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 .
The Examiner for this Application has changed. Please direct all future correspondence to Juliana Candelaria, AU 1634. Additional contact information can be found at the end of this paper
Election/Restrictions
This action is in response to the papers filed on 12/02/2025. Claims 1-23 and 30 are currently pending as per claims filed on 12/02/2025.
Applicant's election without traverse of Group 1, claims 1-17 in the reply filed on 12/02/2025 is acknowledged.
Claim 18-23 and 30 are withdrawn from further consideration by Applicants pursuant to 37 CFR 1.142(b), as being drawn to a nonelected subject matter, there being no allowable generic or linking claim.
The requirement is still deemed proper and is therefore made FINAL. Therefore, claims 1-17 are subject to examination to which the following
grounds of rejection are applicable.
Priority
The instant application is a national stage entry under 35 USC 371 of
PCT/US2021/028903 filed on 04/23/2021 which claims benefit of 63/015,013 filed on 04/24/2020.
Thus, the earliest possible priority for the instant application is 04/24/2020.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 10/19/2022, 06/26/2025, and 09/25/2025 was filed after the mailing date of the current office action.
The information disclosure statement (IDS) submitted on 10/19/2022 and 9/25/2025 is not in compliance with the provisions of 37 CFR 1.97. The following references have not been considered by the examiner, as indicated on Form PTO 1449.
a) Reference WO 2018/022651 has not been considered as it has not been provided in the application.
b) Reference WO 2017/180519 has not been considered as it has not been provided in the application.
c) Reference JP 2019-522008 has not been considered as the provided document is not translated into English.
d) Reference Japanese Office Action for Patent Application No 2022-564592 has been considered to the extent that an English translation of the relevant portions of the document has been provided.
All other documents in said Information Disclosure statement were considered as noted by the Examiner initials in the copy attached hereto.
Claim Objections
Claim 1 is objected to because abbreviations SIRPα and SIRPαlow should be spelled out in first encounter of the claim. Appropriate correction is required.
Claim 2 is objected to because abbreviations CD47 should be spelled out in first encounter of the claim. Appropriate correction is required.
Claim 3 is objected to because abbreviations TLR should be spelled out in first encounter of the claim. Appropriate correction is required.
Claim 14 is objected to because abbreviations TLR should be spelled out in first encounter of the claim. Appropriate correction is required.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claim 8 is rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends. Claim 8 depends from claim 7. Claim 7 requires that the phorbol ester comprises “phorbol 12- myristate 13-acetate (PMA).” Claim 8 broadens the scope of the claimed macrophage activating agent, permitting that it may be “phorbol 12- myristate 13-acetate (PMA) and “LPS, CpG, Poly I:C, LTA, PGN, flagellin, Pam3CSK4, zymosan, and HMGB 1”. It is suggested that applicant intended to recite “The method of claim 5” instead of “The method of 7”.
Applicant may cancel the claim, rewrite the claim in independent form, or present a sufficient showing that the dependent claim complies with the statutory requirements.
The following is a quotation of 35 U.S.C. 112(b):
(B) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 16 and 17 rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which applicant regards as the invention.
Claim 16 which depends on claim 1 is indefinite in its recitation of “further comprising contacting the macrophages with a SHP-1 inhibitor”. Claim 1 already requires contacting the macrophages with an SIRPα inhibitor. Assuming it is the same inhibitor, it is unclear if contacting the macrophages occurs as a separate step, or is the same step as recited in claim 1. As such the metes and bounds of the claim are indefinite.
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.
Claim(s) 1-17 is/are rejected under 35 U.S.C. 103 as being unpatentable over Liu et al (WO 2017/180519 A1) and further in view of Rios et al (Methods in Molecular Bio, page 311-320, 2017), Nilsson et al (Biochemical and Biophysical Research Communications, page 1304-1309, 2012), Christophi et al (Laboratory Investigation, page 742-759, 2009), Shorr et al (Drugs for the Geriatric Patient, page 631-632, 2007), Kundu et al (J. of Immunology, page 6529-6536, 2010), Motz et al (US Patent Publication Number. 2019/0298715 A1), as evidenced by Sigma Aldrich (Page 4, description, downloaded on 1/20/2026).
