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 .
Priority
Acknowledgment is made of applicant’s claim for priority. The certified copy has been filed in parent Application No. 63/135,449, filed on 01/08/2021.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 08/14/2024 and 02/27/2024 are being considered by the examiner.
Specification
The disclosure is objected to because it contains embedded hyperlinks (pages 3, 30, 32, 42 , 65, 71, 72, 73, 74) and/or other form of browser-executable code. Applicant is required to delete the embedded hyperlink and/or other form of browser-executable code; references to websites should be limited to the top-level domain name without any prefix such as http:// or other browser-executable code. See MPEP § 608.01.
Claim Rejections - 35 USC § 102
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 the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claim(s) 31, 33, 35, 37, 39, 41, 43, 45, 47, 49, 51, 53, 55, 57, 59, 61, 65, 69-70 is/are rejected under 35 U.S.C. 102(a)(1)/(2) as being clearly anticipated by HABY (HABY et al., WO2020232130A1, 2020-11-19, IDS).
The applied reference has a common applicant and inventor with the instant application. Based upon the earlier effectively filed date of the reference, it constitutes prior art under 35 U.S.C. 102(a)(2). This rejection under 35 U.S.C. 102(a)(2) might be overcome by: (1) a showing under 37 CFR 1.130(a) that the subject matter disclosed in the reference was obtained directly or indirectly from the inventor or a joint inventor of this application and is thus not prior art in accordance with 35 U.S.C. 102(b)(2)(A); (2) a showing under 37 CFR 1.130(b) of a prior public disclosure under 35 U.S.C. 102(b)(2)(B) if the same invention is not being claimed; or (3) a statement pursuant to 35 U.S.C. 102(b)(2)(C) establishing that, not later than the effective filing date of the claimed invention, the subject matter disclosed in the reference and the claimed invention were either owned by the same person or subject to an obligation of assignment to the same person or subject to a joint research agreement.
The reference HABY teaches (reference claims 1, 3, 5 and 8):
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The reference HABY teaches “In some embodiments, for NSCLC, subjects may have received platinum-based combination therapy and/or targeted therapies (i.e., if molecular testing has identified mutations in EGFR, ALK, or proto-oncogene tyrosine-protein kinase ROS [ROS1] or expression of programmed death-ligand [PD-L1]), prior to receiving AMG 510 (Compound A)” [0119]. The specification anticipates patient populations that received other targeted therapies that are not platinum-based as the platinum based therapies is an optional selection of patient population. This anticipates claim 31 and 65.
The reference HABY teaches “In specific embodiments, Compound A is administered to a subject in need thereof orally and once a day. In some cases, the subject is administered a total daily amount of 180 mg, 360 mg, 720 mg, or 960 mg. In some cases, the total daily amount of Compound A administered is 180 mg. In some cases, the total daily amount of Compound A administered is 360 mg. In some cases, the total daily amount of Compound A administered is 720 mg. In some cases, the total daily amount of Compound A administered is 960 mg. In some cases, Compound A is administered in a divided daily dose, such as two, three, four, five, or six times a day”[0059]. This anticipates claim 33.
The reference HABY teaches “Compound A can be combined with a pharmaceutically acceptable excipient to provide a pharmaceutical formulation (also referred to, interchangeably, as a composition). The excipient can be a diluent or carrier” [0038]. This anticipates claim 35, 37, 39.
The reference HABY teaches “When a therapeutically effective amount of Compound A is administered orally, the composition typically is in the form of a solid (e.g., tablet, capsule, pill, powder, or troche) or a liquid formulation (e.g., aqueous suspension, solution, elixir, or syrup). In one embodiment the therapeutically effective amount of Compound A (e.g., 960 mg) is administered orally in the form of a tablet or multiple tablets (e.g., 8 x 120 mg tablet)” [0041]. This anticipates claim 39, 41, 43, 45.
The reference HABY teaches “When a therapeutically effective amount of Compound A is administered by intravenous, cutaneous, or subcutaneous injection, the composition is in the form of a pyrogen- free, parenterally acceptable aqueous solution. The preparation of such parenterally acceptable solutions, having due regard to pH, isotonicity, stability, and the like, is within the skill in the art. A preferred composition for intravenous, cutaneous, or subcutaneous injection typically contains, in addition to Compound A, an isotonic vehicle. Such compositions may be prepared for administration as solutions of free base or pharmacologically acceptable salts in water suitably mixed with a surfactant, such as hydroxypropylcellulose” [0044]. This anticipates claims 47, 49, 51, 53, 55, 57, 59, 61.
The reference HABY teaches “Compound A Dosing Study: patients identified with a cancer having a KRAS G12C mutation were enrolled in the study. The patients are adult patients with locally advanced or metastatic KRAS G12 C mutant solid tumors. All patients previously received prior standard therapies depending upon the tumor type and stage of disease. No patient exhibited active brain metastases. Patients in the dosing study had the following diagnoses: 14 with non-small cell lung cancer (NSCLC), 10 with colorectal cancer (CRC) and two with another KRAS G12 C mutant solid tumor. Compound A was administered orally once daily at the designated dose. Patients were given a dose of 180 mg, 360 mg, 720 mg, or 960 mg Compound A and adiographic scans were performed every six weeks” [0147]. This anticipates claim 69-70.
