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 .
DETAILED OFFICE ACTION
This Office Action is in response to the papers filed on 31 July 2026.
ELECTION
Applicant’s election of claims 14-30 drawn to a selection method of an anticancer drug composition in the reply filed on 31 July 2026 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.03(a)). The non-elected claims have been cancelled by the Applicant, as being drawn to a nonelected method, there being no allowable generic or linking claim.
CLAIMS UNDER EXAMINATION
Claims 14-30 are pending and have been examined on their merits.
PRIORITY
JP2023-102855 filed on 22 June 2023 is acknowledged.
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claims 14-30 are rejected under 35 U.S.C. 101 because the claimed invention is not directed to patent eligible subject matter.
Based on the claims as a whole, claims 14-30 are determined to be directed to a law of nature/natural principle. The rationale for the determination is explained below.
Claim 14 is directed to a method of selecting an anticancer drug.
Question 1: Is the claim to a process, machine manufacture or composition of matter? Yes, the invention recited in claim 14 is a process.
Question 2A Prong 1: Is the claim directed to a law of nature, a natural phenomenon, or an abstract idea (judicially recognized exceptions)? Yes, claim 14 is directed to a law of nature.
(a) The limitations in the claim that set forth the law of nature are:
The 2019 PEG explains that the abstract idea exception includes the following groupings of subject matter:
Mathematical concepts – mathematical relationships, mathematical formulas or equations, mathematical calculations;
Certain methods of organizing human activity – fundamental economic principles or practices (including hedging, insurance, mitigating risk); commercial or legal interactions (including agreements in the form of contracts; legal obligations; advertising, marketing or sales activities or behaviors; business relations); managing personal behavior or relationships or interactions between people (including social activities, teaching, and following rules or instructions); and
Mental processes – concepts performed in the human mind (including an observation, evaluation, judgment, opinion).
The claim recites selecting an anticancer drug as having an anticancer effect when the number of cells having a proliferation ability in the cell structure is less than the case where the cell structure is cultured without the anticancer drug. The specification does not recite a definition for the term “selecting” of “selection”. Therefore, mentally identifying an anticancer drug based on cell proliferation data reads on the claim limitation. Such mental observations and evaluations fall within the “mental processes” grouping of abstract idea set forth in the 2019 PEG. 2019 PEG Section I, 84 Fed. Reg. at 52. observations and evaluations that can be performed in the human mind (hence within the “mental processes” grouping of abstract ideas).The claim recites using proliferation as an index. This is a mathematical concept and a judicial exception.
Question 2A Prong 2: Does the claim recite additional elements that integrate the judicial exception into a practical application? No.
The claim recites culturing a cell structure in the presence of at least one anticancer drug. This is considered an insignificant extra-solution activity that is required to make the selection.
Question 2B: Do the claims recite any additional elements? Yes.
With respect to Step 2B, limitations that were found to be enough to qualify as “significantly more” when recited in a claim with a judicial exception include:
Improvements to another technology or technical field.
Improvements to the functioning of the computer itself.
Applying the judicial exception with, or by use of, a particular machine.
Effecting a transformation or reduction of a particular article to a different state or thing
Adding a specific limitation other than what is well-understood, routine and conventional in the field, or adding unconventional steps that confine the claim to a particular useful application.
Other meaningful limitations beyond generally linking the use of the judicial exception to a particular technological environment.
With respect to Step 2B, limitations that were found not to be enough to qualify as “significantly more” when recited in a claim with a judicial exception include:
Adding the words ‘‘apply it’’(or an equivalent) with the judicial exception, or mere instructions to implement an abstract idea on a computer
Simply appending well-understood, routine and conventional activities previously known to the industry, specified at a high level of generality, to the judicial exception, e.g., a claim to an abstract idea requiring no more than a generic computer to perform generic computer functions that are well understood, routine and conventional activities previously known to the industry
Adding insignificant extrasolution activity to the judicial exception, e.g., mere data gathering in conjunction with a law of nature or abstract idea
Generally linking the use of the judicial exception to a particular technological environment or field of use.