The applied Liu reference has a common inventor with the instant application. Based upon the earlier effectively filed date of the reference, it constitutes prior art under 35 U.S.C. 102(a)(1). The publication dated for Liu is 19 October 2017. The earliest effective filing date of the instant application is April 23, 2020.
Therefor rejection under 35 U.S.C. 103 CANNOT be overcome by: (1) a showing under 37 CFR 1.130(a) that the subject matter disclosed in the reference was obtained directly or indirectly from the inventor or a joint inventor of this application and is thus not prior art in accordance with 35 U.S.C.102(b)(2)(A); (2) a showing under 37 CFR 1.130(b) of a prior public disclosure under 35 U.S.C. 102(b)(2)(B); or (3) a statement pursuant to 35 U.S.C. 102(b)(2)(C) establishing that, not later than the effective filing date of the claimed invention, the subject matter disclosed and the claimed invention were either owned by the same person or subject to an obligation of assignment to the same person or subject to a joint research agreement. See generally MPEP § 717.02. Because the reference qualifies as prior art under 102(a)(1), the provisions of MPEP 717.02 do not apply.
Regarding claim 1, Liu teaches the methods related to cancer treatment or, more generally to macrophage activation, can be carried out by administering to the patient a first agent that suppresses the expression of SIRPα, inhibits the activity of SIRPα, or disrupts the interaction between SIRPα and CD47 and a second agent that activates macrophage phagocytosis (e.g., of cancer cells) (page 1-2, line 30-3, Summary “a first agent that suppresses the expression of SIRPα inhibits the activity of SIRPα, or disrupts the interaction between SIRPα and CD47 and a second agent that activates macrophage phagocytosis (e.g., of cancer cells)”), rendering obvious a method for producing activated SIRPαlow macrophages, comprising contacting the macrophages with an SIRPα inhibitor; contacting the macrophages with macrophage activating agent, thereby generating a population of macrophages with marked reduction of SIRPα cell-surface expression SIRPαlow, relative to untreated macrophages. .
With regard to claim 1, wherein the SIRPα macrophages have activated phagocytosis towards cancer cells, increased proinflammatory response, and increased immunogenic antigen presentation, it is noted that the claim is directed to an inherent result based on the methodology of the administration of macrophages with marked reduction of SIRPα cell-surface expression SIRPαlow. It is noted that In re Best (195 USPQ 430) and In re Fitzgerald (205 USPQ 594) discuss the support of rejections wherein the prior art discloses subject matter which there is reason to believe inherently includes functions that are newly cited or is identical to a product instantly claimed. In such a situation the burden is shifted to the applicants to "prove that subject matter shown to be in the prior art does not possess characteristic relied on" (205 USPQ 594, second column, first full paragraph). It is noted that, if the prior art discloses identical chemical structure, the properties applicant discloses and/or claims are necessarily present, In re Spada, 911 F.2d 705, 709, 15 USPQ2d. As such the functional limitations would be present in the identical compounds taught by Liu et al and would therefore elicit these effects whenever it is administered.
However, Liu does not teach (a) isolating monocytes from peripheral blood mononuclear cells (PBMC) in a biological sample; (b) differentiate the monocytes in vitro to produce macrophages.
Rios et al teaches a protocol for isolation of PBMCs, isolation of monocytes from PBMCs, and differentiation of monocytes to macrophages (entire document, pages 311-320).
It would have been prima facie obvious to combine the teachings of Liu and Rios to use PBMC as a source of monocytes and to include this step in order to maximize the initial cell population that can be subjected to the inventive method. A skilled artisan would have had a reasonable expectation of success as isolating and differentiating monocytes to become macrophages was a known technique in the art of cell culture before the effective filing date of the claimed invention.
Regarding claim 2, the teachings Liu and Rios render obvious claim 1. Moreover, reference Liu teaches the methods related to cancer treatment or, more generally to macrophage activation, can be carried out by administering to the patient a first agent that suppresses the expression of SIRPα, inhibits the activity of SIRPα, or disrupts the interaction between SIRPα and CD47 and a second agent that activates macrophage phagocytosis (e.g., of cancer cells) (page 1-2, line 30-4, Summary).
