggested by Coligan because combining prior art elements according to known methods would be expected to yield predictable results. One of ordinary skill in the art would recognize that coupling a CD300f inhibitor to a target antigen would enhance/specifically target the delivery of the cancer target antigen to target cells (e.g., antigen presenting dendritic cells) wherein the inhibition of CD300f of said dendritic cells would then facilitate increased cancer target antigen presentation and subsequent T cell activation against said cancer target antigen, wherein such a method would be useful in a more efficacious method of promoting/increasing T cell response to said cancer target antigen.
With regard to claims 24-25, Coligan teaches that the methods of the invention can include administering to the subject a therapeutically effective amount of a pharmaceutical composition comprising a CD300f inhibitor (Page 37, Lines 8-15). It is further noted that the pharmaceutical compositions of Coligan further comprise pharmaceutically acceptable carriers (See Pages 13-14 and/or Page 37, Lines 17-24). As detailed above, one of ordinary skill in the art would have been motivated to administer a CD300f inhibitor coupled to a target antigen (e.g., tumor or cancer antigen), and as such it was prima facie obvious to use a composition (i.e., pharmaceutical composition) comprising a CD300f coupled to an additional agent such as a target antigen, which would result in the increased presentation of said target antigen of an antigen presenting cell (i.e., antigen loading).
With regard to claims 26-27, a composition comprising a CD300f inhibitor and a target antigen with therapeutic applications is rendered obvious by Coligan, as detailed above. However, Coligan does not suggest an immunoconjugate. Hart teaches an antibody, or antigen binding fragment thereof, that specifically binds to a CD300f polypeptide, and to the use of that antibody or antigen binding fragment thereof, in therapy (Page 1, Lines 3-5) and further teaches an immunoconjugate comprising an isolated antibody, or antigen binding fragment thereof, which specifically binds to an extracellular domain of CD300f, wherein the antibody, or antigen binding fragment thereof, is coupled to a moiety (Pages 4-5; see eighth aspect, for example). Examples of moieties include, a radioisotope (e.g., iodine-131, yttrium-90 or indium-111), a detectable label (e.g., a fluorophore or a fluorescent nanocrystal), a therapeutic compound (e.g., a chemotherapeutic or an anti-inflammatory), a colloid (e.g., gold), a toxin (e.g., ricin), a nucleic acid. a peptide (e.g., a serum albumin binding peptide), a protein (e.g., a protein comprising an antigen binding domain of an antibody or serum albumin), a compound that increases the half-life of the antibody or antigen binding protein in a subject (e.g., polyethylene glycol or other water-soluble polymer having this activity) or mixtures thereof (Pages 28-29). Thus, one of ordinary skill in the art could ascertain, from the teachings of Coligan, that administering a CD300f inhibitor (i.e., a CD300f binding protein) and target antigen (e.g., tumor or cancer antigen) would specifically increase the presentation of said target antigen and would subsequently result in the activation of T cells against said target antigen and thus treat a disease/condition associated with said target antigen. Furthermore, it would have been obvious to one of ordinary skill in the art to modify the method suggested by Coligan such that the CD300f inhibitor is coupled to a moiety (i.e., an immunoconjugate), as suggested by Hart, wherein the moiety is the target antigen such as a cancer antigen (i.e., a protein) suggested by Coligan because combining prior art elements according to known methods would be expected to yield predictable results. One of ordinary skill in the art would recognize that coupling a CD300f inhibitor to a target antigen would enhance/specifically target the delivery of the cancer target antigen to target cells (e.g., antigen presenting dendritic cells) wherein the inhibition of CD300f of said dendritic cells would then facilitate increased cancer target antigen presentation and subsequent T cell activation against said cancer target antigen, wherein such a method would be useful in a more efficacious method of promoting/increasing T cell response to said cancer target antigen.
