Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on April 15, 2026 has been entered.
DETAILED ACTION
The amendment filed April 15, 2026 in response to the Office Action of December 17, 2025 is acknowledged and has been entered.
Claims 1, 5, 6, 8, and 9 have been amended.
Claim 2 has been cancelled.
Claims 15-20 have been added.
Claims 1, and 3-20 are pending and under consideration.
In view of amended Specification, the Objection to the Specification set forth in the Office Action of December 17, 2025 is hereby withdrawn.
In view of amendment to claim 5, the Objection to the claim set forth in the Office Action of December 17, 2025 is hereby withdrawn.
In view of cancellation of claim 2, the 112(b) rejection set forth in the Office Action of December 17, 2025 is hereby withdrawn.
In view of claim amendments, 112(f) is invoked for claim limitations: “a means for binding to a human avb3 integrin polypeptide” in claim 1 and claim 20; and “a means for binding to a human macrophage” in claim 13 (see Claim Interpretation below). Thus, these claims are being interpreted to cover only the corresponding structure, material, or acts described in the specification as performing the claimed function, and equivalents thereof. Accordingly, the 112(a) Witten Description rejection set forth in the previous Office Action of 12/17/2025 is hereby withdrawn.
In view of claim amendments of April 15, 2026, the 103 rejections set forth in the Office Action of December 17, 2025 are hereby withdrawn.
In view of claim amendments of April 15, 2026, the double patenting rejections set forth in the Office Action of December 17, 2025 are hereby withdrawn.
Priority
It is acknowledged that this application is a continuation application of U.S. Patent Appl. No. 16/499,623 filed September 30, 2019, which is a national phase application of PCT/US2018/025470, filed March 30, 2018, which claims the benefit of priority to U.S. Provisional Patent Appl. No. 62/479,768, filed March 31, 2017.
Applicant has not complied with one or more conditions for receiving the benefit of an earlier filing date under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) as follows:
The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original nonprovisional application or provisional application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of the first paragraph of 35 U.S.C. 112. See Transco Products, Inc. v. Performance Contracting, Inc., 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994).
The disclosure of the prior-filed applications fails to provide adequate support or enablement in the manner provided by the first paragraph of 35 U.S.C. 112 for one or more amended claims of this application. Examiner has established a priority date of October 4, 2023 for amended claims 1, 3-20 because the claims as currently constituted recite:
“a subject in need thereof that has been administered an effective amount of an RTK inhibitor sufficient to induce an accumulation of tumor associated macrophages (TAMs) in the subject” (claim 1);
“administering an effective amount of erlotinib sufficient to induce an accumulation of tumor-associated macrophages in the cancer or tumor” (claim 16);
“a subject in need thereof that has been administered an effective amount of erlotinib sufficient to induce an accumulation of M2 tumor associated macrophages (TAMs) in the subject” (claim 20);
“wherein administering the effective amount results in macrophage-mediated antibody-dependent cell cytotoxicity of the cancer or tumor” (claim 20).
However, a review of the parent applications does not reveal the newly added limitations in the claimed methods (also see 112(a) NEW MATTER rejection below). Applicant is invited to submit evidence pointing to the serial number, page and line where support can be found establishing an earlier priority date.
It is noted that examiner has established a priority date of October 4, 2023 for claims 5, 8, and 9 because the amended claims introduce NEW MATTER as set forth in the Office Action of December 1, 2025. The 112(a) new matter rejection for these claims are maintained (see maintained rejection below). Thus, the reason for resetting priority date for these claims is still valid.
It is noted that examiner has established a priority date of October 4, 2023 for original claim 12 in the previous Office Action of June 25, 2025. Provisional Patent Appl. No. 62/479,768, PCT/US2018/025470, or U.S. Patent Appl. No. 16/499,623 does not disclose that a method of instant claim 12: “wherein the subject in need thereof expresses a decreased ratio of M1 to M2 macrophages as compared to a healthy subject”, although the specification of U.S. Patent Appl. No. 16/499,623 discloses “A macrophage switch from M1 to M2 has been associated with lung cancer progression” and “the M1/M2 macrophage ratio in avb3-positive tumors was markedly decreased relative to tumor lacking avb3” for example see [0004] and [0078] of US 2020/0109205 A1 (publication of Appl. 16/499,623) which is different from the recitation of claim 12. Thus, the reason for resetting priority date for these claims is still valid.