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claim(s) 31, 33, 47, 49, 63, 64, 65 is/are rejected under 35 U.S.C. 103 as being unpatentable over CANON (CANON J, et al. The clinical KRAS(G12C) inhibitor AMG 510 drives anti-tumour immunity. Nature. 2019;575(7781):217-223, IDS) in view of Dean (Dean et al., Clinical Outcomes of Patients with Rare and Heavily Pretreated Solid Tumors Treated according to the Results of Tumor Molecular Profiling, Biomed Res Int. 2016 Jul 21;2016:4627214. doi: 10.1155/2016/4627214) as evidenced by Stults (Stults et al., Solid State Considerations for Early Development, March 31, 2015).
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The reference CANON teaches “The enhanced potency and efficacy of AMG 510 prompted its selection as, to our knowledge, the first KRAS(G12C) inhibitor to enter clinical trials (clinicaltrials.gov identifier NCT03600883)16. AMG 510 was administered orally, once daily, in escalating dosing cohorts (Fig. 3a). In the first two dosing cohorts there were four patients with non-small-cell lung carcinoma (180 mg, n = 3; 360 mg, n = 1). Treatment with AMG 510 resulted in objective partial responses (as per RECIST 1.1) in two patients (Fig. 3b and Extended Data Fig. 5) and stable disease in two patients”(page 220) and the figures 1 and 3 below that show the structure of AMG 510 and the dosages of the clinical trial. This helps to teach claims 31, 33, 65.
The reference Stults provides evidences that a free base form is the neutral form(page 2), Canon shows that the AMG 510 is the neutral form in figure 1. This helps to teach claims 47 and 49.
The reference CANON also teaches “Here we present the data on the preclinical activity of AMG 510, its ability to induce tumour-cell killing as monotherapy or when combined with other therapies, and the marked impact of AMG 510 on immune cell infiltration, which renders the tumour microenvironment highly sensitive to immunotherapy. We also present promising evidence for clinical efficacy”(page 217). This helps to teach claims 31, 65.
The reference CANON also teaches “Blockade of the immune checkpoint axis that involves programmed cell death 1 (PD-1)–programmed death ligand 1 (PD-L1) is clinically validated in multiple settings. As the long term cures induced by AMG 510 in the CT-26 KRASG12C model were dependent on the engagement of the immune system (Fig. 2h and Extended Data Fig. 4g), strategies such as anti-PD-1
therapy that further boost anti-tumour T cell activity may synergize with AMG 510… Therefore, we used this model to evaluate the combination of anti-PD-1 immune checkpoint inhibition with AMG 510, which was administered at a suboptimal dose to enable the evaluation of combination effects”(page 221) and “Furthermore, the combination of AMG 510 and anti-PD-1 therapy established a memory T cell response against both the CT-26 KRASG12C cells and the parental CT-26 tumour cells. These data support a model of enhanced antigen recognition and T cell memory in which AMG 510-induced tumour cell death and innate immune responses, combined with anti-PD-1 treatment, results in an adaptive immune response that can recognize and eradicate related but nonKRASG12C tumours”(page 223).
The reference CANON also teaches “Patients were recruited at clinical study sites based on the presence of the KRAS p.G12C mutation in their tumor by standard genotype testing”(page 4 of the report summery). This helps to teach claim 63-64’s step 1 assaying a sample obtained from the subject for a KRAS G12C mutation. The reference CANON also teaches “The two patients with a partial response had progressed on multiple previous systemic treatments including carboplatin, pemetrexed and nivolumab with documented disease progression. After 6 weeks of treatment with AMG 510, the first responder (180 mg) exhibited tumour shrinkage of 34%, and the second (360 mg) exhibited a tumour reduction of 67%.”(page 220). This helps to teach claim 63-64’s step 2 determining whether the subject has received a prior systemic platinum-based chemotherapy. This shows it is obvious to a person of ordinary skill in the art to identify medical history including any previous treatments and to identify sensitivity to AMG 510 treatment via tumor response.
The reference CANON teaches does not teach subjects that have not received a prior systemic platinum -based chemotherapy(claim 31, 33, 47, 49, 63, 64, 65) or PD-1 or anti PD-L1 immunotheraру(claim 65).
The reference Dean teaches “Good performance status patients with heavily pretreated tumors and those with rare malignancies represent a difficult therapeutic group”(page 1) and “Patients with heavily pretreated advanced cancer or with rare tumors are difficult to treat. Molecular profiling (MP) of tumors to identify biomarkers that predict potential outcomes with individual therapies is an emerging strategy to guide treatment decisions”(abstract). This helps to teach claim 31 and 65.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON with Dean to produce the instant claims because CANON does not suggest the exclusion of population of patients who had not previously been treated for cancer and Dean indicates that pretreated cancer is often difficult to treat. Thus one would be motivated to treat cancers that would be more likely to respond to treatment such as cancers that had not previously been treated. One would also have reasonable expectation of success because Canon teaches AMG 510 as a monotherapy which means additional treatment was not envisioned as being required. The recited exclusion of patients previously treated with platinum-based chemotherapy does not impart a patentable distinction since the limitation constitutes an obvious patient selection.
