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 .
Election/Restrictions
Applicant’s election without traverse of Group I in the reply filed on 5/13/2024 is acknowledged.
Claim 25, 27, 29-31 and 35 withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected Group II, III, and IV, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 5/13/2024.
Status of Claims
Cancelled: 1, 3, 5, 7, 11, 12, 14-23, 26, 28, 32-34, 36-69
Withdrawn: 25, 27, 29-31, 35
New: 70-76
Examined Herein: 2, 4, 6, 8-10, 13, 24, 70-76
Priority
Priority to PRO 62/789,862 filed on 1/8/2019, PRO 62/913,489 filed on 10/10/2019, and PCT/US2020/012763 filed on 1/8/2020 is acknowledged.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 4/14/2022, 1/3/2023, 4/20/2023, 8/9/2023, 12/14/2023, 10/21/2024, and 5/9/2025 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Drawings
The drawings filed on 7/7/2021 are accepted.
Withdrawn Rejections
All rejections of claim 1 are hereby withdrawn; its cancellation moots the rejection.
The rejection of claims 1, 2, 6, 8, 13, and 24 under 35 U.S.C. 103 over Ingber is hereby withdrawn in view of Applicant’s cancellation of independent claim 1 and substantial amendments to dependent claims 2, 6, 8, 13 and 24.
The rejection of claims 1, 2, 6, 8-10, 13, and 24 under 35 U.S.C. 103 over Ingber and Jain is hereby withdrawn in view of Applicant’s cancellation of independent claim 1 and substantial amendments to dependent claims 2, 6, 8-10, 13 and 24.
The rejection of claims 1, 2, 4, 6, 8, 13, and 24 under 35 U.S.C. 103 over Tardi and Roscoe is hereby withdrawn in view of Applicant’s cancellation of independent claim 1 and substantial amendments to dependent claims 2, 4, 6, 8, 13, and 24.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
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.
Claims 4, 6, and 8 are rejected under 35 U.S.C. 103 as being unpatentable over Tardi (US 5,780,054, Patented 7/14/1998), in view of Roscoe (US 2010/0317020 A1, 12/16/2010), Ariizumi (US 7,071,171 B1, 7/4/2006), and Underhill (US 2016/0317501 A1, Published 11/3/2016).
With respect to claim 4, Tardi discloses a liposome comprising an antifungal agent and a targeting molecule, a protein, wherein the targeting molecule is incorporated into the outer surface of the liposome and wherein the antifungal agent is encapsulated in the liposome. [Tardi, Col. 8, Line 36-58, Col. 9, Line 20-49]
With respect to claim 6, Tardi discloses the antifungal agent is an azole, including miconazole, terconazole, econazole, isoconazole, butaconazole, clotrimazole, itraconazole, or a polyene, including nystatin, naftifine, and amphotericin B. [Tardi, Col. 9, Line 39-42]
With respect to claim 8, Tardi discloses the targeting molecule is conjugated to a lipid. [Tardi, Col. 8, Line 36-50, Col. 9, Line 5-19]
Tardi does not disclose that the targeting molecule is a soluble Dectin-1, Dectin-2 or Dectin-3.
However, with respect to claim 4, Roscoe discloses that Dectin-1 or a derivative of Dectin-1, including recombinant Dectin-1, functions as a recognition element for liposomes. The recognition element enables the liposome to target and bind an analyte (e.g. a cell wall component). Roscoe discloses Dectin-1 binds to a target antigen, such as zymosan. [Roscoe, 0065, 0066] Zymosan is a β-glucan found on the cell wall of fungi.
With respect to claim 8, Roscoe discloses Dectin-1 may be conjugated to a lipid. [Roscoe, 0065, 0066]
Tardi nor Roscoe disclose that the targeting molecule, Dectin-1, is soluble.
However, with respect to claim 4, Ariizumi discloses that soluble Dectin-1 exists as naturally occurring isoforms. [Ariizumi, Col. 54, Line 25-35, Col. 71, Line 34-42] Ariizumi further discloses that His-Dectin-1, which is a derivative of Dectin-1, is a soluble form of Dectin-1. Ariizumi also discloses recombinant Dectin-1 may be produced in soluble and secreted form. [Ariizumi, Col. 53, Line 34-61, Col. 66, Line 35-48] Ariizumi discloses that extracellular domains of Dectin-1, when administered in soluble forms, exhibit beneficial effects to prevent or even treat immunological disorders. [Ariizumi, Col. 62, Line 47-52]
Moreover, with respect to claim 4, Underhill discloses that Dectin-1 is a C-type lectin receptor that recognizes β-1,3-glucans found in the cell walls of nearly all fungi. [Underhill, 0004, 0011] Underhill further discloses soluble Dectin-1 binds with specificity to β-1,3-glucans on fungi. [Underhill, 0016-0018]
Modifying the liposome disclosed by Tardi so that the protein/targeting molecule is soluble Dectin-1 results in the liposome of claim 4.