Claim Interpretation
The following is a quotation of 35 U.S.C. 112(f):
(f) Element in Claim for a Combination. – An element in a claim for a combination may be expressed as a means or step for performing a specified function without the recital of structure, material, or acts in support thereof, and such claim shall be construed to cover the corresponding structure, material, or acts described in the specification and equivalents thereof.
The following is a quotation of pre-AIA 35 U.S.C. 112, sixth paragraph:
An element in a claim for a combination may be expressed as a means or step for performing a specified function without the recital of structure, material, or acts in support thereof, and such claim shall be construed to cover the corresponding structure, material, or acts described in the specification and equivalents thereof.
The claims in this application are given their broadest reasonable interpretation using the plain meaning of the claim language in light of the specification as it would be understood by one of ordinary skill in the art. The broadest reasonable interpretation of a claim element (also commonly referred to as a claim limitation) is limited by the description in the specification when 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, is invoked.
As explained in MPEP § 2181, subsection I, claim limitations that meet the following three-prong test will be interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph:
(A) the claim limitation uses the term “means” or “step” or a term used as a substitute for “means” that is a generic placeholder (also called a nonce term or a non-structural term having no specific structural meaning) for performing the claimed function;
(B) the term “means” or “step” or the generic placeholder is modified by functional language, typically, but not always linked by the transition word “for” (e.g., “means for”) or another linking word or phrase, such as “configured to” or “so that”; and
(C) the term “means” or “step” or the generic placeholder is not modified by sufficient structure, material, or acts for performing the claimed function.
Use of the word “means” (or “step”) in a claim with functional language creates a rebuttable presumption that the claim limitation is to be treated in accordance with 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph. The presumption that the claim limitation is interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, is rebutted when the claim limitation recites sufficient structure, material, or acts to entirely perform the recited function.
Absence of the word “means” (or “step”) in a claim creates a rebuttable presumption that the claim limitation is not to be treated in accordance with 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph. The presumption that the claim limitation is not interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, is rebutted when the claim limitation recites function without reciting sufficient structure, material or acts to entirely perform the recited function.
Claim limitations in this application that use the word “means” (or “step”) are being interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, except as otherwise indicated in an Office action. Conversely, claim limitations in this application that do not use the word “means” (or “step”) are not being interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, except as otherwise indicated in an Office action.
This application includes one or more claim limitations that use the word “means” or “step” which are being interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph because the claim limitation(s) meet the three-prong test. Such claim limitation(s) is/are: “a means for binding to a human avb3 integrin polypeptide” in claim 1 and claim 20; and “a means for binding to a human macrophage” in claim 13.
Because these claim limitations are being interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, they are being interpreted to cover only the corresponding structure, material, or acts described in the specification as performing the claimed function, and equivalents thereof.
MAINTAINED/MODIFIED REJECTION
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 5, 8 and 9 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention. This is a NEW MATTER rejection.
Claim 5 was amended after the filing date. The limitation of “the method of claim 1, further comprising detecting the expression of avb3 expression in a sample isolated from the subject following administration of the RTK inhibitor” in claim 5 has no clear support in the specification as originally filed. Applicant argues in the Remarks of 04/15/2026 that Applicant's Specification as-filed provides clear and unambiguous support for the phrase "detecting the expression of avb3 in a sample". Applicant argues that the specification describes detecting avb3 expression in samples isolated from subjects, specifically using flow cytometry and immunohistochemistry with the LM609 antibody. Applicant specifically pointed to paragraph [0146], Example 1 and associated figures (Fig. 4B, FIG 1E) as supporting evidence for the limitation.
First, "detecting the expression of avb3 in a sample" is different from "detecting the expression of avb3 in a sample isolated from the subject following administration of the RTK inhibitor". In addition, the results disclosed in the specification is only related to a specific RTK inhibitor (erlotinib) in specific cancers (an avb3-negative EGFR-mutant human non-small cell lung cancer: HCC827; and avb3-negative EGFR-mutant PC9 xenografts) (see Figs. 4B and 1E, and paragraphs [0066], [0125], [0135], [0136]). The specification shows the avb3 expression in these cancers is increased after erlotinib treatment.