Do the additional elements result in the claim amounting to significantly more?
No.
Claim 14 recites a signal transduction pathway in the cancer cells stimulated by the recited growth factors is more activated than a signal transduction in a normal cell. This limitation is interpreted to refer to a characteristic of the cells in the cell structure. This limitation does not add more to the selection step (judicial exception).
Regarding claim 15: The claim further limits the signal transduction pathway recited in claim 14. This limitation does not add more to the selection step (judicial exception).
Claims 16 and 27-30 further limits the cancer cell in claim 14. This limitation does not add more to the selection step (judicial exception).
Claims 17-18 further limit the anticancer drug. The culture step is an insignificant extrasolution step needed to make an index (judicial exception) and selection step (judicial exception). The claim limitations do not add more to the judicial exceptions.
Claims 19-26 further limit the cell structure. The claim limitations do not add more to the judicial exceptions.
Therefore claims 14-30 are not eligible subject matter under 35 USC 101.
Claim Rejections - 35 USC § 112
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 14-30 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 14 recites a structure containing “a cancer cell” (singular) and “a stromal cell”(singular). The claim recites an anticancer effect to “the cancer cells” (plural), “the cancer cells in the cell structure” and “a signal transduction pathway in the cancer cells” (plural). The claim language is unclear because the structure contains a single cancer cell, but the claim refers to a plurality of cancer cells. It is unclear if the claim means the structure contains cancer cells (i.e., plural) and “stromal cells” (i.e. plural). Appropriate correction is required. All dependent claims are included in this rejection.
Claim 14 recites a “normal cell”. The metes and bounds of the term “normal” are unclear. It is unclear if the claim is referring to a non-cancerous cell. Appropriate correction is required. All dependent claims are included in this rejection.
Claim 14 recites “wherein a signal transduction pathway in the cancer cells…is more activated than a signal transduction pathway in a normal cell”. It is unclear if this limitation is referring to the cancer cells before or after culture with an anticancer drug. It is unclear if the claim means the cancer cells are cultured with the claimed growth factors. Appropriate correction is required. All dependent claims are included in this rejection. For the purpose of examination, this limitation is interpreted to be an inherent characteristic of the cancer cells used in the cell structure.
Claim 26 recites “mixing cells”. It is unclear if the claim is referring to the cancer cell and the stromal cell recited in claim 14. Appropriate correction is required.
Claims 29-30 recite “the evaluation method…of claim 14”. An evaluation method lacks antecedent basis in claim 14. The metes and bounds of the claim are unclear. Appropriate correction is required.
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.
Claims 19 and 21-22 are 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.
Regarding claim 19: the base claim recites “a cancer cell” (singular). Claim 19 is not further limiting because a cancer cell layer comprises a plurality of cells.
Regarding claim 21: the base claim recites “a stromal cell” (singular). Claim 21 is not further limiting because the claim allows multiple (“one or more”) stromal cells.
Regarding claim 22: the base claim recites “a stromal cell” (singular). Claim 22 is not further limiting because the claim requires multiple types of stromal cells.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Claim Rejections - 35 USC § 103
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 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 14-27 are rejected under 35 U.S.C. 103 as being unpatentable over Kitano et al. (Method for evaluating anticancer effect and method for predicting effectiveness of cancer immunotherapy. US20200191773A1) in view of Fujimoto et al. (Combination treatment with a PI3K/Akt/mTOR pathway inhibitor overcomes resistance to anti-HER2 therapy in PIK3CA-mutant HER2-positive breast cancer cells. Sci Rep 10, 21762 (2020) as evidenced by Koch et al. (Signal transduction by vascular endothelial growth factor receptors. Cold Spring Harb Perspect Med. 2012 Jul;2(7):a006502).
