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 the Claims
Claims 1 – 8, 10 – 15, and 22 were pending. Claim 1, 12, and 15 have been amended, and claims 23 – 25 have been newly added. Claims 1 – 8, 10 – 15, and 22 – 25 are currently pending and are the subject of this Office Action.
Information Disclosure Statement
The information disclosure statements (IDSs) submitted on 09/11/2025 and 11/06/2025 are in compliance with the provisions of 37 CFR 1.97 and have been considered by the examiner.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Previous rejection, withdrawn: claims 12, 13, and 15 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
In view of the claim amendments in the reply of 10/14/2025, this rejection is withdrawn.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
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.
Previous rejection, withdrawn: claims 1, 3 – 6, 8, 10 – 15, and 22 were rejected under 35 U.S.C. 103 as being unpatentable over DE WEERS (US 2016/0237161 A1, published 08/18/2016; see PTO-892 dated 08/27/2024) in view of TESAR (WO 2007/042309 A2, published 04/19/2007, an IDS reference).
In view of the claim amendments in the reply of 10/14/2025, this rejection is withdrawn.
Previous rejection, withdrawn: claims 2 and 6 were rejected under 35 U.S.C. 103 as being unpatentable over DE WEERS in view of TESAR as applied to claims 1, 3 – 5, 8, 10 – 17, and 19 – 22 above, and further in view of OLEINIKA (Oleinika, K et al. “Effector and Regulatory B Cells in Immune-Mediated Kidney Disease.” Nature reviews. Nephrology 15.1 (2019): 11–26) and VAN DE DONK (van de Donk, Niels W. C. J et al. “Monoclonal Antibodies Targeting CD38 in Hematological Malignancies and Beyond.” Immunological Reviews 270.1 (2016): 95–112). See PTO-892 dated 08/27/2024.
In view of the claim amendments in the reply of 10/14/2025, this rejection is withdrawn.
Previous rejection, withdrawn: claim 7 is rejected under 35 U.S.C. 103 as being unpatentable over DE WEERS in view of TESAR as applied to claims 1, 3 – 5, 8, 10 – 17, and 19 – 22 above, and further in view of RAAB (Raab, Marc S et al. “A Phase I/IIa Study of the Human Anti-CD38 Antibody MOR202 (MOR03087) in Relapsed or Refractory Multiple Myeloma (rrMM).” Journal of clinical oncology 33.15_suppl (2015): 8574–8574). See PTO-892 dated 08/27/2024.
After further consideration, this rejection is withdrawn.
New rejection, necessitated by claim amendments: claims 1 – 8, 10 – 15, and 22 – 25 are rejected under 35 U.S.C. 103 as being unpatentable over DE WEERS in view of TESAR, OLEINIKA, and VAN DE DONK 2 (Niels W. C. J. van de Donk, et al. CD38 antibodies in multiple myeloma: back to the future. Blood 2018; 131 (1): 13–29; see IDS submitted 05/27/2025).
The present application is directed to a method for treatment of autoantibody-mediated membranous nephropathy in a subject in need thereof, the method comprising administering to the subject nine infusions of an antibody or antibody fragment specific for CD38 over six 28-day cycles, wherein the antibody or antibody fragment comprises a HCDR1 region of amino acid sequence SEQ ID NO: 1, a HCDR2 region of amino acid sequence SEQ ID NO: 2, a HCDR3 region of amino acid sequence SEQ ID NO: 3, and a LCDR1 region of amino acid sequence SEQ ID NO: 4, a LCDR2 region of amino acid sequence SEQ ID NO: 5 and a LCDR3 region of amino acid sequence SEQ ID NO: 6.
According to the present specification, autoimmune membranous nephropathy is an immune-mediated glomerular disease that is characterized by the presence of anti-PLA2R autoantibodies and/or anti-THSD7A autoantibodies and is also called membranous glomerulonephritis (p. 4, lines 14 – 16; p. 3, lines 24 – 27 and p. 4).
According to the working examples of the present specification, the claimed anti-CD38 antibody is MOR202 (p. 39, lines 34 – 37).