It would be obvious to one of ordinary skill in the art to modify the liposome disclosed by Tardi by selecting soluble Dectin-1 as the protein/targeting molecule and have a reasonable expectation of success. Tardi discloses a liposome comprising an antifungal agent encapsulated in the liposome and a targeting molecule incorporated into the liposome’s outer surface. Tardi further discloses the targeting molecule may be any protein. Roscoe discloses that Dectin-1, or a derivative thereof, functions as a recognition element for liposomes and enables liposomes to target and bind to analyte (e.g. a cell wall component). Roscoe discloses that Dectin-1 binds to a target antigen such as zymosan, a β-glucan found on the cell wall of fungi. Ariizumi discloses that Dectin-1 exists in soluble forms, specifically as naturally occurring isoforms. Underhill discloses that Dectin-1 and soluble Dectin-1 bind to β-glucans found on the cell wall of fungi. Accordingly, the combined teachings of Tardi and Roscoe, Ariizumi, and Underhill reasonably suggest that soluble Dectin-1 may function as the protein/targeting molecule attached to the outer surface of the liposome disclosed by Tardi. One would have been motivated to do so because it is prima facie obvious to combine references when some advantage or expected beneficial result would have been produced by their combination. MPEP 2144(II). In the present case, Roscoe discloses that Dectin-1 recognizes and binds to fungal cell wall components, like zymosan. [Roscoe, 0065, 0066] Furthermore, Ariizumi discloses that extracellular domains of dectin-1, when administered in soluble forms, exhibit beneficial effects to prevent or even treat immunological disorders. [Ariizumi, Col. 62, Line 47-52] Therefore, one would be motivated by the expectation that selecting soluble Dectin-1 as the protein targeting molecule would enable the liposome disclosed by Tardi to target cell wall components of fungi and provide beneficial effects in preventing or treating immunological disorders.
Claims 2, 9, 10, 13, 24, 71, 72, and 74 are rejected under 35 U.S.C. 103 as being unpatentable over Ingber (US 2014/0227723 A1, Published 8/14/2014), in view of Jain (Chitosan-Assisted Immunotherapy for Intervention of Experimental Leishmaniasis via Amphotericin B-Loaded Solid Lipid Nanoparticles, 8/9/2014, Applied Biochemistry and Biotechnology, 174:1309-1330).
With respect to claims 9, 10, 13, and 24, Ingber discloses a liposome, or a plurality of liposomes, comprising a therapeutic agent used to treat an infection and a microbe-targeting molecule, wherein the targeting molecule is incorporated into the outer surface of the liposome, and the therapeutic agent is encapsulated in the liposome. [Ingber, 0056, 0150, 0155] Ingber discloses, in one embodiment, the microbe-targeting molecule is Fc-mannose-binding lectin (MBL) and the therapeutic agent is an antifungal agent. [Ingber, 0176, 0368, 0718, 0727] Mannose-binding lectin (MBL) is soluble and a C-type lectin receptor that binds a target antigen, mannose, on a fungal cell wall.
With respect to claim 2, Ingber discloses the targeting molecule is Fc-MBL. [Ingber, 0176, 0718] Fc-MBL binds the target antigen mannose on a fungal cell wall. Mannose is a fungal cell wall antigen.
With respect to claim 71 and 74, Ingber discloses the targeting molecule is conjugated to a lipid. [Ingber, 0150, 0155]
Ingber does not disclose that the concentration of the antifungal agent is reduced as compared to the concentration of the antifungal agent encapsulated in a liposome that does not comprise a targeting molecule incorporated into the outer surface of the liposome or the liposome has decreased affinity for and/or is less toxic to an animal cell as compared to a liposome that does not comprise a targeting molecule incorporated into the outer surface of the liposome.
