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 .
Claims 1, 7, 11, 13, 14, 31, 32, 35, 58, 59, and 60 have undergone amendments. Claims 61 and 62 are newly added. Thus, Claims 1, 7, 11, 13-14, 22-23, 27, 29, 32, 35, 55-59, and 61-62, submitted on 9 January 2026, represent all claims currently under consideration.
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.
Information Disclosure Statement
One Information Disclosure Statement (IDS), submitted 9 January 2026, is acknowledged and has been considered.
Response to Amendment
The 35 U.S.C. § 112(a) rejection of Claims 1, 7, 11, 13, 14, 17, 22, 23, 25, 27, 29, 32, 35, and 53-59 is withdrawn. Applicant has amended the claims to delete the term “prodrug”.
The 35 U.S.C. § 112(b) rejection of Claims 1, 7, 11, 13, 14, 17, 22, 23, 25, 27, 29, 32, 35, and 53-59 is withdrawn. Applicant has amended Claim 1 to recite the phrase “wherein A is a moiety A1”, providing clarity to what elements are included in the definition of variable A, and has amended Claims 58 and 59 to refer to the compound rather than a composition.
Response to Arguments
The 35 U.S.C. § 112(a) rejection of Claims 1, 7, 11, 13, 14, 17, 22, 23, 25, 27, 29, 32, 35, and 53-59 is maintained as being non-enabling for the treatment of all forms of cancer. The Examiner has considered Applicant’s arguments and does not find them persuasive. While Applicant has provided data demonstrating the treatment of colon, fibroblastoma, breast, and lung cancer utilizing the compounds of the invention, this does not provide evidence for the ability to treat each and every form of cancer. Applicant further provides the Huang reference, and states that “TLR2 is upregulated generally and has been linked to a variety of cancers”. This is not indicative of upregulation in each and every form of cancer. Further, the prior art cited by the Examiner in the previous Office Action states that there are variations in tumor immunophenotypes, and that cancer type and microenvironment condition among other factors affect the clinical outcome of TLR-targeting immunotherapies. Moreover, TLRs are implicated in both cancer progression and suppression, and some patients may derive greater clinical benefit from a TLR antagonist and others from a TLR agonist. Additionally, the state of the art of chemotherapy does not support the notion of a panacea for cancer treatment.
The 35 U.S.C. § 103 rejections of Claims 1, 7, 11, 13, 14, 17, 22, 23, 25, 27, 29, 32, 35, and 53-59 over Bartlett in view of Jackson 2012 and over Jackson 2019 in view of Jackson 2012 are maintained. The Examiner has considered Applicant’s arguments but does not find them persuasive. Applicant claims that the methods of Jackson 2012 are akin to immune response and not therapies for the treatment or minimization of the progression of cancer. Applicant claims that Jackson 2012 teaches the use of a TLR2 agonist, but does not teach the treatment of cancer. The Examiner disagrees. Jackson states “the present invention is concerned with a novel approach to the treatment of infectious diseases and cancers” (Page 1, Lines 21-22). Further, Claims 15 and 16 claims a method for treating a cancer, which can be caused by an infectious agent, including HPV, HCV, or Epstein Barr virus (Claims 15 and 16). Thus, Jackson specifically claims the treatment of cancer using TLR2 agonists, providing a motivation and reasonable expectation of success in applying the TLR2 agonists of Bartlett or Jackson 2019 in the treatment of cancers.
The provisional non-statutory patenting rejection of Claims 1, 7, 11, 13, 14, 22, 23, 27, 29, 32, 35, 53, and 57-59 over Claims 1, 4, 16, and 18-20 of co-pending application No. 18/931,434 (Amended Claims of 30 October 2024) (‘434) is maintained. The Examiner has considered Applicant’s arguments but does not find them persuasive. Applicant claims that ‘434 would not have led one skilled in the art to arrive at methods of treating cancer by TLR2 agonism. The Examiner disagrees. The claims are not patentably distinct because the claims of the examined application are treating cancer by agonism of TLR2, while the claims of the co-pending application are drawn toward the general treatment of diseases by raising an innate immune response in a subject, and /or treating a disease associated with the TRL2 receptor in a subject. These are not patentably distinct as the claims of the examined application are drawn towards the treatment of cancer by raising an innate immune response and the treatment of cancer (a disease associated with the TLR2 receptor).