DE WEERS is directed to isolated monoclonal antibodies which bind to human CD38 and related antibody-based compositions and molecules. See abstract. DE WEERS discloses that anti-CD38 antibodies can treat and prevent autoimmune disorders in which autoantibodies are prominent, such as membranous glomerulonephritis. DE WEERS further discloses a pharmaceutical composition comprising an antibody, an immunoconjugate, a bispecific antibody, or an expression vector and a pharmaceutically acceptable carrier. See paragraphs [0104] and [0449]. DE WEERS teaches the administration in an amount of about 0.1-100 mg/kg, such as 0.5, 0.9, 1.0, 1.1, 1.5, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 40, 45, 50, 60, 70, 80, 90 or 100 mg/kg, per day, on at least one of day 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, or 40, or alternatively, at least one of week 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19 or 20 after initiation of treatment, or any combination thereof. See paragraph 0458.
Although DE WEERS discloses a method for treatment of autoantibody-mediated membranous nephropathy in a subject comprising administering to the subject an antibody or antibody fragment specific for CD38, DE WEERS does not disclose the HCDRs and LCDRs of present independent claim 1.
TESAR is directed to antibodies and methods for using recombinant antigen-binding regions and antibodies and functional fragments containing such antigen-binding regions that are specific for CD38, which play an integral role in various disorders or conditions. See abstract. TESAR discloses the CDRs of SEQ ID NOs: 1 – 6. TESAR’s SEQ ID NO: 21 discloses SEQ ID NOs: 1 – 3 of present claims 1 and 16 with 100% identity, and TESAR’s SEQ ID NO: 51 discloses SEQ ID NOs: 4 – 6 of present claims 1 and 1 with 100% identity.
OLEINIKA is directed to the central role of B cells in autoimmune diseases, including in those with renal involvement, as well as in the immunological response to kidney transplantation. See abstract. OLEINIKA discloses that anti-CD38 monoclonal antibodies that specifically target plasma cells may prove useful for the treatment of antibody-mediated autoimmune diseases (see p. 22, right column, first paragraph). OLEINIKA discloses the proposed mechanism of B cell depletion therapy in autoimmune diseases that involve autoantibodies (see Fig. 4, p. 22) and discloses that Rituximab, which targets B-cell receptor CD20 (see Fig. 3, p.21), has been effective in the treatment of membranous glomerulonephritis in about two-thirds of patients (see Nephrotic syndromes., p. 21, left column). Thus, it would have been obvious to one having ordinary skill in the art to treat membranous glomerulonephritis with antibodies specific for another B-cell receptor CD38.
VAN DE DONK 2 is directed to “CD38 antibodies [that] are currently also being evaluated in smoldering MM and certain monoclonal gammopathies with renal significance (Table 4)” (see New applications for CD38 therapy, p. 25, left column). VAN DE DONK 2’s Table 4 (see p. 23) discloses the use of CD38 antibodies to treat glomerulopathy and glomerulonephritis. Although the CD38 antibodies are daratumumab and not MOR202/Felzartamab (whose CDRs are the sequences of present SEQ ID NOs: 1 – 6 of present claim 1 and whose VH and VL are the sequences of present SEQ ID NOs: 7 and 8, respectively, of present claim 10), VAN DE DONK 2 discloses that “MOR202 treatment is associated with a lower incidence of [(infusion-related reactions)] IRRs (∼10%), which may be explained by low CDC activity. Therefore, MOR202 can be infused faster, compared with daratumumab or isatuximab” (see Infusion-related reactions, p. 20, right column – p. 22, left column) and that Infusion-related reactions [IRR], which typically occur during the first infusion, are the most frequent adverse events went treating MM patients with CD38 antibodies (see abstract). Thus, VAN DE DONK 2 discloses advantages of MOR202/felzartamab over daratumumab. Although these advantages are disclosed in the treatment of MM, the link between MM and glomerulonephritis that VAN DE DONK 2, as well as DE WEERS, teaches makes MOR202/felzartamab an obvious next step in the treatment of glomerulonephritis to one having ordinary skill in the art. MPEP 2143(I)(A) states that “[t]he rationale to support a conclusion that the claim would have been obvious is that all the claimed elements were known in the prior art and one skilled in the art could have combined the elements as claimed by known methods with no change in their respective functions, and the combination yielded nothing more than predictable results to one of ordinary skill in the art.”
