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 .
Status of Claims
Examined Herein: 1-20
Priority
Acknowledgment is made of applicant's claim for priority under based upon an application filed in PRO 63/304,181 on 1/28/2022 and PCT/CA2023/050110 on 1/27/2023.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 1/16/2026 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Drawings
The drawings received on 7/26/2024 are accepted.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 1-20 are rejected under 35 U.S.C. 103 as being unpatentable over Burak (WO 2020/115556 A1, Published 6/11/2020), in view of Morganstern (US 2020/0016281 A1, Published 1/16/2020).
With respect to claim 1, Burak discloses a method for treating a mammal having a cancer expressing a tumor-associated antigen, said method comprising:
administering to the mammal a radioimmunoconjugate, wherein the mammal has received or is receiving one or more checkpoint inhibitors;
administering to the mammal one or more checkpoint inhibitors, wherein the mammal has received or is receiving a radioimmunoconjugate; or
administering to the mammal one or more checkpoint inhibitors at the same time as administering to the mammal a radioimmunoconjugate; [Page 1, Line 28-36; Page 34, Line 18-22]
Moreover, Burak discloses that the radioconjugate comprises (i) a targeting moiety, (ii) a linker, and (iii) a metal complex of a chelating moiety comprising a radionuclide. [Page 2, Line 7-8, 16-17; Page 22, Line 28-37] The targeting moiety is capable of binding to a tumor-specific antigen. [Page 2, Line 9-10] The metal complex of a chelating moiety may be DOTA or another chelator. [Page 31, Line 9-31] The radionuclide may be 225Ac or another alpha-emitter. [Page 2, Line 16-20; Page 32, Line 9-17]
With respect to claim 2, Burak discloses that the method comprises administering to the mammal one or more checkpoint inhibitors wherein the mammal has received or is receiving a radioimmunoconjugate. [Page 1, Line 28-36]
With respect to claim 4, Burak discloses that the one or more checkpoint inhibitors comprise a PD-1 or PD-L1 inhibitor or a CTLA-4 inhibitor. [Page 2, Line 25-30; Page 33, Line 27-34; Page 34, Line 14-15]
With respect to claim 5, Burak discloses that the PD-1 or PD-L1 inhibitor or the CTLA-4 inhibitor is an antibody. [Page 2, Line 25-30; Page 33, Line 27-34; Page 34, Line 14-15]
With respect to claim 6, Burak discloses that the one or more checkpoint inhibitors comprise both a PD-1 or PD-L1 inhibitor and a CTLA-4 inhibitor. [Page 2, Line 25-30; Page 33, Line 27-34; Page 34, Line 14-15]
With respect to claim 7, Burak discloses that the PD-1 or PD- L1 inhibitor camrelizumab, cemiplumab, nivolumab, pembrolizumab, sintilimab, tislelizumab, toripalimab, RMP 1-14, atezolizumab, avelumab, or durvalumab. [Page 34, Line 9-13]
With respect to claim 8, Burak discloses that the CTLA-4 inhibitor is selected from the group consisting of BMS-986218, BMS-986249, ipilimumab, tremelimumab (formerly ticilimumab, CP-675,206), MK-1308, REGN-4659, and 4F10-11. [Page 34, Line 5-8]
With respect to claim 9, Burak discloses that the mammal is a human. [Page 3, Line 2; Page 20, Line 10; Page 34, Line 18-19]
With respect to claim 16, Burak discloses that the cancer is prostate cancer, breast cancer, colorectal cancer, and neuroendocrine cancer. [Page 3, Line 4-7; Page 34, Line 23-34; Page 35, Line 1-3]
With respect to claim 17, Burak discloses that the cancer is prostate cancer or breast cancer. [Page 3, Line 4-5; Page 34, Line 23-34]
With respect to claim 18, the limitation “wherein said administering results in a decrease in tumor volume, a stable tumor volume, or a reduced rate of increase in tumor volume,” which expresses the intended result of a process step (step of administering) positively recited. As a result, this claim is not given weight because the scope of claim 1 is not limited by claim language that does not require steps to be performed, or by claim language that does not limit a claim to a particular structure.