With regard to claim 29, Coligan further teaches that tumor cells, such as apoptotic or killed cells, may be used to deliver antigen to either immature or mature dendritic cells, either freshly isolated or obtained from in vitro culture, wherein expression of CD300f is decreased in the dendritic cells (Page 54, Lines 13-22). In one embodiment, tumor cells comprising an antigen (e.g., tumor antigen) are co-cultured with immature dendritic cells for a time sufficient to allow the antigen to be internalized by the immature dendritic cells wherein the immature dendritic cells are then caused to mature by the addition of a maturation factor to the culture medium; the matured dendritic cells expressing processed antigen on their surface are then exposed to T cells for potent cytotoxic T cell induction to the tumor or, alternatively, one or more specific tumor antigens can be used wherein exemplary tumor antigens that can be used include but are not limited to those shown in Table l (Id.). In this example, the antigen presenting cells are engineered to have reduced CD300f expression, however as indicated by Coligan dendritic cells can also be exposed to CD300f inhibitors to increase antigen presentation. Thus, one of ordinary skill in the art could ascertain, from the teachings of Coligan, that incubating antigen presenting cells with CD300f inhibitor in the presence of a target antigen (e.g., tumor or cancer antigen), which may be coupled to the CD300f inhibitor, would specifically increase the presentation of said target antigen and said antigen presenting cell would be capable of presenting the target antigen to a T cell which would subsequently result in the activation of T cells against said target antigen. Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective filing date of the invention as evidenced by the references.
With regard to claims 35-36, Coligan also teaches that a CD300f inhibitor can be, for example, an antibody or aptamer that specifically binds CD300f (Page 20, Lines 21-24) wherein the CD300f inhibitor can be an antibody, such as a monoclonal antibody, and antibodies that specifically bind CD300f are commercially available, fully human and humanized antibodies that bind CD300f can be produced using methods known to those of skill in the art, and a monoclonal antibody that specifically binds CD300f can be identified and isolated by screening a recombinant combinatorial immunoglobulin library (Pages 20-23). Hart teaches an antibody, or antigen binding fragment thereof, that specifically binds to a CD300f polypeptide, and to the use of that antibody or antigen binding fragment thereof, in therapy (Page 1, Lines 3-5) including embodiments wherein the antibody, or antigen binding fragment thereof, comprises a heavy chain comprising SEQ ID NO: 13 and/or a light chain comprising SEQ ID NO: 14. It is specifically noted that Hart SEQ ID NOs: 13 and 14 are 100% matches to instant SEQ ID NOs: 1 and 5, respectively, and also comprise 100% matches to instant SEQ ID NOs: 2-4 and 6-8, respectively. Thus, it would have been obvious to one of ordinary skill in the art to modify the method of claim 19 such that instead of the CD300f inhibitor (i.e., CD300f binding protein) of Coligan, the CD300f binding protein comprises CDRs corresponding to instant SEQ ID NOs: 2-4 and 6-8 and a heavy chain and light chain corresponding to instant SEQ ID NOs: 1 and 5, as suggested by identical sequences disclosed by Hart, because one of ordinary skill in the art would recognize that any CD300f specific binding protein would be capable of delivering the coupled target antigen to target cells (e.g., antigen presenting dendritic cells), wherein the delivery of the target antigen to said dendritic cells would then facilitate increased target antigen presentation and subsequent T cell activation against said target antigen.
With regard to claims 37-38, Hart further teaches embodiments wherein the CD300f antibody, or antigen binding fragment thereof, comprises a heavy chain comprising SEQ ID NO: 13 and/or a light chain comprising SEQ ID NO: 14. It is specifically noted that Hart SEQ ID NOs: 13 and 14 are 100% matches to instant SEQ ID NOs: 1 and 5, respectively, and also comprise 100% matches to instant SEQ ID NOs: 2-4 and 6-8, respectively. Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective filing date of the invention as evidenced by the references.