However, Jain discloses a liposome comprising an antifungal agent, amphotericin B, and a targeting molecule, chitosan, wherein the targeting molecule is incorporated into the outer surface of the liposome, and the antifungal agent is encapsulated in the liposome. [Jain, Page 1310, Paragraph 5, Page 1311, Paragraph 1 & 5, Page 1312, Paragraph 1]
With respect to claims 9, 10, and 72, Jain discloses the concentration of the antifungal agent is reduced, as compared to the concentration of the antifungal agent encapsulated in a liposome that does not comprise a targeting molecule incorporated into the outer surface of the liposome. [Jain, Page 1324, Figure 6]
With respect to claims 9, 10, and 72, Jain discloses the liposome is less toxic to an animal cell, as compared to a liposome that does not comprise a targeting molecule incorporated into the outer surface of the liposome. [Jain, Page 1321, Figure 3]
Modifying the liposome(s) disclosed by Ingber so that the microbe-targeting molecule is Fc-mannose-binding lectin (MBL) and the therapeutic agent is an antifungal agent and combining the teachings of Ingber and Jain and concluding that the liposome disclosed by Ingber will exhibit a reduced concentration of the antifungal agent and less toxicity to an animal cell, as compared to a liposome that does not comprise a targeting molecule incorporated into the outer surface of the liposome, results in the liposome of claim 9 and 10.
It would be obvious to one of ordinary skill in the art to modify the liposome(s) disclosed by Ingber so that the microbe-targeting molecule is Fc-mannose-binding lectin (MBL) and the therapeutic agent is an antifungal agent and have a reasonable expectation of success. Ingber discloses a liposome, or a plurality of liposomes, comprising a therapeutic agent used to treat an infection and a microbe-targeting molecule that binds a target antigen on a fungal cell. Ingber further discloses the targeting molecule is incorporated into the outer surface of the liposome and the therapeutic agent is encapsulated in the liposome. Ingber discloses that, in one embodiment, the microbe-targeting molecule is Fc-mannose-binding lectin (MBL) and the therapeutic agent is an antifungal agent. Thus, in view of this express teaching by Ingber, it is reasonable to expect the liposome(s) disclosed by Ingber may be modified so that the microbe-targeting molecule is Fc-MBL and the therapeutic agent is an antifungal agent. One would have been motivated to do so because the selection of a known material based on its suitability for its intended use is prima facie obvious. MPEP 2144.07. In the present case, Ingber discloses that the therapeutic agent used to treat an infection may be an antifungal agent and that the microbe targeting molecule may be Fc-MBL. [Ingber, 0176, 0727, 0718] Therefore, selecting a known material, an antifungal agent, based on its suitability as a therapeutic agent for its intended use to treat an infection is prima facie obvious. Likewise, selecting a known material, Fc-MBL, based on its suitability as a microbe-targeting molecule for its intended use to bind a microbe and/or microbial matter is prima facie obvious.
It would be obvious to one of ordinary skill in the art to combine the teachings of Ingber and Jain
and conclude that the liposome disclosed by Ingber will exhibit a reduced concentration of the antifungal agent and less toxicity to an animal cell, as compared to a liposome that does not comprise a targeting molecule incorporated into the outer surface of the liposome, and have a reasonable
expectation of success. Ingber discloses a liposome comprising an antifungal agent encapsulated in the liposome and a targeting molecule, Fc-MBL, incorporated into the outer surface of the liposome. Similarly, Jain discloses a liposome comprising an antifungal agent, amphotericin B, encapsulated in the liposome and a targeting molecule, chitosan, incorporated into the outer surface of the liposome. Jain further discloses that the concentration of the antifungal agent is reduced and the liposome is less toxic to an animal cell, as compared to the concentration of the antifungal agent encapsulated in a liposome that does not comprise a targeting molecule incorporated into the outer surface of the liposome. In view of the structural similarities between the liposome disclosed by Ingber and Jain (a liposome comprising a targeting molecule incorporated on the outer surface thereof and an antifungal agent encapsulated therein), it is reasonable to expect that the liposome disclosed by Ingber, like the liposome disclosed by Jain, will exhibit improved properties relative to a liposome lacking a targeting molecule. Accordingly, it is reasonable to expect the teachings of Ingber and Jain may be combined and conclude that the liposome disclosed by Ingber will exhibit a reduced concentration of the antifungal agent and less toxicity to an animal cell, as compared to a liposome that does not comprise a targeting molecule incorporated into the outer surface of the liposome. One would have been motivated to do so because it is prima facie obvious to combine references when some advantage or expected beneficial result would have been produced by their combination. MPEP 2144(II). In the present case, Jain discloses a liposome comprising a targeting molecule incorporated on the outer surface thereof and an antifungal agent encapsulated therein, wherein the liposome exhibits a reduced concentration of the antifungal agent and less toxicity to an animal cell, as compared to a liposome that does not comprise a targeting molecule incorporated into the outer surface of the liposome. Therefore, one would have been motivated by the expectation that the liposome disclosed by Ingber, which also comprises a targeting molecule incorporated on the outer surface thereof and an antifungal agent encapsulated therein, would exhibit such properties relative to a liposome lacking a targeting molecule.