Furthermore, VAN DE DONK 2 teaches the administration, which consists of infusions (see abstract), of the anti-CD38 antibody Daratumumab (16 mg/kg) weekly for 8 wk, then Q2W for 16 wk, thereafter Q4W. Q4W is Q4W is once every 4 weeks. See Table 1. Because 4 weeks equals 28 days, and VAN DE DONK 2 teaches treatment period of at least 28 weeks (8 weeks plus 16 weeks then at least one additional 4 weeks, which is a total of approximately 6.4 cycles), it would have been obvious to one having ordinary skill in the art to arrive to “infusions of an antibody or antibody fragment specific for CD38 over six 28-day cycles” of present claim 1. Because VAN DE DONK 2 teaches the time period of at least 6 cycles and teaches that an infusion may be administered every 4 weeks (28 days), “nine infusions” of present claim 1 could be determined by routine experimentation. “[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation.” In reAller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955). Similarly, a prima facie case of obviousness exists where the claimed ranges or amounts do not overlap with the prior art but are merely close. Titanium Metals Corp. of Americav.Banner, 778 F.2d 775, 783, 227 USPQ 773, 779 (Fed. Cir. 1985)”. See MPEP 2144.05 (I) and (II).
Thus, because DE WEERS teaches that anti-CD38 antibodies can treat membranous glomerulonephritis and TESAR discloses that the anti-CD38 antibody CDRs of the present claims may be used to treat disorders, it would have been obvious to one having ordinary skill in the art to modify the method of DE WEERS with TESAR’s anti-CD38 CDRs to arrive to a method for treatment of autoantibody-mediated membranous nephropathy of present claim 1. Furthermore, VAN DE DONK 2 also teaches that anti-CD38 antibodies are known to treat glomerulonephritis; VAN DE DONK 2 teaches the MOR202 antibody, which according to the present specification, is the claimed anti-CD38 antibody; and VAN DE DONK 2 renders the claimed dosing regimen obvious as discussed above. Thus, the cited references render the claim 1 obvious.
Regarding claims 2 and 6, OLEINIKA teaches that membranous glomerulonephritis consists of pathogenic anti- phospholipase A2 receptor (PLA2R) or anti- thrombospondin type 1 domain- containing protein 7A (THSD7A) antibodies. See p. 21, left column, second paragraph.
Regarding claim 3, DE WEERS discloses that anti-CD38 antibodies are capable of inducing ADCC. See paragraph [0151].
Regarding claims 4 and 22, while DE WEERS does not expressly state that the disclosed anti-CD38 antibody shows a significant higher specific cell killing on plasma cells than on CD38 low expressing cells, DE WEERS’ antibody anticipates the antibody of claim 1 (which claim 4 depends from) that results in this observation and therefore the anti-CD38 antibody taught by DE WEERS would inherently show a significant higher specific cell killing on plasma cells than on CD38 low expressing cells.
Regarding claims 5 and 6, while DE WEERS does not expressly state that the disclosed anti-CD38 antibody leads to a reduction of endogenous autoantibody titers, specifically anti-PLA2R and/or anti-THSD7A autoantibodies, DE WEERS’ anti-CD38 antibody renders obvious the antibody of claim 1 (which claims 5 and 6 depend from) that results in this observation and therefore the anti-CD38 antibody taught by DE WEERS would inherently lead to a reduction of endogenous autoantibody titers.
Regarding claim 7, VAN DE DONK 2 teaches several CD38 antibodies including daratumumab (fully human), isatuximab (chimeric), and MOR202 (fully human). See abstract.
Regarding claim 8, DE WEERS discloses that the antibody is a full length IgG1 antibody. See paragraph [0082].