With regard to claims 39 and 43, Hart teaches an antibody, or antigen binding fragment thereof, that specifically binds to a CD300f polypeptide, and to the use of that antibody or antigen binding fragment thereof, in therapy (Page 1, Lines 3-5) including embodiments wherein the antibody, or antigen binding fragment thereof, comprises a heavy chain comprising SEQ ID NO: 13 and/or a light chain comprising SEQ ID NO: 14. It is specifically noted that Hart SEQ ID NOs: 13 and 14 are 100% matches to instant SEQ ID NOs: 1 and 5, respectively, and also comprise 100% matches to instant SEQ ID NOs: 2-4 and 6-8, respectively. Hart further teaches an antibody, or antigen binding fragment thereof, that specifically binds to a CD300f polypeptide, and to the use of that antibody or antigen binding fragment thereof, in therapy (Page 1, Lines 3-5) and further teaches an immunoconjugate comprising an isolated antibody, or antigen binding fragment thereof, which specifically binds to an extracellular domain of CD300f, wherein the antibody, or antigen binding fragment thereof, is coupled to a moiety (Pages 4-5; see eighth aspect, for example). Examples of moieties include, a radioisotope (e.g., iodine-131, yttrium-90 or indium-111), a detectable label (e.g., a fluorophore or a fluorescent nanocrystal), a therapeutic compound (e.g., a chemotherapeutic or an anti-inflammatory), a colloid (e.g., gold), a toxin (e.g., ricin), a nucleic acid. a peptide (e.g., a serum albumin binding peptide), a protein (e.g., a protein comprising an antigen binding domain of an antibody or serum albumin), a compound that increases the half-life of the antibody or antigen binding protein in a subject (e.g., polyethylene glycol or other water-soluble polymer having this activity) or mixtures thereof (Pages 28-29). Thus, it would have been obvious to one of ordinary skill in the art to modify the method of claim 19 such that instead of the CD300f inhibitor (i.e., CD300f binding protein) of Coligan, the CD300f binding protein comprises CDRs corresponding to instant SEQ ID NOs: 2-4, 6-8, 1, and 5 as suggested by identical sequences disclosed by Hart, because one of ordinary skill in the art would recognize that any CD300f specific binding protein would be capable of delivering the coupled target antigen to target cells (e.g., antigen presenting dendritic cells), wherein the delivery of the target antigen to said dendritic cells would then facilitate increased target antigen presentation and subsequent T cell activation against said target antigen.
With regard to claims 40 and 42 Hart teaches an antibody, or antigen binding fragment thereof, that specifically binds to a CD300f polypeptide, and to the use of that antibody or antigen binding fragment thereof, in therapy (Page 1, Lines 3-5) including embodiments wherein the antibody, or antigen binding fragment thereof, comprises a heavy chain comprising SEQ ID NO: 13 and/or a light chain comprising SEQ ID NO: 14. It is specifically noted that Hart SEQ ID NOs: 13 and 14 are 100% matches to instant SEQ ID NOs: 1 and 5, respectively, and also comprise 100% matches to instant SEQ ID NOs: 2-4 and 6-8, respectively. Hart further teaches an antibody, or antigen binding fragment thereof, that specifically binds to a CD300f polypeptide, and to the use of that antibody or antigen binding fragment thereof, in therapy (Page 1, Lines 3-5) and further teaches an immunoconjugate comprising an isolated antibody, or antigen binding fragment thereof, which specifically binds to an extracellular domain of CD300f, wherein the antibody, or antigen binding fragment thereof, is coupled to a moiety (Pages 4-5; see eighth aspect, for example). Examples of moieties include, a radioisotope (e.g., iodine-131, yttrium-90 or indium-111), a detectable label (e.g., a fluorophore or a fluorescent nanocrystal), a therapeutic compound (e.g., a chemotherapeutic or an anti-inflammatory), a colloid (e.g., gold), a toxin (e.g., ricin), a nucleic acid. a peptide (e.g., a serum albumin binding peptide), a protein (e.g., a protein comprising an antigen binding domain of an antibody or serum albumin), a compound that increases the half-life of the antibody or antigen binding protein in a subject (e.g., polyethylene glycol or other water-soluble polymer having this activity) or mixtures thereof (Pages 28-29). Thus, it would have been obvious to one of ordinary skill in the art to modify the method of claim 29 such that instead of the CD300f inhibitor (i.e., CD300f binding protein) of Coligan, the CD300f binding protein comprises CDRs corresponding to instant SEQ ID NOs: 2-4, 6-8, 1, and 5 as suggested by identical sequences disclosed by Hart, because one of ordinary skill in the art would recognize that any CD300f specific binding protein would be capable of delivering the coupled target antigen to target cells (e.g., antigen presenting dendritic cells), wherein the delivery of the target antigen to said dendritic cells would then facilitate increased target antigen presentation and subsequent T cell activation against said target antigen.