Taken together, the claims and specification as originally filed provide support for only one specific RTK inhibitor: erlotinib leads to avb3 expression which is associated with erlotinib resistant for two specific cancers (both are avb3-negative EGFR-mutant lung cancers). Thus, the claims and specification as originally filed do not support “the method of claim 2, further comprising detecting the expression of avb3 expression in a sample isolated from the subject following administration of the RTK inhibitor”, which encompassed a broad genus of RTK inhibitors and a broad genus of RTK inhibitor-resistant epithelial cell cancers.
Regarding Applicant’s arguments that "detecting the expression of avb3 in a sample" is enabled for one ordinary skill in the art, new matter is about the origin of the disclosure, arguing that an added feature is “enabled” does not prove that it was originally disclosed. Even if Applicant prove evidence that the public knows how to make and/or use the newly added feature, Applicant have not retroactively proven the Applicant possessed that feature on the application’s original filing date.
Claim 8 was amended after the filing date. The limitation of “the method of claim 1, further comprising detecting the concentration of tumor associated macrophages in the subject following administration of the RTK inhibitor” in claim 8 has no clear support in the specification as originally filed. Applicant argues in the Remarks of 04/15/2026 that Applicant's Specification as-filed provides clear and unambiguous support for the phrase "detecting the concentration of tumor associated macrophages". Applicant argues that the specification describes detecting the concentration of TAMs the subject. Applicant specifically pointed to paragraphs [0136], [0127] and Fig. 1I and associated text as supporting evidence for the limitation.
Fig. 1l, paragraphs [0127] & [0136] show a higher number of TAMs, particularly of M2 type TAM in erlotinib-treated lung adenocarcinoma tumors.
Taken together, the claims and specification as originally filed provide support for only specific RTK inhibitor: erlotinib leads to an increased M2 type TAM in a specific erlotinib-resistant lung adenocarcinoma. Thus, the claims and specification as originally filed do not support “the method of claim 1, further comprising detecting the expression of avb3 expression in a sample isolated from the subject following administration of the RTK inhibitor”, which encompassed a broad genus of RTK inhibitors and a broad genus of RTK inhibitor-resistant epithelial cell cancers.
Regarding Applicant’s enablement arguments, as set forth above, new matter is about the origin of the disclosure, arguing that an added feature is “enabled” does not prove that it was originally disclosed. Even if Applicant prove evidence that the public knows how to make and/or use the newly added feature, Applicant have not retroactively proven the Applicant possessed that feature on the application’s original filing date.
Claim 9 was amended after the filing date. The limitation of “wherein administration of the RTK inhibitor increases the concentration of M2 TAMs” in claim 9 has no clear support in the specification as originally filed. Applicant argues in the Remarks of 04/15/2026 that Applicant's Specification as-filed provides clear and unambiguous support for RTK inhibitor administration in sufficient amounts results in the
accumulation of TAMs in the tumor/cancer microenvironment. Applicant specifically pointed to paragraphs [0127] and Fig. 1I as supporting evidence for the limitation.
As set forth above, Fig. 1l, paragraphs [0127] & [0136] show a higher number of TAMs, particularly of M2 type TAM in erlotinib-treated lung adenocarcinoma patient tumors.
Taken together, the claims and specification as originally filed provide support for only specific RTK inhibitor: erlotinib leads to an increased M2 type TAM in a specific erlotinib-resistant lung adenocarcinoma patients. Thus, the claims and specification as originally filed do not support “wherein administration of the RTK inhibitor increases the concentration of M2 TAMs”, which encompassed a broad genus of RTK inhibitor and a broad genus of RTK inhibitor-resistant epithelial cell cancers.
NEW REJECTION
Claim Rejections - 35 USC § 112(b)
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 7, 10, 11, and 13 are 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 the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 7 recites the limitation "the anti-avb3 integrin antibody" in line 1. There is insufficient antecedent basis for this limitation in the claim because claim 1 recites “an antibody”.
Claim 10 recites the limitation "the anti-avb3 integrin antibody" in line 1. There is insufficient antecedent basis for this limitation in the claim because claim 1 recites “an antibody”.
Claim 11 recites the limitation "the anti-avb3 integrin antibody" in line 1. There is insufficient antecedent basis for this limitation in the claim because claim 1 recites “an antibody”.
Claim 12 recites the limitation "the anti-avb3 integrin antibody" in line 1. There is insufficient antecedent basis for this limitation in the claim because claim 1 recites “an antibody”.
Claim Rejections - 35 USC § 112(a)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1, and 3-20 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention. This is a NEW MATTER rejection.