Claim(s) 69 is/are rejected under 35 U.S.C. 103 as being unpatentable over CANON (CANON J, et al. The clinical KRAS(G12C) inhibitor AMG 510 drives anti-tumour immunity. Nature. 2019;575(7781):217-223, IDS).
The reference CANON also teaches “See clinicaltrials.gov NCT03600883. Key inclusion criteria: age ≥18; documented locally-advanced or metastatic KRASG12C; measurable or evaluable disease; ECOG ≤2; life expectancy >3 months (mo). Key exclusion criteria: active brain metastases…”(report page 4). This helps to teach claim 69.
The reference CANON has been discussed supra and does not disclose patients with no brain metastasis (claim 69).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON to include patients with no brain metastasis because ones with active brain metastasis were explicitly excluded. It would then be obvious to select patients with no brain metastasis at all, as those also exclude active brain metastasis patients. One would have motivation to do this with reasonable expectation of success because they wanted to exclude some of these patients already and the treatment worked.
Claim(s) 70 is/are rejected under 35 U.S.C. 103 as being unpatentable over CANON (CANON J, et al. The clinical KRAS(G12C) inhibitor AMG 510 drives anti-tumour immunity. Nature. 2019;575(7781):217-223, IDS) in view of Janjan (Janjan, Nora. Bone Metastases: Approaches to Management, Seminon in Oncology, Vol 28, No 4, Suppl I I (August), 2001: pp 28-34).
The reference CANON has been discussed supra and does not disclose patients with no bone metastasis (claim 70).
The reference Janjan teaches “Cancer commonly metastasizes to bone and up to 80% of breast, prostate, and lung cancer patients will have bone metastases. The site and distribution of bone metastases, and the presence of skeletal complications such as pathologic fracture and spinal cord compression affect the patient’s prognosis. In many cases, bone metastases are too advanced to be eliminated through chemotherapy or radiotherapy…”(abstract). This helps to teach claim 70.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON with Janjan to produce the instant claims because CANON does not suggest the exclusion of population of patients with bone metastasis and Janjan indicates in many cases, bone metastases are too advanced to be eliminated through chemotherapy. Thus one would be motivated to treat cancers that would be more likely to respond to treatment such as cancers without bone metastases. One would also have reasonable expectation of success because Canon teaches AMG 510 as a monotherapy with no indication of bone metastases. The recited exclusion of patients with bone metastases does not impart a patentable distinction since the limitation constitutes an obvious patient selection.
Claim(s) 31, 33, 35, 37, 39, 41, 43, 45, 51, 53, 55, 57, 59, 61 is/are rejected under 35 U.S.C. 103 as being unpatentable over CANON (CANON J, et al. The clinical KRAS(G12C) inhibitor AMG 510 drives anti-tumour immunity. Nature. 2019;575(7781):217-223, IDS) in view of Dean (Dean et al., Clinical Outcomes of Patients with Rare and Heavily Pretreated Solid Tumors Treated according to the Results of Tumor Molecular Profiling, Biomed Res Int. 2016 Jul 21;2016:4627214. doi: 10.1155/2016/4627214) further in view of Chaudhari (Chaudhari et al., Pharmaceutical Excipients: A review, IJAPBC – Vol. 1(1), Jan- Mar, 2012) as evidenced by Stults (Stults et al., Solid State Considerations for Early Development, March 31, 2015).
The references CANON, Stults and Dean have been discussed supra and does not disclose pharmaceutical excipients (claim 35, 37, 51, 53) or a solid dosage form or tablet (claims 39, 41, 43, 45, 55, 57, 59, 61).
The reference Chaudhari teaches “Excipients play an important role in formulating a dosage form. These are the ingredients which along with Active Pharmaceutical Ingredients make up the dosage forms. Excipients act as protective agents, bulking agents and can also be used to improve bioavailability of drugs in some instances, the following review discusses the various types and sources of excipients along with their uses, and these can be used for different activities”(abstract) and “Tablets are generally considered as a dosage form of choice when oral route is preferred, because of accurate dosing, better patient compliance. Excipients such as binders, disintegrants, diluents, glidants, lubricants etc are used along with the active pharmaceutical ingredient in the tablet manufacturing, These excipient offer in enhancing various properties like dissolution, absorption etc of active pharmaceutical ingredient when in tablet”(pages 23-24). The reference teaches “Many dosage forms formulated today are complex system containing many other components along with the active pharmaceutical ingredient (API); these compounds are generally added along with the active pharmaceutical ingredients…” (page 1). This helps to teach claim 35, 37, 39, 41, 43, 45, 51, 53, 55, 57, 59, 61.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON and Dean with Chaudhari to produce the instant claims because CANON teaches AMG 510 was administered orally to treat cancer and Chaudhari teaches that tablets are generally considered as a dosage form of choice when oral route is used and that tablets often included excipients such as binders, disintegrants, diluents, glidants, lubricants etc. One would be motivated to use a tablet because of accurate dosing, better patient compliance and one would be motivated to use an excipient because excipient offer enhancing various properties like dissolution, absorption etc of active pharmaceutical ingredient when in a tablet. One would have a reasonable expectation of success because excipient are added to many active compounds formulated today and thus it is a common practice.