With regard to claims 44-46, as detailed above, Coligan teaches that the administration of a CD300f inhibitor increases antigen presentation of dendritic cells and said dendritic cells promote the activation of T cells; thus, the administration of CD300f inhibitor activates dendritic cells and said activated dendritic cells subsequently activate T cells. Additionally, Coligan teaches that CD300f is expressed on myeloid cells (i.e., dendritic cells and macrophages) (Page 1, Lines 32-33) and that methods of the invention are disclosed for targeting CD300f in dendritic cells (Page 2, Lines 3-5). Thus, Coligan teaches/suggests antigen presenting cells that are myeloid dendritic cells. Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective filing date of the invention as evidenced by the references.
With regard to claims 48-50, Coligan further teaches that mature dendritic cells can be selected by expression of one or more markers wherein the markers include, but are not limited to, CD86, CD80, CD83, CD58, CDla, HLA-DR, CD40, CDl1c, IL-2-beta, TLR-4 and combinations thereof; dendritic cells can also be identified as lacking or expressing low levels of markers such as CD14 (Pages 53-54). In one embodiment, mature dendritic cells are identified as being CD80+, CD83+, CD86+, and CD14-; greater MHC expression leads to an increase in antigen density on the dendritic cell surface, while up-regulation of costimulatory molecules CD80 and CD86 strengthens the T cell activation signal through the counterparts of the costimulatory molecules, such as CD28 on the T cells (Id.). Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective filing date of the invention as evidenced by the references.
Double Patenting - Maintained
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.
Claims 19-20, 22, 24-27, 29, 35-40, 42-46, and 48-50 stand as rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-13 of U.S. Patent No. 11,987,625 (herein after referred to as “reference patent”) in view of Coligan.
Claims 19-20, 22, 24-27, 29, 35-40, 42-46, and 48-50 stand as provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 23-42 of copending Application No. 18/652,625 (herein after referred to as “’625”) in view of Coligan.
Response to Arguments
With regard to the claim rejections under (i) 35 U.S.C. 103 in view of Coligan and Hart, (ii) nonstatutory double patenting over U.S. Patent No. 11,987,625 in view of Coligan, and (iii) provisional nonstatutory double patenting over copending Application No. 18/652,625 in view of Coligan, Applicant argues the following on Pages 13-15 of Remarks (10/29/2025):
Coligan does not teach or suggest coupling of a target antigen to a CD300f inhibitor or utilizing CD300f to introduce and process a target antigen. Coligan is instead concerned with the inhibition of CD300f. In this regard, Coligan teaches that antisense oligonucleotides, siRNA, or ribozymes, all of which are designed to prevent CD300f protein expression, can be used as an inhibitor of CD300f. In contrast to Coligan, the present invention does not seek to inhibit CD300f, but rather relies on the presence of CD300f to deliver the target antigen payload into the antigen presenting cell.
Hart does not cure the deficiencies of Coligan. Hart does not disclose an immunoconjugate in which a target antigen is coupled to an anti-CD300f antibody. Hart neither teaches nor suggests coupling a target antigen to the anti-CD300f antibody. Instead, Hart is concerned with the use of an anti-CD300f monoclonal antibody to mediate antibody-dependent cell- mediated cytotoxicity (ADCC). Hart teaches coupling cytotoxic molecules (including pro-apoptotic agents, cytotoxic agents, and immunotoxic agents) to an anti-CD300f antibody and then using the anti-CD300f antibody conjugate to target AML blasts and leukemic stem cells, with a view to killing such cells through cytotoxic effects. Such an approach is the exact opposite of the claimed invention, which utilizes viable and functional antigen presenting cells.