Claim 1 was amended after the filing date. The limitation of “a subject in need thereof that has been administered an effective amount of an RTK inhibitor sufficient to induce an accumulation of tumor associated macrophages (TAMs) in the subject” in claim 1 has no clear support in the specification as originally filed. Applicant argues in the Remarks of 04/15/2026 that support for the limitation can be found in the specification as filed, for example, at paragraphs [0024], [0061], [0114], [0116], [0127], [0136], and [0146], as well as FIGS. 3A-E. The paragraphs are shown below:
[0024] In alternative embodiments, provided are methods: wherein the cancer is an epithelial cancer or epithelial tumor cell; or wherein the cancer is a drug resistant cancer, and optionally the drug is a growth factor inhibitor or a kinase inhibitor, wherein optionally the growth factor inhibitor comprises a Receptor Tyrosine Kinase (RTK) inhibitor, optionally erlotinib.
Paragraph [0024] discloses treating RTK inhibitor resistant epithelial cancers with a RTK inhibitor, e.g. erlotinib.
[0061] FIG. 3A-C: LM609 eliminated αvβ3-positive cells via macrophage-mediated ADCC in vitro; ADCC assays with bone marrow derived macrophages (BMDMs) or NK cells were performed with cancer cells with and without αvβ3 integrin treated with the IgG isotype or LM609 10 μg/mL and/or Fc blocker.
[0062] FIG. 3D-E: LM609 eliminated αvβ3-positive tumor growth only in the mice that have macrophages. Nude mice were subcutaneously injected with (33 ectopically expressing HCC827 cells and treated with control liposome and PBS (FIG. 3D left panel, control), control liposome and LM609 (FIG. 3D left panel, LM609), clodronate liposome and PBS (FIG. 3D right panel, control), or clodronate liposome and LM609 (FIG. 3D right panel, LM609), tumor growth was monitored for 15 days, and after the treatments, F4/80 staining in the tumor tissues was quantified (FIG. 3E).
Paragraph [0061] and FIG. 3A-E discloses LM609 eliminates specific avb3-positive cells (HCC827) via macrophage-mediated ADCC in vitro. Importantly, FIG 3C and FIG 3D show that Fc-mediated ADCC is important for the function of LM609. However, claims 1 and 16 encompasses a broad genus of antibodies (even including antibodies without an Fc region).
[0114] In alternative embodiments, a humanized antibody used to practice embodiments provided herein can comprise at least a portion of an immunoglobulin constant region (Fc), typically that of or derived from a human immunoglobulin.
Paragraph [0114] discloses the antibody may comprise an Fc region.
[0116] In alternative embodiments, method comprise use of humanized antibodies capable of specifically binding to an αvβ3 (avb3) integrin polypeptide, including humanized versions of the αvβ3-binding: monoclonal antibody LM609 (Chemicon Int., Temecula, CA) (CVCL_KS89) (the murine hybridoma having ATCC accession number HB 9537) (see e.g., U.S. Pat. No. 7,115,261); monoclonal antibody CBL544, derived from clone 23C6 (MilliporeSigma, Burlington, MA); monoclonal antibody ab7166 (abcam, Cambridge, MA); or, monoclonal antibody ab78289 (abcam, Cambridge, MA), where various humanized versions can be readily determined by one of skill in the art.
Paragraph [0116] discloses exemplary antibodies can be used for treatment.
[0127] Tumor-associated macrophages (TAMs), particularly the M2-type, secrete growth factors, pro-tumorigenic cytokines, and immunosuppressive enzymes to promote tumor progression through induction of angiogenesis, metastasis, and immune suppression. Accordingly, the observation of enriched TAMs in tumor tissues is associated with poor prognosis in various types of cancer, including lung adenocarcinoma. As observed for EGFR inhibitor resistant lung adenocarcinoma patient tumors, we found a higher number of TAMs (CD11b-positive, Ly-6G-negative), particularly of the M2 type (CD206-positive or CD206- and WWII-double negative within the TAM population), within erlotinib-resistant tumors to those from mice treated with a vehicle control (FIG. 1I).