Claim(s) 31, 32, 33, 34, 35, 36, 37,38, 39, 40, 41, 42, 43, 44, 45, 46, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 66 is/are rejected under 35 U.S.C. 103 as being unpatentable over CANON (CANON J, et al. The clinical KRAS(G12C) inhibitor AMG 510 drives anti-tumour immunity. Nature. 2019;575(7781):217-223, IDS) in view of Dean (Dean et al., Clinical Outcomes of Patients with Rare and Heavily Pretreated Solid Tumors Treated according to the Results of Tumor Molecular Profiling, Biomed Res Int. 2016 Jul 21;2016:4627214. doi: 10.1155/2016/4627214) further in view of Chaudhari (Chaudhari et al., Pharmaceutical Excipients: A review, IJAPBC – Vol. 1(1), Jan- Mar, 2012) further in view of Dietel (Dietel et al., Real-world prevalence of programmed death ligand 1 expression in locally advanced or metastatic non–small-cell lung cancer: The global, multicenter EXPRESS study , Lung Cancer 134 (2019) 174–179) as evidenced by Stults (Stults et al., Solid State Considerations for Early Development, March 31, 2015).
The references CANON, Chaudhari, Stults and Dean have been discussed supra and do not disclose PD-L1 tumor proportion score (TPS)(claim 32, 34, 36, 38, 40, 42, 44, 46, 48, 50, 52, 54, 56, 58, 60, 62, 66).
The reference Dietel teaches “PD-L1 expression is reported as a tumor proportion score (TPS), which represents the percentage of viable tumor cells that show partial or complete membrane staining irrespective of staining intensity; expression levels can range from 0% to 100%...”(page 175). The reference also teaches “Tumor programmed death ligand 1 (PD-L1) expression is associated with improved clinical benefit from immunotherapies targeting the PD-1 pathway. We conducted a global, multicenter, retrospective observational study to determine real-world prevalence of tumor PD-L1 expression in patients with NSCLC…Of 2617 patients who met inclusion criteria, 2368 (90%) had PD-L1 data; 530 (22%) patients had PDL1 TPS ≥ 50%, 1232 (52%) had PD-L1 TPS ≥ 1%, and 1136 (48%) had PD-L1 TPS < 1%”(abstract). This helps to teach claim 32, 34, 36, 38, 40, 42, 44, 46, 48, 50, 52, 54, 56, 58, 60, 62, 66.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON, Dean and Chaudhari with Dietel because Canon teaches AMG 510 to treat non–small-cell lung cancer and Dietel teaches treating non–small-cell lung cancer. It would have been obvious to treat TPS < 1% because a large percent of the patient population 48% fall into this category and AMG 510 is not a PD-1 inhibitor( Canon page 221) so it works on an alternate pathway and thus it has a reasonable expectation to function when the TPS is low. One would be motivated to do so to treat non–small-cell lung cancer with low TPS with a reasonable expectation of success.
Claim(s) 67 and 68 is/are rejected under 35 U.S.C. 103 as being unpatentable over CANON (CANON J, et al. The clinical KRAS(G12C) inhibitor AMG 510 drives anti-tumour immunity. Nature. 2019;575(7781):217-223, IDS) in view of Hallin (Hallin et al., The KRASG12C Inhibitor MRTX849
Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients, AACR, CANCER DISCOVERY, 55-71, JANUARY 2020).
The reference CANON have been discussed supra and does not disclose loss-of-function mutation of STK11 and KEAP1 (claims 67 and 68).
The reference Hallin teaches “The identification of MRTX849 as a highly selective
KRASG12C inhibitor capable of near-complete inhibition of KRAS in vivo provides a renewed opportunity to better understand the role of this mutation as an oncogenic driver in
various cancers and to guide rational clinical trial design… The demonstration that MRTX849 exhibited significant antitumor efficacy in all evaluated KRASG12C mutated cancer models and demonstrated marked regression in the majority (65%) confirms that this mutation is a broadly operative oncogenic driver and that MRTX849 represents a compelling therapeutic opportunity”(page 66) and “In addition, KRAS mutations often co-occur with other key genetic alterations including TP53 and CDKN2A in multiple cancers, KEAP1 and/or STK11 in lung adenocarcinoma, or APC and PIK3CA in colon cancer”(page 55). This helps to teach claims 67-68.