With regard to the recitation of “ wherein the SIRPα inhibitor suppresses the expression of SIRPα, diminishes the abundance of SIRPα on the surface of a cell, inhibits the activity of SIRPα, disrupts the interaction between SIRPα and CD47, or a combination thereof.” it is noted that the claim is directed to an inherent result based on the methodology of the administration of macrophages with marked reduction of SIRPα cell-surface expression SIRPαlow as disclosed by the combined teachings of Liu and Rios..
Regarding claim 3, the teachings Liu and Rios render obvious claims 1 and 2. Moreover, reference Liu teaches ligands for TLRs or agents that activate TLRs can be used as either a first or second agent in compositions and methods for activating macrophages (page 3, lines 17-19), rendering obvious wherein the SIRPα inhibitor comprises a cytokine, a TLR ligand, a glucocorticoid, or a combination thereof.
Regarding claim 4, the teachings Liu and Rios render obvious claims 1- 3. Moreover, reference Liu teaches SIRPα can be a ligand for a Toll-like receptor (TLR) (e.g., lipopolysaccharide (LPS), polyinosinic:polycytidylic acid (poly I:C), lipoteichoic acid (LTA), flagellin, GARDIQUIMOD™ (an imidazoquinoline compound currently manufactured by InvivoGen; CAS number 1020412-43-4), IMIQUIMOD™ (l-isobutyl-1H-imidazo[4,5-c]quinoline-4- amine; CAS number 99011-02-6), or a CpG oligonucleotide), or a cytokine such as IFNy, IL-I, or IL-6 (these three cytokines may advantageously be used together) (page 2 line 20-25), rendering obvious wherein the SIRPα inhibitor is selected from the group consisting of IFNa, IFNP,IFNy, IL-1, IL-6, IL-12, IL-18, LPS, CpG, Poly I:C, LTA, PGN, flagellin, Pam3CSK4, zymosan, and HMGB1.
Regarding claims 5 and 6, the teachings Liu and Rios render obvious claim 1. Moreover, reference Liu teaches the second agent included in a composition or administered in a method that activates macrophages can be a cytokine (e.g., an interleukin such as IL-1, IL-1β, IL-6, IL-17 ( also known as IL-17 A), a lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNFα), or phorbol 12-myristate 13- acetate (PMA). As PMA is a PKC stimulator, it is an agent that activates macrophages by stimulating the PKC-Syk pathway (page 3, line 5-10), rendering obvious a cytokine selected from the group consisting of IFNa, IFNf3, IL-6, IL-1, IL-17, IL-18, TNFα, and IL-12.
Regarding claim 7, the teachings Liu and Rios render obvious claims 1 and 5. Moreover, reference Liu teaches the second agent included in a composition or administered in a method that activates macrophages can be a cytokine (e.g., an interleukin such as IL-I, IL-1β, IL-6, IL-17 (also known as IL-17 A), a lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNFα), or phorbol 12-myristate 13-acetate (PMA). As PMA is a PKC stimulator, it is an agent that activates macrophages by stimulating the PKC-Syk pathway (page 3, line 5-10), rendering obvious wherein the phorbol ester comprises phorbol 12- myristate 13-acetate (PMA).
Regarding claim 8, the teachings Liu and Rios render obvious claim 7. Moreover, reference Liu teaches SIRPα can be a ligand for a Toll-like receptor (TLR) (e.g., lipopolysaccharide (LPS), polyinosinic:polycytidylic acid (poly I:C), lipoteichoic acid (LTA), flagellin, GARDIQUIMOD™ (an imidazoquinoline compound currently manufactured by InvivoGen; CAS number 1020412-43-4), IMIQUIMOD™ (l-isobutyl-1H-imidazo[4,5-c]quinoline-4- amine; CAS number 99011-02-6), or a CpG oligonucleotide), or a cytokine such as IFNy, IL-I, or IL-6 (these three cytokines may advantageously be used together) (page 2 line 20-25), rendering obvious wherein the TLR ligand is selected from the group consisting of LPS, CpG, Poly I:C, LTA, PGN, flagellin, Pam3CSK4, zymosan, and HMGB1.
Regarding claim 9, the teachings Liu and Rios render obvious claims 1-3.
However, they do not teach wherein the glucocorticoid comprises methylprednisolone or dexamethasone.
Nilsson teaches “dexamethasone-treated macrophages did also show enhanced phagocytosis” (abstract, page 1), therefore exposing macrophages to dexamethasone in the treatment.