Regarding claim 10, TESAR’s SEQ ID NO: 21 discloses present SEQ ID NO: 7 with 100% identity and TESAR’s SEQ ID NO: 51 discloses present SEQ ID NO: 8 with 100% identity.
Regarding claims 11 – 13, DE WEERS discloses that the anti-CD38 antibodies of the present invention may also be administered in combination therapy, i.e., combined with other therapeutic agents relevant for the disease or condition to be treated. See paragraph [0464]. DE WEERS further discloses that a therapeutic agent for use in combination with the anti-CD38 antibody for treating the disorders may be dexamethasone. See paragraph [0486].
Regarding claim 14, DE WEERS discloses that administration of the anti-CD38 composition may be intravenous. See paragraph [0452].
Regarding claim 15, DE WEERS discloses that the anti-CD38 antibodies may be administered at about 16 mg/kg. See paragraph [0451]. DE WEERS further discloses that the anti-CD38 antibodies may be administered once a week for a period of 6 months. See paragraph [0456].
Although DE WEERS discloses that that an antibody or antibody fragment specific for CD38 may be used to the treatment and/or prophylaxis of membranous nephropathy which may be caused by autoantibodies and TESAR discloses anti-CD38 antibody sequences that may be used in treating disorders, neither DE WEERS nor TESAR discloses much detail about how anti-CD38 antibodies may specifically reduce endogenous anti-PLA2R and/or anti-THSD7A autoantibodies.
Regarding claim 23 – 25, VAN DE DONK 2 teaches the administration of 16 mg/kg of an anti-CD38 antibody weekly for 8 wk, then Q2W for 16 wk, thereafter Q4W. Q4W is Q4W is once every 4 weeks. See Table 1. Thus, the administration once per week in a first cycle of the six 28-day cycles of present claim 23, once per month in the second, third, fourth, fifth, and sixth cycles of present claim 24 could be determined by routine experimentation. “[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation.” In reAller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955). Similarly, a prima facie case of obviousness exists where the claimed ranges or amounts do not overlap with the prior art but are merely close. Titanium Metals Corp. of Americav.Banner, 778 F.2d 775, 783, 227 USPQ 773, 779 (Fed. Cir. 1985)”. See MPEP 2144.05 (I) and (II).
Response to Arguments
On page 5, second – third paragraphs, of the reply of 10/14/2025, Applicant argues that “[a]s explained in Rovin et al. (2024) ‘Phase lb/2a Study Assessing the Safety and Efficacy of Felzartamab in Anti-Phospholipase A2 Receptor Autoantibody-Positive Primary Membranous Nephropathy’ Kidney Int'l. Rep. 9:2635-47, 76.9% of efficacy-evaluable patients who received the 9-dose course of felzartamab achieved an anti-PLA2R titer reduction >50%. Rovin et al. (2024) reports that forty four percent of these patients experienced the reduction in anti-PLA2R titer within the first week of treatment, and 53.8% of patients achieved the response by 7 months after last felzartamab dose (Abstract). By the end of the study (EOS), serum albumin increased from baseline to EOS in 76.9% of efficacy-evaluable patients (Id.). In other words, in this population with membranous nephropathy, felzartamab treatment as presently claimed achieved rapid immunologic responses and improvements in serum albumin in some patients (Id.). Further, Rovin et al (2024) explain on page 2643 that while ‘[i]n clinical studies of rituximab for PMN, immunologic responses were more likely to occur in patients with lower baseline anti-PLA2R titers,’ with felzartamab, ‘[i]mmunologic responses occurred regardless of baseline titer.’”