The reference Hallin teaches “Interestingly, despite the implication that certain mutations that co-occur with KRAS including TP53, STK11, and KEAP1 may limit therapeutic response in KRASG12C-positive lung cancers, none of these mutations correlated with response or resistance in the cell-line panel. In addition, the partial response we reported in the patient with lung adenocarcinoma was observed in a patient harboring deleterious comutations in both STK11 and KEAP1”(page 67) and “Targeted next-generation sequencing (NGS) demonstrated a KRASG12C mutation (c.34G>T). In addition, loss-of- function KEAP1 (K97M) and STK11 (E223*) mutations were detected and are predicted to be deleterious to their respective proteins. The patient was administered MRTX849 (600 mg twice a day) and had marked clinical improvement within 2 weeks, including complete resolution of baseline cough and oxygen dependency”(page 60). This helps to teach claims 67-68.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON with Hallin because both teach KRASG12C inhibitors to treat KRASG12C-positive lung cancers. It would have been obvious to one of ordinary skill in the art to use the KRASG12C inhibitor found in Canon the same way the Hallin KRASG12C inhibitor was used and found success because they are both KRASG12C inhibitors used to treat lung cancer. It is obvious to substitute equivalents known for the same purpose. Thus one would be motivated to do so to treat cancers that included , loss-of- function KEAP1 (K97M) and STK11 mutations and one would have a reasonable expectation of success because another KRASG12C inhibitor was able to successfully treat the same patient population.
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 31-70 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-28 of copending Application No. 19/112,616, over claims 1-21 of copending Application No. 19/123,697, over claims 1-20 of copending Application No. 19/309,299, over claims 1-20, 25, 30, 33-37, 40, 43-47 of copending Application No. 19/472,476, over claims 1- 31 of copending Application No. 18/562,107, over claims 87-138 of copending Application No. 18/558,827, over claims 1, 87-115 of copending Application No. 18/545,953, over claims 2, 4, 8, 10, 12-13, 65-90 of copending Application No. 17/696,758 in view of CANON (CANON J, et al. The clinical KRAS(G12C) inhibitor AMG 510 drives anti-tumour immunity. Nature. 019;575(7781):217-223, IDS) in view of Dean (Dean et al., Clinical Outcomes of Patients with Rare and Heavily Pretreated Solid Tumors Treated according to the Results of Tumor Molecular Profiling, Biomed Res Int. 2016 Jul 21;2016:4627214. doi: 10.1155/2016/4627214) as evidenced by Stults (Stults et al., Solid State Considerations for Early Development, March 31, 2015) in view of Janjan (Janjan, Nora. Bone Metastases: Approaches to Management, Seminon in Oncology, Vol 28, No 4, Suppl I I (August), 2001: pp 28-34) further in view of Chaudhari (Chaudhari et al., Pharmaceutical Excipients: A review, IJAPBC – Vol. 1(1), Jan- Mar, 2012) further in view of Dietel (Dietel et al., Real-world prevalence of programmed death ligand 1 expression in locally advanced or metastatic non–small-cell lung cancer: The global, multicenter EXPRESS study , Lung Cancer 134 (2019) 174–179), in view of Hallin (Hallin et al., The KRASG12C Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients, AACR, CANCER DISCOVERY, 55-71, JANUARY 2020).
This is a provisional nonstatutory double patenting rejection.
The application ‘616 claims:
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The application ‘697 claims:
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The application ‘299 claims:
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The application ‘476 claims:
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The reference applications help to teach instant claims 31-70 as shown above.
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59
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The application ‘107 claims:
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The application ‘827 claims:
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831
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The application ‘953 claims:
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397
702
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The application ’758 claims:
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These helps to teach claims 31-70.
The reference applications do not teach subjects that have not received a prior systemic platinum -based chemotherapy(claim 31, 33, 47, 49, 63, 64, 65) or PD-1 or anti PD-L1 immunotheraру(claim 65), patients with no brain metastasis (claim 69), patients with no bone metastasis (claim 70), pharmaceutical excipients (claim 35, 37, 51, 53) or a solid dosage form or tablet (claims 39, 41, 43, 45, 55, 57, 59, 61), PD-L1 tumor proportion score (TPS)(claim 32, 34, 36, 38, 40, 42, 44, 46, 48, 50, 52, 54, 56, 58, 60, 62, 66), loss-of-function mutation of STK11 and KEAP1 (claims 67 and 68).