Kitano et al. teach “a method for testing an anticancer effect including culturing a cell structure including cancer cells and stromal cells in a presence of an anticancer drug and immune cells, and measuring the number of living cancer cells in the cell structure after the culturing, as an indicator of an anticancer effect of the anticancer drug or the immune cells” (Abstract). Kitano teaches the anticancer effect of an anticancer drug in the presence of the anticancer drug and immune cells is evaluated using, as an indicator (hence, an index), the number of living cancer cells in the cell structure after the culture step. Kitano teaches the anticancer effect refers to an effect of suppressing the growth (i.e. proliferation) of cancer cells or an effect of killing cancer cells ([0082]).
Kitano teaches when the number of living cancer cells in the cell structure is smaller than (hence, less than) that cultured in the absence of the anticancer drug and immune cells, at least one of the anticancer drug and the immune cells used is evaluated to have an anticancer effect on the cancer cells contained in the cell structure ([0083]).
It is noted Kitano teaches the cancer cell in the structure can be a breast cancer cell ([0033]).
Kitano is silent regarding a breast cancer cell with the claimed signal transduction activation.
Fujimoto et al. teach gene amplification, overexpression, and mutation of human epidermal growth factor receptor 2 (HER2), is observed in approximately 20% of breast cancers and are associated with poor prognosis. Oncogenic activation of HER2 constitutively activates the downstream signaling pathways: PI3K/AKT pathway, and the RAS/RAF/mitogen-activated ERK/MAPK pathway (see page 1, first paragraph).
Fujimoto administers a HER2 inhibitor (Abstract; see page 2, third paragraph). Fujimoto teaches some patient populations demonstrate clinical resistance to anti-HER2 therapies (see page 1, first paragraph bridging first sentence of page 2).
As evidenced by Koch et al., ERK/MAPK pathway is activated by VEGF (see Figure 3). Therefore the cells taught by Koch read on the claim limitation.
It would have been obvious to use a HER-2 breast cancer cell in the cell structure taught by Kitano. One would have been motivated to do so to evaluate the effect of anti-HER cancer drugs on a patient with HER-2 cancer in vitro. One would have been motivated to do so since Fujimoto teaches some patients are resistant to drug treatment. One would have had a reasonable expectation of success since Kitano teaches breast cancer cells can be used in the cell structure. One would have expected similar results since Kitano and Fujimoto both analyze drugs that treat cancer. Therefore claim 14 is rendered obvious.
Fujimoto teaches oncogenic activation of HER2 constitutively activates PI3K/AKT pathway, and the ERK/MAPK pathways (supra). Claim 15 is included in this rejection.
A HER2 positive cancer cell is rendered obvious on the grounds set forth above. Claim 16 is included in this rejection.
Fujimoto administers small molecule inhibitors of AKT and HER2 (see page 2, third paragraph). As evidenced by Koch et al., AKT is a molecule in a signal transduction pathway activated by VEGF (see Figure 3). Claim 17 is included in this rejection.
Fujimoto teaches a HER2 inhibitor (supra). Claim 18 is included in this rejection.
Kitano teaches it is preferred to use a cell structure including a cancer cell layer on the top surface ([0099]). Claim 19 is included in this rejection.
Kitano teaches the cancer cell can be obtained from a cancer patent ([0209]). Claim 20 is included in this rejection.
Kitano teaches the cell structure may contain at least one selected from the group consisting of fibroblasts and mast cells as cells constituting a stroma ([0200]). This reads on claim 21.
Kitano teaches when both vascular endothelial cells and lymphatic endothelial cells are contained as endothelial cells, the total number of vascular endothelial cells and lymphatic endothelial cells is preferably 0.1% or more, and more preferably 0.1% to 5.0% of the number of fibroblasts. ([0031]). Claim 22 is included in this rejection.
Kitano teaches the cell structure preferably has a thickness of 5 μm or more ([0037]). Therefore claim 23 is included in this rejection.
Kitano teaches a cell structure having a blood vessel network structure ([0104]). Claim 24 is included in this rejection.
Kitano teaches culture for 24 to 96 hours ([0080]). Claim 25 is included in this rejection.