Claim Rejections - 35 USC § 112(a)- NEW GROUNDS OF REJECTION
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, 7, 11, 13-14, 22-23, 27, 29, 32, 35, 55-59, and 61-62 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for the treatment or minimization of progression of certain types of cancer wherein TLR2 is downregulated or dysregulated, it does not reasonably provide enablement for treatment of all forms of cancer. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the invention commensurate in scope with these claims. Consideration of the relevant factors sufficient to establish a prima facie case for lack of enablement is set forth below:
The nature of the invention and breadth of the claims:
The claims are directed towards a method of treating cancer comprising administering to a patient in need a therapeutically effective amount of a compound of Formula (I). The compounds of Formula (I) are TLR2 agonists. Thus, the claims are directed to a method which can be used for the treatment of any cancer, by agonizing TLR2 using the compounds of the invention.
The state of the prior art and the predictability or unpredictability of the art:
Pahlavanneshan (Journal of Immunology Research, 2021 May 22; 2021:9912188) provides a review of toll-like receptors (TLRs) in cancer and current treatment strategies targeting these receptors. TLRs are expressed in a variety of immune cell types involved in tumor immunity, and there is data on the pharmacological targeting of TLR using agonist molecules that boost antitumor immune responses. A recent body of research also points to the systemic administration of TLR antagonists (Abstract). These receptors are expressed on a variety of cells, including innate immune system cells such as macrophages, neutrophils, dendritic cells, natural killer cells, and mast cells, as well as the adaptive immune system (T and B lymphocytes), stromal cells, and different types of tumor cells (Introduction). These immune cells are found throughout the tumor microenvironment, and play key roles in cancer immunity. For example, macrophages can function as tumor-protective M1 or tumor-promoting M2 subtypes. TLR3 activation can revert M2 to M1. Various types of TLR agonists are being developed including natural microbial components or synthetic compounds and being used in anti-cancer therapy. These agents are considered immune-stimulating factors which enhance TLR signaling and activate an innate immune response which results in long-lasting adaptive immunity. These molecules can stimulate cytotoxic lymphocytes, NK cells, and dendritic cells, and can also be used as vaccine adjuvants to increase the immune response. TLR2 agonists such as Pam3Cys have been used for bladder cancer. Although current studies have shown the proof of concept for the application of TLR-targeted drugs for cancer treatment, given the variations in tumor immunophenotypes, it is likely that cancer type and microenvironment condition among other factors may affect the clinical outcome of TLR-targeting immunotherapies. These differences need to be addressed especially when preclinical animal experiments are conducted. Rolfo (Precision Oncology, 7: 26, 2023) provides a review of TLR agonists that are being evaluated clinically as new therapies for solid tumors. TLR agonists have the potential to convert “cold tumors” to “hot tumors”, making TLRs potential targets for cancer therapies (Abstract). As a family, TLRs have been implicated in both cancer progression and suppression, with the effects of individual receptors varying by tumor histology. The anti-tumor effects of TLRs are mediated by the secretion of pro-inflammatory cytokines and the induction of tumor cell death, while their pro-tumor effects include facilitating cancer cell proliferation, survival, and metastasis, as well as immunosuppression. TLRs can also stimulate regulatory T-cells, which further contribute to the creation of a tumor-permissive immune environment. The antithetical effects of TLRs have been attributed to variations in the response and expression of individual receptors by tumor cells and cells in the tumor microenvironment. As a consequence, it is not possible to regard all TLRs and tumor types as equal; rather, it is necessary to parse out the role of a particular TLR in a given treatment setting, as some patients may derive greater clinical benefit from a TLR antagonist and others from a TLR agonist (Role of TLRs in cancer). Given the conflicting roles of different TLRs and of the same TLR in different tumor types, novel clinical study designs, namely adaptive designs, may be of value in effectively evaluating the efficacy and safety of novel TLR agonists (Conclusions). In view of these teachings, not all cancers can be successfully treated in this manner, as the prior art indicates that each cancer has specific tumor microenvironments with differing expression patterns of TLRs and presence of the cells within the tumor itself, and there is currently no known treatment that can be used to treat all forms of cancer.