The secondary references further teach that all needed changes would be obvious as outlined in the 103 rejection (which is incorporated herein by reference).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified the reference applications with CANON and Dean to produce the instant claims because the reference applications teach AMG 510 for non-small cell lung cancer treatment the same as CANON. CANON and the reference application do not suggest the exclusion of population of patients who had not previously been treated for cancer and Dean indicates that pretreated cancer is often difficult to treat. Thus one would be motivated to treat cancers that would be more likely to respond to treatment such as cancers that had not previously been treated. One would also have reasonable expectation of success because Canon teaches AMG 510 as a monotherapy which means additional treatment was not envisioned as being required. The recited exclusion of patients previously treated with platinum-based chemotherapy does not impart a patentable distinction since the limitation constitutes an obvious patient selection.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON to include patients with no brain metastasis because ones with active brain metastasis were explicitly excluded. It would then be obvious to select patients with no brain metastasis at all, as those also exclude active brain metastasis patients. One would have motivation to do this with reasonable expectation of success because they wanted to exclude some of these patients already and the treatment worked.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON with Janjan to produce the instant claims because CANON does not suggest the exclusion of population of patients with bone metastasis and Janjan indicates in many cases, bone metastases are too advanced to be eliminated through chemotherapy. Thus one would be motivated to treat cancers that would be more likely to respond to treatment such as cancers without bone metastases. One would also have reasonable expectation of success because Canon teaches AMG 510 as a monotherapy with no indication of bone metastases. The recited exclusion of patients with bone metastases does not impart a patentable distinction since the limitation constitutes an obvious patient selection.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON and Dean with Chaudhari to produce the instant claims because CANON teaches AMG 510 was administered orally to treat cancer and Chaudhari teaches that tablets are generally considered as a dosage form of choice when oral route is used and that tablets often included excipients such as binders, disintegrants, diluents, glidants, lubricants etc. One would be motivated to use a tablet because of accurate dosing, better patient compliance and one would be motivated to use an excipient because excipient offer enhancing various properties like dissolution, absorption etc of active pharmaceutical ingredient when in a tablet. One would have a reasonable expectation of success because excipient are added to many active compounds formulated today and thus it is a common practice.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON, Dean and Chaudhari with Dietel because Canon teaches AMG 510 to treat non–small-cell lung cancer and Dietel teaches treating non–small-cell lung cancer. It would have been obvious to treat TPS < 1% because a large percent of the patient population 48% fall into this category and AMG 510 is not a PD-1 inhibitor( Canon page 221) so it works on an alternate pathway and thus it has a reasonable expectation to function when the TPS is low. One would be motivated to do so to treat non–small-cell lung cancer with low TPS with a reasonable expectation of success.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON with Hallin because both teach KRASG12C inhibitors to treat KRASG12C-positive lung cancers. It would have been obvious to one of ordinary skill in the art to use the KRASG12C inhibitor found in Canon the same way the Hallin KRASG12C inhibitor was used and found success because they are both KRASG12C inhibitors used to treat lung cancer. It is obvious to substitute equivalents known for the same purpose. Thus one would be motivated to do so to treat cancers that included , loss-of- function KEAP1 (K97M) and STK11 mutations and one would have a reasonable expectation of success because another KRASG12C inhibitor was able to successfully treat the same patient population.
Claims 31-70 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-37 of U.S. Patent No. 12280056 B2, over claims 1-31 of U.S. Patent No. 11918584 B2, over claims 1-30 of U.S. Patent No. 11439645 B2, over claims 1-47 of U.S. Patent No. 11426404 B2, over claims 1-29 of U.S. Patent No. 12421234 B1, over claims 1-22 of U.S. Patent No. 12415806 B1, over claims 1-16 of U.S. Patent No. 11827635 B2, over claims 1-42 of U.S. Patent No. 12398133 B2, over claims 1-42 of U.S. Patent No. 11236091 B2, over claims 1-55 of U.S. Patent No. 11306087 B2, over claims 1-54 of U.S. Patent No. 12252486 B2, over claims 1-5 of U.S. Patent No. 12083121 B2, over claims 1-4 of U.S. Patent No. 12440491 B2 in view of CANON (CANON J, et al. The clinical KRAS(G12C) inhibitor AMG 510 drives anti-tumour immunity. Nature. 019;575(7781):217-223, IDS) in view of Dean (Dean et al., Clinical Outcomes of Patients with Rare and Heavily Pretreated Solid Tumors Treated according to the Results of Tumor Molecular Profiling, Biomed Res Int. 2016 Jul 21;2016:4627214. doi: 10.1155/2016/4627214) as evidenced by Stults (Stults et al., Solid State Considerations for Early Development, March 31, 2015) in view of Janjan (Janjan, Nora. Bone Metastases: Approaches to Management, Seminon in Oncology, Vol 28, No 4, Suppl I I (August), 2001: pp 28-34) further in view of Chaudhari (Chaudhari et al., Pharmaceutical Excipients: A review, IJAPBC – Vol. 1(1), Jan- Mar, 2012) further in view of Dietel (Dietel et al., Real-world prevalence of programmed death ligand 1 expression in locally advanced or metastatic non–small-cell lung cancer: The global, multicenter EXPRESS study , Lung Cancer 134 (2019) 174–179), in view of Hallin (Hallin et al., The KRASG12C Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients, AACR, CANCER DISCOVERY, 55-71, JANUARY 2020).