Kitano teaches the cell structure is produced by mixing cells with an extracellular matrix component in a cationic buffer solution to obtain a mixture; seeding the mixture in a cell culture vessel; and (obtaining a cell structure in which cells are multi-layered in the cell culture vessel after step ([0043]). the cells are preferably further mixed with a strong electrolyte polymer. When the cells are mixed with a cationic substance, a strong electrolyte polymer, and an extracellular matrix component, a thick three-dimensional cell tissue with few voids can be obtained ([0045]). Therefore claim 26 is included in this rejection.
Fujimoto teaches a HER2-positive cancer cell and a HER2 inhibitor. Claim 27 is included in this rejection.
Therefore Applicant’s invention is rendered obvious as claimed.
Claims 14-26 and 28 are rejected under 35 U.S.C. 103 as being unpatentable over Kitano et al. in view of Hrustanovic et al. (RAS signaling in ALK fusion lung cancer. Small GTPases. 2016;7(1):32-3) as evidenced by Koch et al.
The teachings of Kitano as set forth above are reiterated. Kitano teaches the cancer cell in the structure can be a malignant lymphoma ([0033]).
Kitano is silent regarding a lymphoma cell with the claimed signal transduction activation.
Hrustanovic investigate resistance to targeted therapies acting against the anaplastic lymphoma kinase (ALK) in ALK gene rearrangement-positive lung adeno carcinoma (ALKC). The art teaches RAS-RAF MEK-ERK signaling is the crucial downstream pathway (Abstract; see Figure1). As evidenced by Koch et al., RAS-RAF MEK-ERK signaling activated by VEGF (see Figure 3). These patients are treated with ALK inhibitors. The art teaches initial ALK inhibitor response is typically incomplete and transient in these patients, or resistant to ALK inhibitor treatment (see page 32, left column, second paragraph).
It would have been obvious to use an ALKC cancer cell in the cell structure taught by Kitano. One would have been motivated to do so to study the effect of ALK-inhibitor therapy on ALKC in vitro. One would have had a reasonable expectation of success since Kitano teaches lymphoma cancer cells can be used in the cell structure. One would have been motivated to do so since Hrustanovic teaches response to treatment is incomplete and transient in some patients. One would have expected similar results since Kitano and Hrustanovic both analyze drugs that treat cancer. Claim 14 is rendered obvious.
Hrustanovic teaches RAS-RAF-MEK ERK (RAS-MAPK) activation in ALK positive cells (see Figure 1). Claim 15 is included in this rejection.
Hrustanovic teaches an ALK-positive cell. Claim 16 is included in this rejection.
Hrustanovic teaches a MEK inhibitor (see Figure 1). administers small molecule inhibitors of AKT and HER2 (see page 2, third paragraph). As evidenced by Koch et al., MEK is a molecule in a signal transduction pathway activated by VEGF (see Figure 3). Claim 17 is included in this rejection.
Hrustanovic teaches an ALK-inhibitor (supra, see Figure 1). Claim 18 is included in this rejection.
Claims 19-26 are rejected over the teachings of Kitano as set forth above.
Hrustanovic teaches an ALK-positive cell and an ALK-inhibitor. Claim 28 is included in this rejection.
Therefore Applicant’s Invention is rendered obvious as claimed.
Claims 14-26 and 29 are rejected under 35 U.S.C. 103 as being unpatentable over Kitano et al. in view of Zhao et al. (Dual Inhibition of MAPK and JAK2/STAT3 Pathways Is Critical for the Treatment of BRAF Mutant Melanoma. Mol Ther Oncolytics. 2020 Jun 5;18:100-108) as evidenced by Koch et al.
The teachings of Kitano as set forth above are reiterated. Kitano teaches the cancer cell in the structure can be a melanoma, thyroid, ovarian, colon or rectal cancer ([0033]).
Kitano is silent regarding cancer cells with the claimed signal transduction activation.