Still, Burak discloses that said administering results in a decrease in tumor volume, a stable tumor volume, or a reduced rate of increase in tumor volume. [Page 3, Line 9-11]
With respect to claim 19, the limitation “wherein said administering results in a decreased
incidence of recurrence or metastasis,” which expresses the intended result of a process step (step of administering) positively recited. As a result, this claim is not given weight because the scope of claim 1 is not limited by claim language that does not require steps to be performed, or by claim language that does not limit a claim to a particular structure.
Still, Burak discloses that said administering results in a decreased incidence of recurrence or metastasis. [Page 3, Line 11-12]
With respect to claim 20, Burak discloses that the method comprises administering to the mammal one or more checkpoint inhibitors, wherein:
the mammal has received or is receiving radioimmunoconjugate; and
the one or more checkpoint inhibitors comprise both a PD-1 inhibitor and a CTLA-4 inhibitor. [Page 1, Line 28-36; Page 2, Line 25-30; Page 33, Line 27-34; Page 34, Line 14-22]
Burak does not disclose that the radioimmunoconjugate comprises 225Ac chelated with a compound of Formula I. (Claim 1, 3, 20) Burak does not disclose the dosage (Bq/kg) or unitary dosage (Bq) that the radioimmunoconjugate is administered at. (Claim 10-15) Burak does not disclose that the radioimmunoconjugate is administered at a dosage of 0.5-1.5 MBq/kg of body weight of said mammal. (Claim 20)
However, with respect to claims 1, 3, and 20, Morganstern discloses a method for treating PSMA-expressing cancers or cancer cells, comprising administering to a patient in need thereof the following compound, 225Ac-PSMA-I&T. 225Ac-PSMA-I&T comprises 225Ac chelated with a compound of Formula I, or a stereoisomer thereof. [0008; Page 2, Formula C and E]
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[Page 2, Formula C and E]
With respect to claims 10 and 20, Morganstern discloses that the radiopharmaceutical is administered at a dosage of 0.025-0.4 MBq/kg (including less than 2 MBq/kg) of body weight of said mammal. [0034-0037, 0041-0042]
With respect to claims 11 and 12, Morganstern discloses that the radiopharmaceutical is administered at a dosage of 0.025-0.4 MBq/kg or 25 kBq/kg-400 kBq/kg of said mammal. [0034-0037, 0041-0042]
With respect to claims 13, 14, and 15, Morganstern discloses the radiopharmaceutical is administered as a unitary dosage of 3-30 MBq to said mammal. [0034-0037, 0042]
With respect to claim 16, Morganstern discloses that the cancer is prostate cancer, breast cancer, colorectal cancer, renal cell cancer, bladder cancer, testicular-embryonal cancer, neuroendocrine cancer, and brain tumor. [0039]
With respect to claim 17, Morganstern discloses that the cancer is prostate cancers or breast cancer. [0039]
Modifying the method disclosed by Burak by replacing the radioimmunoconjugate with 225Ac-PSMA-I&T results in the method of claims 1 and 3.
Further modifying the method disclosed by Burak by administering the compound at a dosage of 0.025-0.4 MBq/kg of body weight of said mammal results in the method of claim 10-12 and 20.
Alternatively, further modifying the method disclosed by Burak by administering the compound as a unitary dosage of 3-30 MBq results in the method of claim 13-15.
It would be obvious to one of ordinary skill in the art to modify the method disclosed by Burak by replacing the radioimmunoconjugate with 225Ac-PSMA-I&T and have a reasonable expectation of success. Burak discloses a method for treating a mammal having a cancer expressing a tumor-associated antigen comprising administering a radioimmunoconjugate. Burak further discloses that the radioconjugate comprises (i) a targeting moiety capable of binding to a tumor-specific antigen, (ii) a linker, and (iii) a metal complex of a chelating moiety (i.e., DOTA) comprising a radionuclide (i.e., 225Ac).