Applicant’s argument has been considered but not found persuasive because the cited references under the 103 rejections above discuss the success of anti-CD38 antibodies in the treatment of nephropathy and thus the treatment of with felzartamab/MOR202 with a reasonable expectation of success. For example, VAN DE DONK 2 teaches “the development of several CD38 antibodies including daratumumab (fully human), isatuximab (chimeric), and MOR202 ([also known as felzartamab;] fully human). CD38 antibodies have pleiotropic mechanisms of action including Fc-dependent immune-effector mechanisms, direct apoptotic activity, and immunomodulatory effects by the elimination of CD38+ immune-suppressor cells. CD38-targeting antibodies are generally well tolerated and induce partial response or better in ∼30% of heavily pretreated MM patients as monotherapy. Based on their distinct mechanisms of action, favorable toxicity profile, and single-agent activity, CD38 antibodies are attractive partners in combination regimens.” See abstract. While the use of anti-CD38 antibodies is often described within the context of MM treatments, VAN DE DONK 2 teaches that they are also used to treat other conditions such as glomerulonephritis. See Table 4, p. 23.
On p. 6, Applicant argues that there was no clear connection between treating MM and treating autoantibody-mediated membranous nephropathy with anti-CD38 antibodies. However, the cited references establish CD38 as the connection between MM and autoantibody-mediated diseases such as nephropathy. DE WEERS states that anti-CD38 antibodies treat “disorder[s] involving cells expressing CD38 is an immune disorder in which CD38 expressing B cells, macrophages, plasma cells, monocytes and T cells are involved, such as an inflammatory and/or autoimmune disease . . . Examples of immune disorders in which CD38 expressing B cells, plasma cells, monocytes and T cells are involved include autoimmune disorders, such as . . . glomerulonephritis” (see paragraph 0447) and “[f]urther examples of inflammatory, immune and/or autoimmune disorders in which autoantibodies and/or excessive B and T lymphocyte activity are prominent and which may be treated [with the anti-CD38 antibodies] include . . . membranous glomerulonephritis” (see paragraph 0449). DE WEERS teaches that a disorder involving cells expressing CD38 is also MM (see paragraph 0440). Thus, DE WEERS clearly state that MM and autoantibody-mediated membranous nephropathy are two disorders involving cells expressing CD38 that are treated with anti-CD38 antibodies.
On p. 6, last paragraph – p. 7, first paragraph, Applicant argues that “the claimed invention has the unexpected result of not significantly reducing a patient's humoral immunity, whereas the objective evidence shows that daratumumab, the CD38 antibody cited in the prior art, significantly reduced patients' humoral immunity. Specifically, Rovin et al. (2022) "Immunologic Responses After COVID-19 Vaccination in Patients with Membranous Nephropathy Receiving Anti-CD38 Felzartamab Therapy: Results from the Phase lb/2a M-PLACE Study" Kidney Int'l. Rep. 7:2086-90 details the effects of treatment according to Example 5 on antibody titers as a result of felzartamab treatment. Rovin et al. (2022) find that anti-SARS CoV2 antibody titers are measured after COVID19 vaccination in the treated patients are comparable to those in the healthy general population following COVID19 vaccination. Similarly, there was no statistically significant difference in anti-SARS CoV2 titers among the M- PLACE participants who received their COVID19 vaccines after starting felzartamab treatment compared to those who were vaccinated before starting felzartamab treatment (see, Discussion on page 2087 of Rovin et al. (2022)). This is notable because myeloma patients receiving daratumumab were significantly impaired in anti-SARS CoV2 serum titers following COVID19 vaccination compared to similarly situated myeloma patients not receiving daratumumab (Pimpinelli et al. (2021) J. Hematol. & Oncol. 14:81, pg. 10, col. 1). Moreover, this effect is not limited to anti-SARS-CoV2 antibodies. The enclosed Rule 132 declaration from Dr. Donna Flesher ("Flesher Declaration") establishes that a similar effect was seen in anti-tetanus toxoid serum titers from patients dosed with felzartamab, but not in patients dosed with placebo in the same trial. In other words, even as felzartamab successfully treats autoantibody mediated nephropathy, it does not interfere with humoral immunity. Dr. Flesher also provides clinical trial data from patients post-COVID19 vaccination to further evidence such findings. Flesher Declaration at 8. Dr. Flesher explains that this is an unexpected advantage over the antibodies of de Weers, which could not have been predicted from the prior art. See id. at 17-9.”