Claims 2, 9, 10, 13, 24, 70, 71, 72, 73, 74, 75, and 76 are rejected under 35 U.S.C. 103 as being unpatentable over Ingber and Jain, as applied to claim 2, 9, 10, 13, 24, 71, 72, and 74 above, and further in view of Ariizumi (US 7,071,171 B1, 7/4/2006) and Underhill (US 2016/0317501 A1, Published 11/3/2016).
With respect to claims 9 and 10, Ingber and Jain disclose the teachings above.
Ingber further discloses the targeting molecule may comprise a microbe surface-binding domain derived from a C-type lectin. [Ingber, 0061, 0070]
With respect to claim 75, Ingber and Jain disclose that the liposome exhibits a reduced concentration of the antifungal agent and less toxicity to an animal cell, compared to a liposome that does not comprise a targeting molecule incorporated into the outer surface of the liposome. Ingber and Jain further disclose that a targeting molecule/C-type lectin receptor conjugated to a lipid. [See citations of Ingber and Jain above]
With respect to claim 76, Ingber discloses the antifungal agent is an azole. [Ingber, 0368]
Ingber and Jain do not disclose that the soluble C-type lectin receptor is selected from the group consisting of a soluble Dectin- 1, a soluble Dectin-2, and a soluble Dectin-3.
However, with respect to claims 70, 73, 75, and 76, Ariizumi discloses Dectin-1 is a C-type lectin receptor. [Arrizumi, Abstract] Moreover, Ariizumi discloses soluble Dectin-1 exists as naturally occurring isoforms. [Ariizumi, Col. 54, Line 25-35, Col. 71, Line 34-42] Ariizumi further discloses His-Dectin-1, which is a derivative of Dectin-1, is a soluble form of Dectin-1. Ariizumi also discloses recombinant Dectin-1 may be produced in soluble and secreted form. [Ariizumi, Col. 53, Line 34-61, Col. 66, Line 35-48] Ariizumi discloses that extracellular domains of Dectin-1, when administered in soluble forms, exhibit beneficial effects to prevent or even treat immunological disorders. [Ariizumi, Col. 62, Line 47-52]
Moreover, with respect to claims 70, 73, 75, and 76, Underhill discloses that Dectin-1 is a C-type lectin receptor that recognizes β-1,3-glucans found in the cell walls of nearly all fungi. [Underhill, 0004, 0011] Underhill further discloses that soluble Dectin-1 binds with specificity to β-1,3-glucans on fungi. [Underhill, 0016-0018]
Modifying the liposome disclosed by Ingber and Jain by replacing the targeting molecule, Fc-MBL, with soluble Dectin-1 results in the liposome of claim 70, 73, 75, and 76.