It would have been prima facie obvious to one of ordinary skill, in the art at the time of the effective filing date, to modify the teachings of Liu and Rios with exposing the macrophages to dexamethasone as taught by Nilsson, to enhance phagocytosis. One would be motivated to do so to maximize the ability of the macrophages to enhanced phagocytosis with a reasonable expectation of success.
Regarding claims 10-11, the teachings Liu and Rios render obvious claim 1. Moreover, reference Liu teaches the first and second agents can be mixed together in a single container or contained within separate containers, allowing them to be mixed in varying amounts prior to administration or administered sequentially or via separate routes of administration (page 19 line 8-10), rendering obvious wherein the SIRPα inhibitor and macrophage activating agent are administered sequentially, simultaneously or concurrently.
Regarding claim 12, the teachings Liu and Rios render obvious claim 1. Moreover, Liu teaches the first and second agents can be mixed together in a single container or contained within separate containers, allowing them to be mixed in varying amounts prior to administration or administered sequentially or via separate routes of administration (page 19 line 8-10), rendering obvious wherein the SIRPα inhibitor and macrophage activating agent are present in the same composition.
Regarding claim 13, the teachings Liu and Rios render obvious claims 1 and 12. Moreover, Liu teaches the first agent that suppresses the expression of SIRPα can be a ligand for a Toll-like receptor (TLR) (e.g., lipopolysaccharide (LPS), polyinosinic:polycytidylic acid (poly I:C), a CpG oligonucleotide, or a cytokine such as IFNy (page 17, line 4-13), rendering obvious wherein the composition comprises recombinant human interferon-gamma (IFNy), CpG oligodeoxynucleotide, and polyinosinic:polycytidylic acid (Poly I:C).
However, they do not teach comprising recombinant human interferon-alpha A2 (IFNa).
Shorr teaches interferon alfa-2a (Brand name: Roferon-A (alfa-2a)) is a biologic response modifier that increases phagocytic action of macrophages (page 631-632).
It would have been prima facie obvious to one of ordinary skill, in the art at the time of the effective filing date, to modify the teachings of Liu and Rios to include poly I:C, a CpG oligodeoxynucleotide, and IFNy in a composition with recombinant human interferon-alpha A2 as taught by Shorr. One would be motivated to do so to maximize the efficacy of SIRPα inhibition and macrophage activation (phagocytosis).
Regarding claim 14, the teachings Liu and Rios render obvious claim 1.
However, they do not teach the SIRPα inhibitor comprises a SHP-1 inhibitor.
Christophi teaches SHP-1 is a crucial negative regulator of proinflammatory cytokine signaling, TLR signaling, and inflammatory gene expression. Furthermore, mice genetically lacking SHP-1 display a profound susceptibility to inflammatory CNS demyelination relative to wild-type mice. In particular, SHP-1 deficiency may act predominantly in inflammatory macrophages to increase CNS demyelination as SHP-1-deficient macrophages display coexpression of inflammatory effector molecules (Page 1, abstract).
Therefore, it would have been prima facie obvious to one of ordinary skill, in the art at the time of the effective filing date, to select a SHP-1 inhibitor as the SIRPα inhibitor particularly because Christophi teaches that SHP-1 deficiency may act predominantly in inflammatory macrophages to increase CNS demyelination. One would be motivated to do so in order to reduce CNS demyelination and reduce coexpression of inflammatory effector molecules in macrophages. r
Regarding claim 15, the teachings of Liu, Rios, and Christophi render obvious claims 1 and 14.
However, they do not teach the SHP-1 inhibitor is selected from a species group recited in claim 15.
Kundu teaches “TPI-1 and the analogs as novel SHP-1 inhibitors with anti-tumor activity likely via an immune mechanism, supporting SHP-1 as a novel target for cancer treatment” (Page 1, abstract).
It would have been prima facie obvious to one of ordinary skill, in the art at the time of the effective filing date, to modify the teachings of Liu, Rios, and Christophi with the teachings of using TP1-1 and analogs as SHP-1 inhibitors from Kundu to maximize anti-cancer activity of macrophages as a cancer treatment.
Regarding claim 16, the teachings Liu and Rios render obvious claim 1.