The relative skill of those in the art:
The artisan would generally have an advanced degree related to the treatment or study of various cancers; however, their high level of training and knowledge would not be sufficient to overcome the lack of understanding of how to use the claimed compounds to treat all forms of cancer, as not all forms of cancer are sensitive to treatment by modulating the innate immune system, specifically, through agonizing TLR2. Further, there is yet to be evidence of a therapeutic which can be used as a cancer panacea.
The amount of direction or guidance presented and the presence or absence of working examples:
The specification provides experimental data demonstrating the efficacy of the compounds of the invention in the treatment of certain cancers. Example 1 (Page 112) demonstrates that compound A101 has in vivo efficacy in xenograft mouse models of colon carcinoma (MC38 cells), melanoma (B16F10 cells), and breast cancer (4T1.2 cells). Example 2 (Page 115) demonstrates compound A108 is effective in treatment of a murine model of colon carcinoma (MC38 cells). Example 3 (Page 115) demonstrates that compound A108 is effective in treatment of a murine model of fibroblastoma (WEHI164 cells). Examples 4 and 5 (Page 116) show efficacy of compound A108 in reducing lung metastasis in murine models of colon and lung cancer. Example 6 (Page 116) provides data showing efficacy of other compounds of the invention in murine models of colon cancer. The specification does not provide data demonstrating efficacy in the treatment of all forms of cancer.
The quantity of experimentation necessary:
Considering the state of the art as described above, in particular with regards to the lack of a panacea for the treatment of cancer due to the heterogenous nature of the disease, and the high unpredictability of the art as evidenced therein, and the lack of guidance provided in the specification, one of ordinary skill in the art would be burdened with undue experimentation to practice the invention commensurate with the scope of the claims.
Claim Rejections - 35 USC § 103- NEW GROUNDS OF REJECTION
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Claims 1, 7, 11, 13-14, 22-23, 27, 29, 32, 35, 55-59, and 61-62 are rejected under 35 U.S.C. 103 as being unpatentable over Bartlett (WO 2018/176099; Publication date: 4 October 2018) in view of Jackson (WO 2012/037612; Publication Date: 29 March 2012).
Bartlett (See IDS, 23 June 2022) discloses methods for inhibiting a rhinovirus infection in a subject comprising administering a composition consisting of a compound comprising a TLR2 agonist and a pharmaceutically acceptable carrier (Abstract). In a preferred embodiment, the TLR2 agonist comprises Pam2Cys (Page 4, Lines 17-18). Preferably, the TRL2 agonist and solubilizing agent are linked. The TLR2 agonist may be PEGylated (Page 4, Lines 26-27). In any aspect of the invention, the compound or composition is administered to the respiratory tract (Page 4, Lines 27-28). Compound INNA-011
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(Page 85) is identical in structure to Compound A108 of the examined application; this compound is a preferred embodiment of the invention (Page 21).
Bartlett does not teach the treatment or minimization of cancer progression using the TLR2 agonist of the examined application.
Jackson (See IDS, 23 June 2022) discloses a method for treating or preventing a disease by raising an innate immune response in a subject, comprising administering to the subject an effective amount of a composition comprising a TLR2 moiety (Abstract). The present invention is concerned with the development of a novel approach to the treatment of infectious diseases and cancers (Page 1, Lines 21-22). In a fourth aspect of the present invention, there is provided a pharmaceutical composition comprising an effective amount of a TLR2 moiety in solution together with a pharmaceutically acceptable carrier or excipient for treating or preventing disease by raising an innate immune response in a subject (Page 2, Lines 16-19). The present invention is predicated on the observation that a TLR2 agonist such as Pam2Cys demonstrates the ability to raise an innate immune response in a subject (Page 8, Lines 20-22). Where it is desired to use the TLR2 agonist in a polar or aqueous solvent, the TLR2 agonist may be conjugated with a solubilizing agent (Page 11, Lines 11-12). The solubilizing agent includes one or more of the group consisting of PEG and a polar polypeptide, such as a hyper-branched tetra arginine complex, a hyperbranched tetrahistidine complex, a linear peptide containing histidine residues, or a linear peptide containing glutamate residues (Page 11, Lines 19-26). In a particularly preferred form according to the present invention, the TLR2 moiety comprises a conjugate comprising Pam2Cys conjugated to PEG (Page 13, Lines 14-15). The present invention also contemplates the use of a TLR2 moiety as defined herein for treating cancer in a subject. Another aspect of the invention provides a method for treating or preventing cancer by raising an innate immune response in a subject, the method comprising administering to the subject a therapeutically effective amount of a composition comprising a TLR2 moiety in solution. In some embodiments, administration of the TLR2 moiety inhibits the growth or spread of cancer (metastasis) (Page 17, Lines 19-27). The invention claims a method for treating a cancer, which can be caused by an infectious agent, including HPV, HCV, or Epstein Barr Virus (Claims 15 and 16). The present invention also provides a pharmaceutical composition comprising an effective amount of a TLR2 moiety in solution together with a pharmaceutically acceptable carrier or excipient for treating or preventing a disease by raising an innate immune response in a subject (Page 20, Lines 15-17). The compositions of the present invention may be administered by any means known to those skilled in the art, including, but not limited to, intranasally, orally, and intravenously (Page 20, Lines 22-24).