There is nothing in either Coligan or Hart, alone or in combination, to suggest that a CD300f binding protein coupled to a target antigen could be introduced into an antigen presenting cell, let alone that the antigen presenting cell could subsequently present the target antigen in a manner that promotes a T cell response to the target antigen, as achieved by the claimed invention
Applicant's arguments have been fully considered but they are deemed not persuasive.
With regard to Applicant’s arguments, the following are noted:
Arguments (i) and (ii) above are based on piecemeal analysis of the references; it has been held that one cannot show non-obviousness by attacking references individually where, as here, the rejections are based on combinations of references. In re Keller, 208 USPQ 871 (CCPA 1981).
Applicant is reminded that preferred embodiments are not the only teaching of a reference. “The use of patents as references is not limited to what the patentees describe as their own inventions or to the problems with which they are concerned. They are part of the literature of the art, relevant for all they contain.” In re Heck, 699 F.2d 1331, 1332-33, 216 USPQ 1038, 1039 (Fed. Cir. 1983) (quoting In re Lemelson, 397 F.2d 1006, 1009, 158 USPQ 275, 277 (CCPA 1968)). A reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill the art, including nonpreferred embodiments. Merck & Co. v. Biocraft Laboratories, 874 F.2d 804, 10 USPQ2d 1843 (Fed. Cir.), cert. denied, 493 U.S. 975 (1989). See also > Upsher-Smith Labs. v. Pamlab, LLC, 412 F.3d 1319, 1323, 75 USPQ2d 1213, 1215 (Fed. Cir. 2005)(reference disclosing optional inclusion of a particular component teaches compositions that both do and do not contain that component); < Celeritas Technologies Ltd. v. Rockwell International Corp., 150 F.3d 1354, 1361, 47 USPQ2d 1516, 1522-23 (Fed. Cir. 1998) (The court held that the prior art anticipated the claims even though it taught away from the claimed invention. “The fact that a modem with a single carrier data signal is shown to be less than optimal does not vitiate the fact that it is disclosed.”). Disclosed examples and preferred embodiments do not constitute a teaching away from a broader disclosure or nonpreferred embodiments. In re Susi, 440 F.2d 442, 169 USPQ 423 (CCPA 1971). “A known or obvious composition does not become patentable simply because it has been described as somewhat inferior to some other product for the same use.” In re Gurley, 27 F.3d 551, 554, 31 USPQ2d 1130, 1132 (Fed. Cir. 1994). Furthermore, “[t]he prior art’s mere disclosure of more than one alternative does not constitute a teaching away from any of these alternatives because such disclosure does not criticize, discredit, or otherwise discourage the solution claimed….” In re Fulton, 391 F.3d 1195, 1201, 73 USPQ2d 1141, 1146 (Fed. Cir. 2004).
With regard to argument (i), it is noted that Coligan teaches using an antibody/aptamer that specifically binds to CD300f. The instant claims only require a CD300f binding protein, of which the CD300f antibodies/aptamers of Coligan read on. The fact that the CD300f antibodies/aptamers of Coligan are CD300f inhibitors does not teach away from the instant claims. Specifically, Coligan indicates that the use of such inhibitor CD300f antibodies/aptamers still function to facilitate antigen presentation and wherein the CD300f inhibitors increase antigen presentation which subsequently activates T cells (i.e., activates T cells against the antigen). Thus, Coligan discloses concurrent use of CD300f binding proteins and a target antigen to increase antigen presentation and subsequently activate T cells.