Applicant’s argument has been considered but not found persuasive because VAN DE DONK 2, for example, teaches the advantages of felzartamab (MOR202) over daratumumab. For example, VAN DE DONK 2 teaches that “Isatuximab-induced IRRs [IRR: infusion-related reactions] have similar characteristics as those mediated by daratumumab, and occur in 55% to 56% of patients. MOR202 treatment is associated with a lower incidence of IRRs (∼10%), which may be explained by low CDC activity. Therefore, MOR202 can be infused faster, compared with daratumumab or isatuximab.” Although, the cited references do not address the advantages of MOR202 over daratumumab within the context of COVID19, the method of treatment with MOR202 taught by the cited references renders the method of claim 1 (that results in Applicant’s observation) obvious, and therefore the taught method by the cited references would inherently achieve the result of not significantly reducing a patient's humoral immunity.
On p. 8, second paragraph, Applicant argues that “Oleinika is cited for the proposed idea of B cell depletion therapy in autoimmune diseases that involve autoantibodies. van de Donk is cited to reinforce this idea with the hypothesis that CD38-targeting antibodies may also abrogate the production of autoantibodies in autoimmune disorders and thereby reduce autoantibody-dependent effector mechanisms. In other words, neither of these references do anything to remedy the defects noted above in the rejection over de Weers and Tesar. Nor do Oleinika and/or van de Donk contribute any information that would make the results from Rovin et al. detailed above any less surprising. Therefore, claims 2 & 6 are not obvious for the same reasons articulated above with regards to claim 1.”
Applicant’s argument is not persuasive because as discussed above, the method of the cited references renders the claimed method obvious and thus would inherently achieve the results from Rovin et al.
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.
Previous rejection, withdrawn: claims 1 – 8, 10 – 15, and 22 were rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 5, 11, and 12 of U.S. Patent No. 8,877,899 in view of DE WEERS and OLEINIKA.
In view of the claim amendments in the reply of 10/14/2025, this rejection is withdrawn.
Previous rejection, withdrawn: claims 1 – 8, 10 – 15, and 22 were rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 5, 11, and 12 of U.S. Patent No. 8,088,896 in view of DE WEERS and OLEINIKA.
In view of the claim amendments in the reply of 10/14/2025, this rejection is withdrawn.
Previous rejection, withdrawn: claims 1 – 8, 10 – 15, and 22 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 5, 11, and 12 of U.S. Patent No. 9,579,378 in view of DE WEERS and OLEINIKA.
In view of the claim amendments in the reply of 10/14/2025, this rejection is withdrawn.
Previous rejection, withdrawn: claims 1 – 8, 10 – 15, and 22 were rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 5, 11, and 12 of U.S. Patent No. 9,486,547 in view of DE WEERS and OLEINIKA.
In view of the claim amendments in the reply of 10/14/2025, this rejection is withdrawn.
Previous rejection, withdrawn: claims 1 – 8, 10 – 15, and 22 were rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 of U.S. Patent No. 9,289,490 in view of DE WEERS and OLEINIKA.
In view of the claim amendments in the reply of 10/14/2025, this rejection is withdrawn.
Previous rejection, withdrawn: claims 1 – 8, 10 – 15, and 22 were rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 – 8 of U.S. Patent No. 9,765,152 in view of DE WEERS and OLEINIKA.
In view of the claim amendments in the reply of 10/14/2025, this rejection is withdrawn.
Previous rejection, withdrawn: claims 1 – 8, 10 – 15, and 22 were rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 4, and 5 of U.S. Patent No. 10,533,057 in view of DE WEERS and OLEINIKA.
In view of the claim amendments in the reply of 10/14/2025, this rejection is withdrawn.
Previous rejection, withdrawn: claims 1 – 8, 10 – 15, and 22 were rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, and 4 of U.S. Patent No. 10,308,722 in view of DE WEERS and OLEINIKA.
In view of the claim amendments in the reply of 10/14/2025, this rejection is withdrawn.