Morganstern discloses a method for treating a PSMA-expressing cancer or cancer cell comprising administering to a patient in need thereof 225Ac-PSMA-I&T. PSMA is a tumor-associated antigen, and
225Ac-PSMA-I&T comprises (i) a targeting moiety, PSMA, capable of binding to a tumor-specific antigen, PSMA-I&T, (ii) a linker, and (iii) a metal complex of a chelating moiety, DOTA, comprising a radionuclide, 225Ac. Accordingly, the combined teachings of Burak and Morganstern reasonably suggest that 225Ac-PSMA-I&T is a species of the radioconjugate disclosed by Burak. Therefore, it is reasonable to expect that 225Ac-PSMA-I&T may be administered as the radioconjugate in the method disclosed by Burak. One would have been motivated to do so because it is prima facie obvious to combine references when some advantage or expected beneficial result would have been produced by their combination. MPEP 2144(II). In the present case, Morganstern discloses that PSMA-expressing cancers, notably prostate and breast cancers, indubitably rank among the most frequent cancers and a reliable and efficient therapy for these cancers is highly desirable. [Morganstern, 0006] Accordingly, a method for treating PSMA-expressing cancers comprising administering 225Ac-PSMA-I&T allows for an efficient treatment of the cancer, while having as few side effects as possible. [Morganstern, 0007] Therefore, one would have been motivated by the expectation that replacing the radioimmunoconjugate with 225Ac-PSMA-I&T and administering 225Ac-PSMA-I&T according to the method disclosed by Burak allows for an efficient treatment of PSMA-expressing cancer, while having as few side effects as possible.
Claims 1-9 and 13-19 are rejected under 35 U.S.C. 103 as being unpatentable over Leamon (US 2023/0098279 A1, Filed 2/18/2021), in view of Bander (US 2024/0000979 A1, Filed 9/8/2021).
With respect to claim 1, Leamon discloses a method for treating a mammal having cancer expressing PSMA, said method comprising:
administering to the mammal a PSMA therapeutic agent, wherein the mammal has received or is receiving one or more checkpoint inhibitors (e.g., PD-1 inhibitors, PD-L1 inhibitors, and CTLA-4 inhibitors);
administering to the mammal one or more checkpoint inhibitors (e.g., PD-1 inhibitors, PD-L1 inhibitors, and CTLA-4 inhibitors), wherein the mammal has received or is receiving a PSMA therapeutic agent; or
administering to the mammal one or more checkpoint inhibitors (e.g., PD-1 inhibitors, PD-L1 inhibitors, and CTLA-4 inhibitors) at the same time as administering to the mammal a PSMA therapeutic agent. [0002, 0015, 0061, 0062, 0173, 0255, 0355, 0356, 0360]
Moreover, Leamon discloses that in a specific embodiment, the PSMA therapeutic agent is radiolabeled Compound I. Compound I is a small molecule that specifically binds to PSMA composed of a pharmacophore ligand, glutamate-urea-lysine; a chelator, DOTA (complexing 177Lu or 225Ac); and a linker connecting the ligand and the chelator. [0008, 0015, 0293]
With respect to claim 2, Leamon discloses administering to the mammal one or more checkpoint inhibitors (LAG-3 inhibitors, TIM-3 inhibitors, GITR agonists, TGF-β inhibitors, IL15/IL-15RA complex, PD-1 inhibitors, PD-L1 inhibitors, and CTLA-4 inhibitors), wherein the mammal has received or is receiving a PSMA therapeutic agent. [0002, 0015, 0173]
With respect to claim 4, Leamon discloses the one or more checkpoint inhibitors comprise a PD-1 or PD-L1 inhibitor or a CTLA-4 inhibitor. [0002, 0015, 0173]
With respect to claim 5, Leamon discloses the PD-1 or PD-L1 inhibitor or the CTLA-4 inhibitor is an antibody. [0002, 0015, 0142, 0173]
With respect to claim 6, Leamon discloses the one or more checkpoint inhibitors comprise both a PD-1 or PD-L1 inhibitor and a CTLA-4 inhibitor. [0002, 0015, 0142, 0173]