Bartlett and Jackson are considered analogous to the claimed invention as all are involved in the development of TLR2 agonist therapeutics. Therefore, it would have been prima facie obvious to one of ordinary skill in the art the time of the effective filing date of the instant application to apply the TLR2 agonist of Bartlett (INNA-011) to the treatment of cancers, including those that are claimed in the examined application. The use of the known TLR2 agonist of Bartlett for the treatment of cancers by targeting TLR2 as taught by Jackson is prima facie obvious simple substitution of one known element for another to obtain predictable results (See MPEP § 2143 I (B)). The compounds of Bartlett are known TLR2 agonists, and are of similar structure to those used by Jackson for the treatment of cancer. The artisan would recognize this, and would have a reasonable expectation of success in substituting this compound for those disclosed by Jackson for the treatment of cancers.
Regarding Claim 53, Jackson teaches a method for the treatment of cancer. It flows from this art that would require identifying a subject which has cancer prior to administering the treatment to said subject.
Regarding Claims 55 and 56, Jackson teaches that this treatment method can be used to inhibit the growth or spread of cancer (metastasis), and that these cancers can be caused by an infectious agent including HPV, HCV, or the Epstein Barr Virus. Epstein-Barr virus is associated with the development of lymphomas, nasopharyngeal carcinomas, and carcinomas which can develop at other sites such as the thymus, tonsils, lungs, stomach, skin, or the uterine cervix. HPV is a known factor in the development of oral, cervical, and laryngeal cancers. HCV is a leading cause of liver and bile duct cancers. The artisan would recognize this, and apply the method of Jackson for the treatment of these specific cancers, and for the inhibition of metastasis, including that to the lungs.
Claims 1, 7, 11, 13-14, 22-23, 27, 29, 32, 35, 55-59, and 61-62 are rejected under 35 U.S.C. 103 as being unpatentable over Jackson (WO 2019/119067; Publication Date: 27 June 2019) (Jackson 2019) in view of Jackson (WO 2012/037612; Publication Date: 29 March 2012).
Jackson 2019 discloses TLR2 agonist compounds and their compositions, and the use of such compounds and compositions in the prevention and/or treatment of respiratory infections, or diseases or conditions associated with bacterial or viral infections (Abstract). Compound 8 (Page 52) is identical to compound A108 of the examined application
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. The invention also provides for compositions comprising a compound of the invention and a pharmaceutically acceptable carrier, diluent, or excipient (Page 53, Lines 1-3). The invention provides a method for treating a disease, comprising raising an innate immune response in a subject by administering an effective amount of a compound as described herein to the subject in need thereof (Page 53, Lines 4-7). The present invention also provides a method of treating a disease or condition associated with the TLR2 receptor, comprising administering a compound of the invention as described (Page 53, Lines 26-28). Example 8 (Page 138) demonstrates that TRL2 is activated by compounds of the invention, showing that the compounds as claimed function as TLR2 receptor agonists. The results demonstrate that the most potent compounds were those with a single serine, threonine or homoserine separating the Pam2Cys and PEG, or a length or 12, 28 or two groups of 28 ethylene oxide monomers. All compounds resulted in successful receptor binding and subsequent signal transduction (Page 139, Lines 1-4).
Jackson 2019 does not teach the use of the TLR2 agonist for the treatment or minimization of progress of cancer.
Jackson, as previously described, discloses the use of TLR2 agonists of similar structure as those claimed in the examined application for the treatment of cancers.