Zhao et al. teach BRAF mutations are common in melanoma, papillary thyroid cancer, ovarian cancer, and colorectal cancer. The mutant BRAF protein continuously activates the mitogen-activated protein kinase (MAPK) pathway (also known as the RAS-RAF-MAPK kinase [MEK]-extracellular signal-regulated kinase [ERK] pathway) to promote tumor cell proliferation and survival (see first paragraph of introduction on page 100).
Zhao teaches patients are treated with BRAF inhibitors, but most patients develop tumor recurrence after 11-14 months of targeted therapy (see page 100, right column first paragraph). As evidenced by Koch et al., RAS-RAF MEK-ERK signaling activated by VEGF (see Figure 3).
It would have been obvious to use a BRAF positive cancer cell in the structure taught by Kitano. One would have been motivated to do so to study the effect of BRAF inhibitors on BRAF positive cancers in vitro. One would have been motivated to do so since Zhao teaches response to treatment is transient in some patients. One would have had a reasonable expectation of success since Kitano teaches the cancer cells taught in Zhao can be used in the cell structure. One would have expected similar results since Kitano and Zhao are both analyze drugs that treat cancer. Therefore claim 14 is rendered obvious.
Zhao teaches RAS-RAF-MEK ERK (RAS-MAPK) activation in BRAF positive cells (see Figure 1). Claim 15 is included in this rejection.
Zhao teaches a BRAF-positive cell. Claim 16 is included in this rejection.
Zhao administers a combination of MAPK pathway inhibitors (Abstract). As evidenced by Koch et al., MEK is a molecule in a signal transduction pathway activated by VEGF (see Figure 3). Claim 17 is included in this rejection.
Zhao teaches a BRAF-inhibitor. Claim 18 is included in this rejection.
Claims 19-26 are rejected over the teachings of Kitano as set forth above.
Zhao teaches an BRAF-positive cell and a BRAF-inhibitor. Claim 29 is included in this rejection.
Therefore Applicant’s Invention is rendered obvious as claimed.
Claims 14, 16, 18-26 and 30 are rejected under 35 U.S.C. 103 as being unpatentable over Kitano et al. in view of Zer et al. (Promising Targets and Current Clinical Trials in Metastatic Non-Squamous NSCLC. Front. Oncol. 4:329) as evidenced by Sohn et al. (Foretinib Inhibits Cancer Stemness and Gastric Cancer Cell Proliferation by Decreasing CD44 and c-MET Signaling. Onco Targets Ther. 2020 Feb 3;13:1027-1035).
The teachings of Kitano as set forth above are reiterated. Kitano teaches a non-small cell lung cancer cell can be used in the disclosed cell structure ([0033]).
Kitano is silent regarding cancer cells with the claimed signal transduction activation.
Zer teaches ROS1 fusion genes, with oncogenic transformation potential, has been described in lung cancer non-small cell lung cancer (page 2, right column, first paragraph). As evidenced by the instant specification, the signal transduction pathway stimulated by HGF, PIGF, VEGF, or bFGF is activated ([0046]). The art teaches foretinib is being studied for treatment (Table 1). As evidenced by Sohn et al., foretinib inhibits Wnt (page 1033, left column, first paragraph).
It would have been obvious to use a ROS-1 non-small cell lung cancer cell in the structure taught by Kitano. One would have been motivated to do so to study the effect of drugs that treat NSCLC. One would have had a reasonable expectation of success since Kitano teaches the cancer cells taught in Zhao can be used in the cell structure. One would have expected similar results since Kitano and Zhao are both analyze drugs that treat cancer. Therefore claim 14 is rendered obvious.
Zer teaches a ROS-1 positive cancer cell. Therefore claim 16 is included in this rejection. Zer teaches a WNT inhibitor (supra). Therefore claim 18 is included in this rejection.
Claims 19-26 are rejected over the teachings of Kitano as set forth above.
Zer teaches a ROS-1 positive cancer cell and a WNT inhibitor (supra). Therefore claim 30 is included in this rejection.