It would be obvious to one of ordinary skill in the art to modify the liposome disclosed by Ingber and Jain by replacing the targeting molecule, Fc-MBL, with soluble Dectin-1 and have a reasonable expectation of success. Ingber and Jain disclose a liposome comprising an antifungal agent encapsulated in the liposome and a targeting molecule, Fc-MBL, incorporated into the liposome’s outer surface. However, Ingber further discloses that a microbe surface-binding domain derived from a C-type lectin may alternatively function as the targeting molecule. Ariizumi discloses that Dectin-1 is a C-type lectin receptor that exists in soluble forms, specifically as naturally occurring isoforms. Underhill also discloses that Dectin-1 is a C-type lectin receptor and further discloses that Dectin-1 recognizes β-1,3-glucans found in the cell walls of nearly all fungi, and that soluble Dectin-1 binds with specificity to β-1,3-glucans on fungi. So, Ingber and Jain disclose a liposome comprising a C-type lectin receptor, Fc-MBL, that functions as a targeting molecule on the outer surface thereof, but further disclose that another C-type lectin may function as the targeting molecule. Arrizumi and Underhill establish that Dectin-1 and soluble Dectin-1 are C-type lectin receptors that target β-1,3-glucans found in the cell walls of nearly all fungi. Thus, the combined teachings of Ingber, Jain, Arrizumi, and Underhill suggest that soluble Dectin-1 may serve as the C-type lectin receptor/targeting molecule attached to the outer surface of the liposome disclosed by Ingber and Jain. Therefore, it is reasonable to expect that the liposome the liposome disclosed by Ingber and Jain may be modified by replacing the targeting molecule, Fc-MBL, with soluble Dectin-1. One would have been motivated to do so because it is prima facie obvious to combine references when some advantage or expected beneficial result would have been produced by their combination. MPEP 2144(II) In the present case, Ariizumi discloses that extracellular domains of dectin-1, when administered in soluble forms, exhibit beneficial effects to prevent or even treat immunological disorders. [Ariizumi, Col. 62, Line 47-52] Therefore, one would be motivated by the expectation that the replacing the targeting molecule, Fc-MBL, with soluble Dectin-1 would enable the liposome disclosed by Ingber and Jain to provide beneficial effects in preventing or treating immunological disorders.
Response to Arguments
Applicant's arguments filed 10/6/2025 have been fully considered but they are not persuasive.
Applicant asserts “The Office Action cites Ingber at [0150] and [0155] as allegedly teaching the MBL conjugated to a lipid. There is no teaching or suggestion in these paragraphs of MBL being conjugated to a lipid. Thus, Ingber does not teach or suggest a soluble C-type lectin receptor conjugated to a lipid or pegylated lipid as recited in claim 8.” [Remarks 10/6/2025, Page 6 – Page 7, Paragraph 1]
Applicant’s arguments are not persuasive because Applicant falsely suggests that the rejection only relies on paragraph 0150 and 0155 to teach the MBL conjugated to a lipid. In actuality, the Examiner also cites paragraph 0056, 0176, 0368, 0718, and 0727 for this teaching.
Applicant asserts “Independently of the amendment of claim 8, this rejection as applied to previously presented claim 8 is traversed on the ground that Ingber does not teach or suggest the Fc-mannose binding lectin (MBL) conjugated to a lipid or a pegylated lipid as alleged. The remarks provided
above are incorporated herein by reference. Jain does not rectify this deficiency of Ingber. Thus, the combination of Ingber and Jain do not teach or suggest a soluble C-type lectin receptor conjugated to a lipid or pegylated lipid as recited in claim 8.” [Remarks 10/6/2025, Page 7, Paragraph 5]
Applicant’s arguments are not persuasive because Ingber does suggest a soluble C-type lectin receptor conjugated to a lipid. Ingber discloses a microparticle/liposome comprising a microbe-targeting molecule. [0150 and 0155] Ingber discloses that the microbe-targeting molecule is on the surface of the microparticle/liposome. [0150] The surface of a liposome is composed of lipids. Ingber discloses, in one embodiment, the microbe-targeting molecule is Fc-mannose-binding lectin (MBL) [0176] Therefore, Ingber discloses a microparticle/liposome comprising a microbe-targeting molecule, Fc-MBL, composed on the lipid surface thereof.
Applicant asserts “Thus, the chitosan-coated liposomes of Jain (chitosan) would be targeted to completely different targets than the alleged MBL-coated liposomes of Ingber and would have different downstream effects. The alleged chitosan-coated liposomes of Jain would accordingly not have provided teachings relevant to the alleged MBL-coated liposomes of Ingber. At least for these reasons, claims 9 and 10 are not obvious over Ingber in view of Jain.” [Remarks 10/6/2025, Page 6 – Page 7, Paragraph 1] [See also Page 7, Paragraph 3-6]
Applicant’s arguments are not persuasive because Applicant incorrectly suggests that for the disclosures of Ingber and Jain to be considered relevant to each other, the references must teach the same binding target and have the same downstream effects. However, this is not required to establish a prima facie case of obviousness. Rather, it is sufficient that Ingber and Jain both teach a liposome comprising an antifungal agent and a targeting molecule, wherein the targeting molecule is incorporated into the outer surface of the liposome, and the antifungal agent is encapsulated in the liposome. Ingber and Jain are relevant to each other because they teach a structurally and functionally analogous liposome, and would be recognized by one of ordinary skill in the art as such.