Fig. 1l and paragraphs [0127] show a higher number of TAMs, particularly of M2 type TAM in erlotinib-treated lung adenocarcinoma tumors. The paragraph does not disclose treating “a subject in need thereof that that has been administered an effective amount of an RTK inhibitor sufficient to induce an accumulation of tumor associated macrophages (TAMs) in the subject”. In addition, the claims encompass a broad genus of RTK inhibitors, a broad genus of TAMs and a broad genus of RTK inhibitor-resistant epithelial cell cancers, and a broad genus of antibodies (e.g. including antibodies without an Fc domain).
[0136] TAMs were isolated from tumor tissues as previously described (4). Snap frozen tumor tissues were thawed, minced, and dissociated in HBSS containing collagenase IV (Sigma, C5138, 0.5 mg/mL), hyaluronidase (Sigma, H2654, 0.1 mg/mL), dispase 11 (Roche, 04942078001, 0.6 U/mL), and DNase IV (Millipore, 260913-10MU, 5 U/mL) at 37° C. for 15 minutes. Cell suspensions were filtered through 70 μm cell strainer and washed with PBS. Single cell suspensions (106 cells/100 μL in 5% BSA in PBS) were incubated with Mouse BD Fc Block™ (BD Biosciences, 553142, 1:50) for 10 minutes at 4° C. and fluorescently labeled antibodies, CD11b (eBioscience, 17-0112-81, 1:100), Ly-6G (eBioscience, 25-5931, 1:100), CD206 (BioRad, MCA2235PET), and MHC11 (BD Biosciences, 562928) for one hour at 4° C. Flow cytometry was performed on BD LSRFortessa™, and the ratio of TAMs (CD11b-positive, Ly-6G-negative), M1 (CD206-negative, MHC11-positive within TAMs), and M2 (non-M1 population within TAMs) in the tumor tissue was calculated using the flow cytometry analysis program FlowJo™ (Treestar).
Paragraph [0136] discloses the method of measuring TAMs.
[0146] Cell pellets were washed blocked with 1% BSA in PBS for 30 minutes at room temperature and stained with LM609 (5 μg/mL in 1% BSA in PBS) and a fluorescently labeled secondary antibody (Thermo, A21235, 1:500). After the staining, the cells were incubated with PI (Sigma, P4864, 1:1000), and flow cytometry was performed on BD LSRFortessa™. The levels of αvβ3 integrin were analyzed using the flow cytometry analysis program FlowJo™ (Treestar).
Paragraph [0146] discloses the method of measuring expression of avb3.
It’s noted that, as set forth above, claim 1 encompasses a broad genus of RTK inhibitors, a broad genus of TAMs and a broad genus of RTK inhibitor-resistant epithelial cell cancers, and a broad genus of antibodies (e.g. including antibodies without an Fc domain).
Taken together, the claims and specification as originally filed do not support “a subject in need thereof that has been administered an effective amount of an RTK inhibitor sufficient to induce an accumulation of tumor associated macrophages (TAMs) in the subject” of amended claim 1.
Similarly, the claims and specification as originally filed do not support “administering an effective amount of erlotinib sufficient to induce an accumulation of tumor-associated macrophages in the cancer or tumor, followed by administering an effective amount of an antibody comprising the heavy chain and light chain CDR regions of an antibody selected from the group of the LM609, the monoclonal antibody CBL544, the monoclonal antibody ab7166, or the monoclonal antibody ab78289” of the newly added claim 16, or “a subject in need thereof that has been administered an effective amount of erlotinib sufficient to induce an accumulation of M2 tumor associated macrophages (TAMs) in the subject, …” of the newly added claim 20.
New claim 20 further recites “wherein administering the effective amount results in macrophage-mediated antibody-dependent cell cytotoxicity of the cancer or tumor” which has no clear support in the specification as originally filed. As set forth above, paragraph [0061] and FIG. 3A-E discloses LM609 eliminates specific avb3-positive cells (HCC827) via macrophage-mediated ADCC in vitro. Claim 20 encompasses a broad genus of RTK inhibitor-resistant epithelial cell cancers, and a broad genus of antibodies, which are not supported by the claims and specification as originally filed.
Claims 3-15 and 17-19 are also rejected because these claims encompass the new matter of claim 1 or claim 16.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to CHENG LU whose telephone number is (571)272-0334. The examiner can normally be reached Monday-Friday 8-5.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Samira Jean-Louis can be reached at (571)270-3503. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/CHENG LU/Examiner, Art Unit 1642
/SAMIRA J JEAN-LOUIS/Supervisory Patent Examiner, Art Unit 1642
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