Therefore Applicant’s Invention is rendered obvious as claimed.
Double Patenting
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 14-27 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 6-10 and 13-16 of U.S. Patent No. US12523647B2 in view of Fujimoto et al.
Regarding claim 14: Claim 1 of the ‘647 Patent recites method for evaluating effectiveness of a cancer immunotherapy, comprising culturing a cell structure comprising stromal cells and cancer cells in the presence of an anticancer drug; and measuring the number of living cancer cells in the multi-layered cell structure after the culture; wherein a reduction of the number of living cancer cells in the multi-layered cell structure after the culture period compared to the number of living cancer cells in a control cell structure cultured in the absence of the anticancer drug indicates effectiveness of the cancer immunotherapy.
While the ‘647 Patent does not teach the signal transduction limitation recited in instant claim 14, Fujimoto teaches oncogenic activation of HER2 constitutively activates the downstream signaling pathways: PI3K/AKT pathway, and the RAS/RAF/mitogen-activated ERK/MAPK pathway (see page 1, first paragraph).Fujimoto administers a HER2 inhibitor (Abstract; see page 2, third paragraph). Fujimoto teaches some patient populations demonstrate clinical resistance to anti-HER2 therapies (see page 1, first paragraph bridging first sentence of page 2). As evidenced by Koch et al., ERK/MAPK pathway is activated by VEGF (see Figure 3). Therefore the cells taught by Koch read on the claim limitation.
It would have been obvious to use a HER-2 breast cancer cell in the cell structure taught by Kitano. One would have been motivated to do so to evaluate the effect of anti-HER cancer drugs on a patient with HER-2 cancer in vitro. One would have been motivated to do so since Fujimoto teaches some patients are resistant to drug treatment. One would have had a reasonable expectation of success since Kitano teaches breast cancer cells can be used in the cell structure. One would have expected similar results since Kitano and Fujimoto both analyze drugs that treat cancer.
Regarding instant claim 15: Fujimoto teaches oncogenic activation of HER2 constitutively activates PI3K/AKT pathway, and the ERK/MAPK pathways (supra).
Regarding instant claim 16: A HER2 positive cancer cell is rendered obvious on the grounds set forth above.
Regarding instant claim 17: Fujimoto administers small molecule inhibitors of AKT and HER2 (see page 2, third paragraph). As evidenced by Koch et al., AKT is a molecule in a signal transduction pathway activated by VEGF (see Figure 3).
Regarding instant claim 18: Fujimoto teaches a HER2 inhibitor (supra).
Regarding instant claim 27: Fujimoto teaches a HER2-positive cancer cell and a HER2 inhibitor.
Regarding instant claim 21: claim 7 of the ‘647 Patent recites the stromal cells include at least one of a fibroblast or a mast cell, an epithelial cell.
Regarding instant claim 22: claim 6 of the ‘647 Patent recites the stromal cells include fibroblasts and at least one endothelial cell type selected from vascular endothelial cells and lymphatic endothelial cells. Claim 13 of the ‘647 Patent recites the stromal cells comprise a plurality of endothelial cells and a plurality of fibroblasts, and the ratio of endothelial cells to fibroblasts is from 0.1% to 5.0%.
Regarding instant claim 23: claim 8 of the ‘647 Patent recites the thickness of the multi-layered cellular structure is from 50 μm to 500 μm.
Regarding instant claim 24: claim 9 of the ‘647 Patent recites the cellular structure includes a vascular network structure.
Regarding instant claim 26: claim 14-16 of the ‘647 Patent disclose the cell structure is made prepared with a strong electrolyte polymer and an extracellular matrix component.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to NATALIE MOSS whose telephone number is (571) 270-7439. The examiner can normally be reached on Monday-Friday, 8am-5pm EST.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Sharmila Landau can be reached on (571) 272-0614. The fax phone number for the organization where this application or proceeding is assigned is (571) 270-8439.
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/NATALIE M MOSS/ Examiner, Art Unit 1653
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