The patent ‘056 claims:
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The patent ‘584 claims:
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The patent ‘645 claims:
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The patent ‘404 claims:
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The patent ‘234 claims:
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The patent ‘806 claims:
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The patent ‘635 claims:
“1. A compound, wherein the compound is a crystalline anhydrous form of the M atropisomer of 6-fluoro-7-(2-fluoro-6-hydroxyphenyl)-1-(4-methyl-2-(2-propanyl)-3-pyridinyl)-4-((2S)-2-methyl-4-(2-propenoyl)-1-piperazinyl)pyrido[2,3-d]pyrimidin-2(1H)-one (Compound 1) and wherein the compound is characterized by an x-ray powder diffraction pattern comprising a peak at 9.0±0.2 degrees 2 theta as measured by using an x-ray wavelength of 1.54 Å.
11. A method of treating cancer having a KRAS G12C mutation in a patient in need thereof, the method comprising administering to the patient a therapeutically effective amount of the compound of any one of claims 1- 7, wherein the cancer having a KRAS G12C mutation is non-small cell lung cancer, small intestine cancer, appendix cancer, colorectal cancer, endometrial cancer, pancreatic cancer, liver cancer, small cell lung cancer, cervical cancer, germ cell tumor, ovarian cancer, pancreatic neuroendocrine tumor, bladder cancer, myelodysplastic/myeloproliferative neoplasms, head and neck cancer, esophageal cancer, soft tissue sarcoma, malignant mesothelioma, thyroid cancer, skin cancer, gastric cancer, nasal cavity cancer, or bile duct cancer. claims 1”
The reference patents do not teach subjects that have not received a prior systemic platinum -based chemotherapy(claim 31, 33, 47, 49, 63, 64, 65) or PD-1 or anti PD-L1 immunotheraру(claim 65), patients with no brain metastasis (claim 69), patients with no bone metastasis (claim 70), pharmaceutical excipients (claim 35, 37, 51, 53) or a solid dosage form or tablet (claims 39, 41, 43, 45, 55, 57, 59, 61), PD-L1 tumor proportion score (TPS)(claim 32, 34, 36, 38, 40, 42, 44, 46, 48, 50, 52, 54, 56, 58, 60, 62, 66), loss-of-function mutation of STK11 and KEAP1 (claims 67 and 68).
The patent ‘133 claims:
“1. A compound, wherein the compound is a crystalline form of the M atropisomer of 6-fluoro-7-(2-fluoro-6-hydroxyphenyl)-1-(4-methyl-2-(2-propanyl)-3-pyridinyl)-4-((2S)-2-methyl-4-(2-propenoyl)-1-piperazinyl)pyrido[2,3-d]pyrimidin-2(1H)-one (Compound 1) and wherein the compound is characterized by 19 F solid state NMR comprising peaks at approximately −109 and −120 ppm.
4. A pharmaceutical composition comprising the compound of claim 1 and a pharmaceutically acceptable excipient.
11. The pharmaceutical composition of claim 10, wherein the pharmaceutical composition is a tablet.
13. A method of treating cancer having a KRAS G12C mutation in a patient in need thereof, the method comprising administering to the patient a therapeutically effective amount of the compound of claim 1, wherein the cancer having a KRAS G12C mutation is non-small cell lung cancer, small intestine cancer, appendix cancer, colorectal cancer, endometrial cancer, pancreatic cancer, liver cancer, small cell lung cancer, cervical cancer, germ cell tumor, ovarian cancer, pancreatic neuroendocrine tumor, bladder cancer, myelodysplastic/myeloproliferative neoplasms, head and neck cancer, esophageal cancer, soft tissue sarcoma, malignant mesothelioma, thyroid cancer, skin cancer, gastric cancer, or bile duct cancer.
15. The method of claim 14, wherein the cancer having a KRAS G12C mutation is non-small cell lung cancer.”
The patent ‘091 claims:
“1. A compound, wherein the compound is a crystalline form of the M atropisomer of 6-fluoro-7-(2-fluoro-6-hydroxyphenyl)-1-(4-methyl-2-(2-propanyl)-3-pyridinyl)-4-((2S)-2-methyl-4-(2-propenoyl)-1-piperazinyl)pyrido[2,3-d]pyrimidin-2(1H)-one (Compound 1) and wherein the compound is characterized by a powder X-ray diffraction pattern comprising peaks at 9.0, 12.0, 12.6, and 19.0±0.2 degrees 2 theta as measured by x-ray powder diffraction using an x-ray wavelength of 1.54 Å.
16. A pharmaceutical composition comprising the compound of claim 1 and a pharmaceutically acceptable excipient.
claim 1
17. The pharmaceutical composition of claim 16, wherein the pharmaceutical composition is a dosage form for oral administration.
claim 16
18. The pharmaceutical composition of claim 17, wherein the dosage form is a solid dosage form.
claim 17
19. The pharmaceutical composition of claim 18, wherein the solid dosage form is a tablet.
21. A method of treating a cancer having a KRAS G12C mutation in a patient in need thereof, the method comprising administering to the patient a therapeutically effective amount of the compound of claim 1, wherein the cancer having a KRAS G12C mutation is non-small cell lung cancer, pancreatic cancer, colorectal cancer, appendix cancer, endometrial cancer, esophageal cancer, gastric cancer, small intestine cancer, nasal cavity cancer, paranasal sinus cancer, bile duct cancer, skin cancer, or intraocular melanoma.
claim 1
22. The method of claim 21, wherein the cancer having a KRAS G12C mutation is non-small cell lung cancer”
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The patent ‘087 claims:
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Further, it is generally noted that the substitution of methyl for hydrogen on a known compound is not a patentable modification absent unexpected or unobvious results. In re Druey, 319 F.2d 237, 138 U.S.P.Q. 39 (C.C. P.A. 1963). Given that applicant did not provide unexpected or unobvious results of the invention, it is concluded that the normal desire of scientists or artisans to improve upon what is already generally known would provide the motivation to substitute the H group for a Me. 2144.08(II)(A)(4)(c).