With respect to claim 7, Leamon discloses the PD-1 or PD- L1 inhibitor is pembrolizumab, durvalomab, atezolizumab, avelumab, nivolumab, ipilimumab, tremelimumab, REGN2810 (cemiplimab), TSR-042 (dostarlimab), BGB-A317 (tislelizumab), or INCSHR1210 (camrelizumab). [0015, 0142, 0173]
With respect to claim 8, Leamon discloses the CTLA-4 inhibitor is ipilimumab or tremelimumab. [0015, 0142, 0173]
With respect to claim 9, Leamon discloses the mammal is a human. [0360]
With respect to claims 13, 14, and 15, Leamon discloses that the PSMA agent (Compound I bound to 225Ac) is administered as a unitary dosage of 1-20 MBq to said mammal. [0295, 0358]
With respect to claim 16, Leamon discloses the cancer is prostate cancer, breast cancer, colorectal cancer, renal cell cancer, bladder cancer, testicular - embryonal cancers, neuroendocrine cancer, and brain tumor. [0084, 0207, 0255] ADD CANCER FROM 0084
With respect to claim 17, Leamon discloses the cancers are prostate cancer, breast cancer, colorectal cancer. [0084, 0207, 0255]
With respect to claim 18, the limitation “wherein said administering results in a decrease in tumor volume, a stable tumor volume, or a reduced rate of increase in tumor volume,” which expresses the intended result of a process step (step of administering) positively recited. As a result, this claim is not given weight because the scope of claim 1 is not limited by claim language that does not require steps to be performed, or by claim language that does not limit a claim to a particular structure.
Still, Leamon discloses said administering results in an anti-cancer effect or anti-tumor effect including a decrease in tumor volume. [0061, 0082, 0083, 0084]
With respect to claim 19, the limitation “wherein said administering results in a decreased
incidence of recurrence or metastasis,” which expresses the intended result of a process step (step of administering) positively recited. As a result, this claim is not given weight because the scope of claim 1 is not limited by claim language that does not require steps to be performed, or by claim language that does not limit a claim to a particular structure.
Still, Leamon discloses said administering results in a decreased incidence of metastasis. [0061, 0082, 0083, 0084]
Leamon does not disclose that the PSMA agent comprises 225Ac chelated with a compound of Formula I. (Claim 1, 3)
However, with respect to claims 1 and 3, Bander discloses that 225Ac-PSMA I&T is a PSMA receptor targeting agent. [0066, 0070]
Modifying the method disclosed by Leamon by replacing the PSMA therapeutic agent with 225Ac-PSMA-I&T results in the method of claims 1 and 3.
It would be obvious to one of ordinary skill in the art to modify the method disclosed by Leamon by replacing the PSMA agent with 225Ac-PSMA-I&T and have a reasonable expectation of success. Leamon discloses a method for treating a mammal having a PSMA-expressing cancer comprising administering a PSMA therapeutic agent represented by 225Ac-Compound I. Compound I is a small molecule that specifically binds to PSMA composed of (i) a pharmacophore ligand, glutamate-urea-lysine, (ii) a chelator, DOTA; and (iii) a linker connecting the ligand and the chelator.
One would have been motivated to do so because the selection of a known material based on its suitability for its intended use is prima facie obvious. MPEP 2144.07. In the present case, Leamon discloses that the PSMA therapeutic agent is a small molecule that specifically binds to PSMA. [Leamon, 0008] Bander discloses that 225Ac-PSMA-I&T, which is a small molecule, targets (i.e., specifically binds to) the PSMA receptor. [Bander, 0066, 0070] Therefore, the selection of a known material, 225Ac-PSMA-I&T, based on its suitability as an agent that specifically binds to the PSMA, for use in the method for treating PSMA-expressing cancers disclosed by Leamon is prima facie obvious.
Claims 1-9 and 16-19 are rejected under 35 U.S.C. 103 as being unpatentable over McCann (US 11,129,912 B1, Patented 9/28/2021), in view of Bander.