However, they do not teach further contacting the macrophages with a SHP-1 inhibitor in addition to a first agent that suppresses the expression of SIRPα, inhibits the activity of SIRPα, or disrupts the interaction between SIRPα and CD47 as taught by Liu.
Motz teaches immune effector cell (macrophage) described herein is administered to a subject in combination with a protein tyrosine phosphatase inhibitor, e.g., a protein tyrosine phosphatase inhibitor described herein. In one embodiment, the protein tyrosine phosphatase inhibitor is an SHP-1 inhibitor (Page 143, col 1, para 1284).
It would have been obvious for one of ordinary skill in the art to combine the teachings of Liu, Rios, and Motz in order for the macrophages to receive the effects from the SHP-1 requiring directly contacting the macrophages with the inhibitor.
Regarding claim 17, the teachings of Liu and Rios render obvious claim 1 and 16. Moreover, Kundu teaches “TPI-1 and its analogs were identified as more effective than SSG in SHP-1 inhibition, immune cell activation, and anti-tumor action. Our results provide important evidence supporting targeting SHP-1 to activate immune cells as an anti-cancer strategy and designate TPI-1 and the analogs as promising leads” (page 6530, para 1) where TPI-1 is an irreversible SHP-1 inhibitor as evidenced by Sigma Aldrich (page 4, Description; Downloaded on 1/20/2026).
Double Patenting – Non-statutory – Secondary Reference(s)
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 1-23 and 30 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1-11 of US Patent 11,026,972 B2 in view of Rios et al (Methods in Mol. Bio, page 311-320, 2017). Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims are obvious over the cited claims of US Patent 11,026,972 (reference patent ‘972).
Claim 1 of reference patent ‘972:
“A method of generating macrophages with enhanced cancer phagocytosis, the method comprising:
(a) providing a biological sample from a subject, wherein the biological sample comprises macrophages;
(b) exposing the sample to an effective amount of a first composition comprising at least 100 units/ml IFNγ to suppress the expression or activity of signal regulatory protein α (SIRPα); and
(c) exposing the sample from step (b) to an effective amount of a second composition that activates Protein kinase C (PKC)-Spleen tyrosine kinase (Syk) pathway, thereby generating macrophages with enhanced cancer phagocytosis.”
Claim 1 of the instant application recites:
A method for producing activated SIRPa low macrophages, comprising
(a) isolating monocytes from peripheral blood mononuclear cells (PBMC) in a biological
sample;
(b) differentiate the monocytes in vitro to produce macrophages; and
(c) contacting the macrophages with an SIRPa inhibitor; and
(d) contacting the macrophages with macrophage activating agent, thereby generating a
population of macrophages with marked reduction of SIRPa cell-surface expression
(SIRPa10w), relative to untreated macrophages, wherein the SIRPa1ow macrophages have activated phagocytosis towards cancer cells, increased proinflammatory response, and increased immunogenic antigen presentation.
In relation to steps (c) and (d) of instant claim 1, requiring (c) contacting the macrophages with an SIRPa inhibitor; and (d) contacting the macrophages with macrophage activating agent, steps b) and c) in claim 1 of reference patent ‘972 are species of the genus
claimed in steps (c) and (d) of instant claim 1.
The instant claims differ from claims 1-11 by requiring differentiating monocytes in the
biological sample in vitro to produce macrophages.
However, before the effective filing date of the claimed invention, Rios et al., exemplified prior that teaches a protocol for isolation of PBMCs, isolation of monocytes from PBMCs, and differentiation of monocytes to macrophages (entire document, pages 311-320).
Therefore, in view of the benefit of using PBMC as a source of monocytes, it would have been obvious for one of ordinary skill in the art to include this step as taught by Rios et al., in the claimed method in an attempt to maximize the initial cell population of macrophages in a biological sample. Thus, the claims of the instant application are encompassed by, or overlap in scope significantly with, the claims of U.S. Patent 11,026,972.
Conclusion
Claim 1-17 are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Juliana Candelaria whose telephone number is (571)272-5488. The examiner can normally be reached Monday - Friday 8am - 5pm.
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/JULIANA IRENE CANDELARIA/Examiner, Art Unit 1634
/MARIA G LEAVITT/
Supervisory Patent Examiner, Art Unit 1634