Applicant asserts “The Office has alleged that it would have been obvious in view of Roscoe and Ariizumi to modify the liposome of Tardi to comprise soluble Dectin-1 as an alleged targeting agent on its surface.… However, the cited prior art does not teach or suggest that soluble Dectin-1 would be capable of binding cell wall components of fungi and/or otherwise targeting to fungi. Soluble Dectin-1 is alleged as being taught only by Ariizumi. Ariizumi, however, fails to teach or suggest that soluble Dectin-1 would be capable of binding fungal cell wall components and/or otherwise targeting to fungi…” [Remarks 10/6/2025, Page 7, Paragraph 6 – Page 8, Paragraph 1]
Applicant is reminded that the rejection of record is made over the combined teachings of Tardi, Roscoe, and Ariizumi, not Ariizumi alone. Roscoe explicitly teaches that Dectin-1, or a derivative thereof, recognizes fungal cell wall components, such as zymosan. Ariizumi teaches that soluble Dectin-1 is a derivative of Dectin-1. So, Roscoe teaches a derivative of Dectin-1 recognizes fungi, and Ariizumi teaches that soluble Dectin-1 is a derivative of Dectin-1. Thus, a person of ordinary skill in the art would reasonably conclude, in view of the combined teachings of Roscoe and Ariizumi, that soluble dectin-1 recognizes fungi.
Regardless, the ability of soluble dectin-1 to bind fungal cell wall components and/or otherwise target fungi is necessarily present in any reference that teaches soluble dectin-1.
Applicant asserts “The Office has also alleged it would have been obvious to substitute the Dectin-1 of Roscoe for the soluble Dectin-1 of Ariizumi for the purpose of providing beneficial effects in preventing or treating immunological disorders triggered by fungal cell wall components… First, the cited prior art does not teach or suggest that soluble Dectin-1 would have been capable of preventing or treating immunological disorders triggered by fungal cell wall components. Ariizumi is completely silent regarding any immunological disorders specifically triggered by fungal cell wall components. [Remarks 10/6/2025, Page 9, Paragraph 2]
The Examiner does not agree with the Applicant’s assertion; however, the noted statement has been removed, as it is not essential to maintain the instant prima facie case of obviousness.
Applicant asserts “Second, Ariizumi fails to teach or suggest that soluble Dectin-1 would have any functions or properties whatsoever when coated on a liposome. Thus, it would not have been obvious to substitute the Dectin-1 of Roscoe for the soluble Dectin-1 of Ariizumi for the alleged purpose of providing beneficial effects in preventing or treating immunological disorders triggered by fungal cell wall components.” [Remarks 10/6/2025, Page 9, Paragraph 2]
Without acquiescing to Applicant’s assertion, it is unclear why Ariizumi wound need to teach or suggest that “soluble Dectin-1 would have any functions or properties whatsoever when coated on a liposome, when this is not a claimed limitation. Further clarification is requested.
Applicant asserts “In view of the foregoing, the cited prior art fails to provide a motivation and reasonable likelihood of success for modifying the liposome of Tardi to comprise soluble Dectin-1 as an alleged targeting agent on the surface. As outlined in MPEP 2143(I)(A), Example 8, "the 'predictable result' discussed in KSR refers not only to the expectation that prior art elements are capable of being physically combined, but also that the combination would have worked for its intended purpose." [Remarks 10/6/2025, Page 9, Paragraph 3]
Applicant’s arguments are not persuasive because MPEP 2143(1)(A) is not relevant to the instant rejection, as this is not the rationale used to support the instant rejection. The rationale supporting the instant rejection is MPEP 2143(1)(G). Furthermore, the rationales listed in MPEP 2143 are examples of rationales that may support a conclusion of obviousness; they are not an all-inclusive list and other rationales to support a conclusion of obviousness may be relied upon by Office personnel. Therefore, Applicant’s assertions are also unpersuasive because they incorrectly suggest that the Office personnel must satisfy MPEP 2143(1)(A) example to establish a prima facie case of obviousness.
Conclusion
Applicant's amendment, filed 10/6/2025, necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/K.A.C./Examiner, Art Unit 1618 /Michael G. Hartley/Supervisory Patent Examiner, Art Unit 1618
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