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The patent ‘486 claims:
The patent ‘121 claims:
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Further, it is generally noted that the substitution of methyl for hydrogen on a known compound is not a patentable modification absent unexpected or unobvious results. In re Druey, 319 F.2d 237, 138 U.S.P.Q. 39 (C.C. P.A. 1963). Given that applicant did not provide unexpected or unobvious results of the invention, it is concluded that the normal desire of scientists or artisans to improve upon what is already generally known would provide the motivation to substitute the H group for a Me. 2144.08(II)(A)(4)(c).
The patent ‘491 claims:
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These helps to teach claims 31-70.
The secondary references further teach that all needed changes would be obvious as outlined in the 103 rejection (which is incorporated herein by reference).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified the reference patents with CANON and Dean to produce the instant claims because the reference applications teach AMG 510 for non-small cell lung cancer treatment the same as CANON. CANON and the reference application do not suggest the exclusion of population of patients who had not previously been treated for cancer and Dean indicates that pretreated cancer is often difficult to treat. Thus one would be motivated to treat cancers that would be more likely to respond to treatment such as cancers that had not previously been treated. One would also have reasonable expectation of success because Canon teaches AMG 510 as a monotherapy which means additional treatment was not envisioned as being required. The recited exclusion of patients previously treated with platinum-based chemotherapy does not impart a patentable distinction since the limitation constitutes an obvious patient selection.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON to include patients with no brain metastasis because ones with active brain metastasis were explicitly excluded. It would then be obvious to select patients with no brain metastasis at all, as those also exclude active brain metastasis patients. One would have motivation to do this with reasonable expectation of success because they wanted to exclude some of these patients already and the treatment worked.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON with Janjan to produce the instant claims because CANON does not suggest the exclusion of population of patients with bone metastasis and Janjan indicates in many cases, bone metastases are too advanced to be eliminated through chemotherapy. Thus one would be motivated to treat cancers that would be more likely to respond to treatment such as cancers without bone metastases. One would also have reasonable expectation of success because Canon teaches AMG 510 as a monotherapy with no indication of bone metastases. The recited exclusion of patients with bone metastases does not impart a patentable distinction since the limitation constitutes an obvious patient selection.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON and Dean with Chaudhari to produce the instant claims because CANON teaches AMG 510 was administered orally to treat cancer and Chaudhari teaches that tablets are generally considered as a dosage form of choice when oral route is used and that tablets often included excipients such as binders, disintegrants, diluents, glidants, lubricants etc. One would be motivated to use a tablet because of accurate dosing, better patient compliance and one would be motivated to use an excipient because excipient offer enhancing various properties like dissolution, absorption etc of active pharmaceutical ingredient when in a tablet. One would have a reasonable expectation of success because excipient are added to many active compounds formulated today and thus it is a common practice.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON, Dean and Chaudhari with Dietel because Canon teaches AMG 510 to treat non–small-cell lung cancer and Dietel teaches treating non–small-cell lung cancer. It would have been obvious to treat TPS < 1% because a large percent of the patient population 48% fall into this category and AMG 510 is not a PD-1 inhibitor( Canon page 221) so it works on an alternate pathway and thus it has a reasonable expectation to function when the TPS is low. One would be motivated to do so to treat non–small-cell lung cancer with low TPS with a reasonable expectation of success.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified CANON with Hallin because both teach KRASG12C inhibitors to treat KRASG12C-positive lung cancers. It would have been obvious to one of ordinary skill in the art to use the KRASG12C inhibitor found in Canon the same way the Hallin KRASG12C inhibitor was used and found success because they are both KRASG12C inhibitors used to treat lung cancer. It is obvious to substitute equivalents known for the same purpose. Thus one would be motivated to do so to treat cancers that included , loss-of- function KEAP1 (K97M) and STK11 mutations and one would have a reasonable expectation of success because another KRASG12C inhibitor was able to successfully treat the same patient population.
Conclusion
Claims 31-70 are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ALISON AZAR SALAMATIAN whose telephone number is (703)756-4584. The examiner can normally be reached Mon-Thurs 7:30am-5pm EST Friday 7:30-4pm EST (every other Friday off).
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/A.A.S./Examiner, Art Unit 1627
/Kortney L. Klinkel/Supervisory Patent Examiner, Art Unit 1627