With regard to argument (ii), Hart is specifically relied upon for its disclosure of using CD300f binding proteins (i.e., antibodies) in therapeutic methods, wherein it is specifically noted that such CD300f binding proteins may be used in immunoconjugate formats (including coupling to proteins) and that the disclosed antibodies of Hart comprise the instantly claimed sequences. Hart does not explicitly disclose coupling a target antigen to the CD300f binding proteins, but in view of the teachings of Coligan one of ordinary skill in the art would have been motivated to do so. Specifically, an immunoconjugate wherein a CD300f binding protein (that of Coligan or Hart) would be able to specifically target antigen-presenting cells, as suggested by both Coligan and Hart, and deliver the target antigen to said antigen-presenting cells. Based on the teachings of Coligan, one of ordinary skill in the art would recognize that the delivery of said target antigen to said antigen-presenting cells would facilitate increased antigen presentation and would serve to promote T cell activation against said target antigen, ultimately resulting in a larger immune response against said target antigen. Coligan and Hart are considered to be analogous to the present invention as they are in the same field of CD300f (e.g., CD300f binding proteins) and therapeutics (directed at antigen-presenting cells and/or subsequent T cell activation) and thus it would have been obvious to one of ordinary skill in the art to modify the method suggested by Coligan such that the CD300f inhibitor is coupled to a moiety (i.e., an immunoconjugate), as suggested by Hart, wherein the moiety is the target antigen such as a cancer antigen (i.e., a protein) suggested by Coligan because combining prior art elements according to known methods would be expected to yield predictable results; one of ordinary skill in the art would recognize that coupling a CD300f inhibitor to a target antigen would enhance/specifically target the delivery of the cancer target antigen to target cells (e.g., antigen presenting dendritic cells) wherein the inhibition of CD300f of said dendritic cells would then facilitate increased cancer target antigen presentation and subsequent T cell activation against said cancer target antigen, wherein such a method would be useful in a more efficacious method of promoting/increasing T cell response to said cancer target antigen.
The same rationale as presented above can be applied to the claim rejections under nonstatutory double patenting. It is specifically noted that (i) the reference patent is generally drawn to an antibody, antigen binding fragment thereof, or immunoconjugate, and compositions thereof, wherein the antibody specifically binds to the extracellular domain of CD300f and comprises the instantly claimed sequences and (ii) copending application ‘625 is generally drawn to therapeutic methods comprising the administration of a CD300f-specific antibody, antigen binding fragment thereof, or immunoconjugate wherein the CD300f-specific antibody comprises the instantly claimed sequences. The reference patent, copending application ‘625, and Coligan are considered to be analogous to the present invention as they are in the same field of CD300f (e.g., CD300f binding proteins) and therapeutics (directed at antigen-presenting cells and/or subsequent T cell activation) and thus it would have been obvious to one of ordinary skill in the art to modify the method suggested by Coligan such that the CD300f inhibitor is coupled to a moiety (i.e., an immunoconjugate), as suggested by the reference patent or copending application ‘625, wherein the moiety is the target antigen such as a cancer antigen (i.e., a protein) suggested by Coligan because combining prior art elements according to known methods would be expected to yield predictable results; one of ordinary skill in the art would recognize that coupling a CD300f inhibitor to a target antigen would enhance/specifically target the delivery of the cancer target antigen to target cells (e.g., antigen presenting dendritic cells) wherein the inhibition of CD300f of said dendritic cells would then facilitate increased cancer target antigen presentation and subsequent T cell activation against said cancer target antigen, wherein such a method would be useful in a more efficacious method of promoting/increasing T cell response to said cancer target antigen.
In view of the above, it is maintained that the combination of Coligan and Hart render obvious the instant claims. As such, the updated claim rejections under 35 U.S.C. 103 are deemed proper. Additionally, the teachings of the reference patent or copending application ‘625 in view of Coligan further render obvious the instant claims. As such, the claim rejections under (i) nonstatutory double patenting over the reference patent in view of Coligan and (ii) provisional nonstatutory double patenting over copending application ‘625 in view of Coligan are deemed proper and are maintained.
Conclusion
Claims 19-20, 22, 24-27, 29, 35-40, 42-46, and 48-50 are pending. Claims 19-20, 22, 24-27, 29, 35-40, 42-46, and 48-50 are rejected. No claims are allowed.
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/ALYSSA RAE STONEBRAKER/Examiner, Art Unit 1642
/SAMIRA J JEAN-LOUIS/Supervisory Patent Examiner, Art Unit 1642