With respect to claim 1, McCann discloses a method for treating a mammal having a PSMA-expressing cancer comprising:
administering to the mammal a 177Lu-radiopharmaceutical, wherein the mammal has received or is receiving a 177Lu-radiopharmaceutical
administering to the mammal one or more checkpoint inhibitors, ipilimumab and/or nivolumab, wherein the mammal has received or is receiving a 177Lu-radiopharmaceutical; or
administering to the mammal one or more checkpoint inhibitors, ipilimumab and/or nivolumab, at the same time as administering to the mammal a 177Lu-radiopharmaceutical;
wherein:
in each occurrence said 177Lu-radiopharmaceutical comprises 177Lu chelated with a compound of Formula I. [Col. 16, Line 6-14; Col. 24, Line 30-34, 63-67; Col. 25, Line 1-35]
With respect to claim 2, McCann discloses that said method comprises administering to the mammal one or more checkpoint inhibitors wherein the mammal has received or is receiving a 177Lu-radiopharmaceutical. [Col. 16, Line 6-14; Col. 24, Line 30-34, 63-67; Col. 25, Line 1-35]
With respect to claim 3, McCann discloses said 177Lu-radiopharmaceutical comprises 177Lu chelated with the following structure or a stereoisomer thereof:
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With respect to claim 4, McCann discloses the one or more checkpoint inhibitors comprise a PD-1 inhibitor, nivolumab, or a CTLA-4 inhibitor, ipilimumab. [Col. 25, Line 1-6]
With respect to claim 5, McCann discloses the PD-1 inhibitor and CTLA-4 inhibitor is an antibody. [Col. 25, Line 1-6]
With respect to claim 6, McCann disclsoes the one or more checkpoint inhibitors comprise both a PD-1 inhibitor, nivolumab, and a CTLA-4 inhibitor, ipilimumab. [Col. 25, Line 1-6]
With respect to claim 7, McCann discloses the PD-1 inhibitor is nivolumab. [Col. 25, Line 1-6]
With respect to claim 8, McCann discloses the CTLA-4 inhibitor is ipilimumab. [Col. 25, Line 1-6]
With respect to claim 9, McCann discloses the mammal is a human patient. [Col. 16, Line 6-14]
With respect to claims 16 and 17, McCann discloses the cancer is prostate cancer. [Col. 24, Line 63-67; Col. 25, Line 1-6]
With respect to claim 18, the limitation “wherein said administering results in a decrease in tumor volume, a stable tumor volume, or a reduced rate of increase in tumor volume,” which expresses the intended result of a process step (step of administering) positively recited. As a result, this claim is not given weight because the scope of claim 1 is not limited by claim language that does not require steps to be performed, or by claim language that does not limit a claim to a particular structure.
With respect to claim 19, the limitation “wherein said administering results in a decreased
incidence of recurrence or metastasis,” which expresses the intended result of a process step (step of administering) positively recited. As a result, this claim is not given weight because the scope of claim 1 is not limited by claim language that does not require steps to be performed, or by claim language that does not limit a claim to a particular structure.
McCann does not disclose that the radiopharmaceutical comprises 225Ac chelated with a compound of Formula I.
However, with respect to claims 1 and 3, Bander discloses that either 225Ac or 177Lu may be chelated with PSMA I&T (a compound of Formula I). [0070]
Also, with respect to claims 1 and 3, Leamon discloses a small molecule that specifically binds to PSMA (“Compound 1”) composed of a pharmacophore ligand, glutamate-urea-lysine; a chelator, DOTA (complexing 177Lu or 225Ac); and a linker connecting the ligand and the chelator. Leamon discloses that Compound 1 may be radiolabeled with 177Lu or 225Ac. [0008, 0015, 0293] Leamon further discloses that the type of cellular damage inflicted by either isotope (177Lu or 225Ac) is expected to be different due to the difference in the characteristics of each warhead. 177Lu is believed to provide a longer path length of radiation and therefore can be effective in delivering radiation to adjacent cells. The preponderance of single strand breaks, especially in the presence of oxygen, provides the opportunity to repair sublethal damage (SLD), and/or potentially lethal damage (PLD) providing the optimal conditions for normal tissue repair. On the contrary, 225Ac delivers extremely powerful, high LET radiation, and the potential for repair of normal tissue is much more limited. The radiological biological effectiveness of alpha radiation is at least 5 times that of beta irradiation and for administered doses the relative biological effectiveness (RBE) has to be taken into account. With 225Ac therapy, the type of DNA damage inflicted does not require the presence of oxygen, so it will also be more effective in hypoxic tumor regions. [0011]
Modifying the method disclosed by McCann by replacing 177Lu with 225Ac results in the method of claims 1 and 3.