Jackson 2019 and Jackson are considered analogous to the claimed invention as all are involved in the development of TLR2 agonist therapeutics. Therefore, it would have been prima facie obvious to one of ordinary skill in the art the time of the effective filing date of the instant application to apply the TLR2 agonist of Jackson 2019 to the treatment of cancers, including those that are claimed in the examined application. The use of the known TLR2 agonist of Jackson 2019 for the treatment of cancers by targeting TLR2 as taught by Jackson is prima facie obvious simple substitution of one known element for another to obtain predictable results (See MPEP § 2143 I (B)). The compounds of Jackson 2019 are known TLR2 agonists, and are of similar structure to those used by Jackson for the treatment of cancer. The artisan would recognize this, and would have a reasonable expectation of success in substituting this compound for those disclosed by Jackson for the treatment of cancers.
Regarding Claim 53, Jackson teaches a method for the treatment of cancer. It flows from this art that would require identifying a subject which has cancer prior to administering the treatment to said subject.
Regarding Claims 55 and 56, Jackson teaches that this treatment method can be used to inhibit the growth or spread of cancer (metastasis), and that these cancers can be caused by an infectious agent including HPV, HCV, or the Epstein Barr Virus. Epstein-Barr virus is associated with the development of lymphomas, nasopharyngeal carcinomas, and carcinomas which can develop at other sites such as the thymus, tonsils, lungs, stomach, skin, or the uterine cervix. HPV is a known factor in the development of oral, cervical, and laryngeal cancers. HCV is a leading cause of liver and bile duct cancers. The artisan would recognize this, and apply the method of Jackson for the treatment of these specific cancers, and for the inhibition of metastasis, including that to the lungs.
Double Patenting- NEW GROUNDS OF REJECTION
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, 7, 11, 13-14, 22-23, 27, 29, 32, 35, 55-59, and 61-62 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4, 16 and 18-20 of copending Application No. 18/931,434 (Amended Claims of 30 October 2024) (‘434).
Claim 1 of ‘434 is directed to a compound of Formula (VII)
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wherein A has the structure
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; Y is
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; n is 10 to 100, m is 1, 2, 3, or 4; each g is independently 10-18; p is 2, 3, or 4; q is null or 1; one of R1 and R2 is hydrogen and the other is H, CH2OH, CH2CH2OH, CH(CH3)OH, CH2OPO(OH)2, CH2C(=O)NH2, CH2CH2C(=O)OH, and CH2C(=O)OR8, wherein any of the alkyl hydrogens can be replaced with halogen; R6 and R7 are independently selected from H, straight or branched C1-C4 alkyl, and -C(=O)CH3; R8 is H or straight or branched C1-C6 alkyl; R9 and R10 are independently selected from -NH-, -O-, and bond; z is 1 or 2; X is S or S(=O); wherein when q is 1, R3 is -NH2 or -OH; wherein when q is 0, R3 is H; L is null or consists of 1 to 10 units wherein each unit is a natural alpha amino acid or derived from a natural alpha amino acid, and has the formula
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wherein R4 is H and R5 is the side chain or second hydrogen of the amino acid. Claim 4 claims the compound of claim 1 wherein A is Pam2Cys
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. Claim 16 claims the compound of Claim 1 wherein the compound is the R diastereomer around the following chiral center
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and/or the L-diastereomer of the compound around the following chiral center
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and/or the L-diastereomer around the following
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. Claim 18 claims the compound of Claim 1 that is
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, which is identical to the compound claimed in the examined application. Claim 19 claims a composition comprising a compound of claim 1 and a pharmaceutically acceptable carrier, diluent, or excipient. Claim 20 claims a method of treating a subject by raising an innate immune response in a subject, and/or preventing a disease caused by an infectious agent in a subject and/or treating or preventing a disease or condition associated with the TLR2 receptor comprising administering a therapeutically effective amount of a compound of Claim 1. The method of treating cancer in the examined application raises an innate immune response, and is used to treat a disease which is associated with the TLR2 receptor.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
Claims 1, 7, 11, 13-14, 22-23, 27, 29, 32, 35, 55-59, and 61-62 are rejected.
Applicant's amendment 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to PHILLIP MATTHEW RZECZYCKI whose telephone number is (703)756-5326. The examiner can normally be reached Monday Thru Friday 730AM-5PM EST.
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/P.M.R./Examiner, Art Unit 1625 /Andrew D Kosar/Supervisory Patent Examiner, Art Unit 1625