It would be obvious to one of ordinary skill in the art to modify the method disclosed by McCann by replacing 177Lu with 225Ac and have a reasonable expectation of success. McCann discloses a method for treating a mammal having a PSMA-expressing cancer comprising administering to the mammal 177Lu-PSMA I&T. Bander discloses that PSMA I&T may be radiolabeled with either 177Lu or 225Ac. Accordingly, the combined teachings of McCann and Bander suggest that the radiopharmaceutical, PSMA I&T, administered according to the method disclosed by McCann may alternatively be radiolabeled with 225Ac. One would have been motivated to do so because it is prima facie obvious to combine references when some advantage or expected beneficial result would have been produced by their combination. MPEP 2144(II). In the present case, Leamon discloses that the radiological biological effectiveness of alpha radiation is at least 5 times that of beta irradiation, and that for administered doses, the relative biological effectiveness (RBE) must be taken into account. With 225Ac therapy, the type of DNA damage inflicted does not require the presence of oxygen, so it will also be more effective in hypoxic tumor regions. [Leamon, 0011] Therefore, one would have been motivated by the expectation that replacing 177Lu, a β-emitter, with 225Ac, an α-emitter, will enable the administered pharmaceutical to exhibit at least 5 times the radiological biological effectiveness and to be more effective in hypoxic tumor regions.
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 1-20 provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-7, 12, 16, 19, and 22-25 of copending Application No. 19/474,981 in view of Leamon.
Although the claims at issue are not identical, they are not patentably distinct from each other.
The present application (claims 1-20) is drawn to a method of treating PSMA-expressing cancer comprising administering 225Ac-PSMA-I&T in combination with an immune checkpoint inhibitor, selected from a PD-1 inhibitor, PD-L1 inhibitor, or CTLA-4 inhibitor.
The reference application (claims 1-7, 12, 16, 19, 22-25) is drawn to a method of treating PSMA-expressing cancer comprising administering 225Ac-PSMA-I&T in combination with a DDR inhibitor selected from a PARP inhibitor, CHK1 inhibitor or CHK2 inhibitor.
The present application differs from the reference application in the type of inhibitor co-administered with the PSMA agent.
However, Leamon discloses a method of treating PSMA-expressing cancer comprising administering a PSMA therapeutic agent in combination with an immuno-oncology agent/immune checkpoint inhibitor including PD-1 inhibitors, PD-L1 inhibitors, and CTLA-4 inhibitors (i.e., pembrolizumab, durvalomab, atezolizumab, avelumab, nivolumab, ipilimumab, tremelimumab, cemiplimab, dostarlimab, tislelizumab, and camrelizumab), or, an anti-cancer agent/DDR inhibitor including checkpoint Kinase (CHK) inhibitors and PARP inhibitors (i.e., Olaparib, rucaparib, Niraparib, Talazoparib, Veliparib). [Leamon, 0015, 0297 0299, 0306, 0351, 0353, 0354]
Accordingly, Leamon establishes that immune checkpoint inhibitors (i.e., PD-1 inhibitors, PD-L1 inhibitors, and CTLA-4 inhibitors) and DDR inhibitors (i.e., CHK inhibitors and PARP inhibitors) are classes of therapeutic agents that are combined with a PSMA therapeutic agent to treat PSMA-expressing cancer.
Therefore, a person of ordinary skill in the art would recognize that immune checkpoint inhibitors (i.e., PD-1 inhibitors, PD-L1 inhibitors, and CTLA-4 inhibitors) are obvious variants of DDR inhibitors (i.e., CHK inhibitors and PARP inhibitors) in a method of treating PSMA-expressing cancer because they both represent classes of therapeutic agents that are combined with a PSMA therapeutic agent and employed in such a method.
This is a provisional nonstatutory double patenting rejection.
Conclusion
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/K.A.C./Examiner, Art Unit 1618
/Michael G. Hartley/Supervisory Patent Examiner, Art Unit 1618
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