Previous rejection, withdrawn: claims 1 – 8, 10 – 15, and 22 were rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4, 9 – 11, 13 – 15, and 19 and 4 of U.S. Patent No. 10,184,005 in view of DE WEERS and OLEINIKA.
In view of the claim amendments in the reply of 10/14/2025, this rejection is withdrawn.
Previous rejection, withdrawn: claims 1 – 8, 10 – 15, and 22 were provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3, 7, 11, and 17 – 31 of U.S. Application No. 17/298,156 in view of DE WEERS and OLEINIKA.
In view of the claim amendments in the reply of 10/14/2025, this rejection is withdrawn.
New rejection, necessitated by claim amendments: claims 1 – 8, 10 – 15, and 22 – 25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 5, 11, and 12 of U.S. Patent No. 8,877,899 in view of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2.
Patented claim 1 recites an antibody specific for CD38.
Patented SEQ ID NOs: 10 and 11 (claim 2) disclose present SEQ ID NOs: 7 and 8, respectively, of present claim 10 with 100% identity.
The main difference between the present claims and the patented claims is that the present claims recite the anti-CD38 antibody in a method to treat autoantibody-mediated membranous nephropathy with the limitations of present claim 1. However, DE WEERS and VAN DE DONK 2 disclose this difference. The teachings of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2, and how they relate to the claims, are set forth in the rejections under 35 U.S.C. 103 above.
Because the patented claims disclose an antibody specific for CD38, and DE WEERS and VAN DE DONK 2 disclose that the anti-CD38 antibody may be used in a method to treat autoantibody-mediated membranous nephropathy of present claim 1, it would have been obvious to one having ordinary skill in the art to use the patented claims’ anti-CD38 antibody to treat autoantibody-mediated membranous nephropathy as claimed.
Response to Arguments
On page 8 – 9, under the heading Obviousness-type Double Patenting over each of '899 in view of de Weers and Oleinika, Applicant argues that “[c]laims 1-5, 11, & 12 of the '899 patent are directed to drug combinations that comprise an anti-CD38 antibody in combination with (a) thalidomide, lenalidomide, or pomalidomide, or (b) a proteasome inhibitor for use in the treatment of multiple myeloma and/or non-hodgkins lymphoma. Oleinika mentions the use of rituximab (an anti-CD20 antibody) against membranous glomerulonephritis, but mentions anti-CD38 antibodies only in passing when Oleinika speculates that "anti-CD38 monoclonal antibodies... may prove useful in antibody-mediated autoimmune diseases." The rejection, in other words, combines de Weers mention of anti-CD38 antibodies with a prior report of anti-CD20 antibodies for the treatment of autoantibody-mediated membranous nephropathy. A double patenting rejection is proper only when the examined application claim either is anticipated by or obvious over the reference claim(s). See M.P.E.P. § 804. The purpose of the rejection is to prevent extension of patent rights by issuing two claims to the same invention or an obvious variant thereof. Id. The claimed method for treatment of autoantibody-mediated membranous nephropathy in a subject in need thereof, the method comprising administering to the subject nine infusions of an antibody or antibody fragment specific for CD38 over six 28-day cycles is not the same invention or an obvious variant of the claims of the '899 patent. Indeed, the '899 patent published more than a year before the priority date of the present application, yet it has not been cited in any prior art rejection, which further highlight the fact that it fails to disclose or suggest the claimed invention. Further, the Federal Circuit has confirmed that unexpected results "evidence should be considered" when considering an obviousness-type double patenting rejection. Eli Lilly & Co. v. Teva Parenteral Medicines, 689 F.3d 1368, 1381 (Fed. Cir. 2012); see also Abbvie Inc. v. Kennedy Inst. of Rheumatology, 764 F.3d 1366, 1372 (Fed. Cir. 2014). Just as in the rejections discussed above, the claimed invention has unexpected results over the claims of the '899 patent even if they are viewed with de Weers and Oleinika. For at least these reasons, the rejected claims are not obvious over the cited references.”
Applicant’s argument is not persuasive because the present claims recite the patented claims’ antibody specific for CD38 and DE WEERS and VAN DE DONK 2 teach a method of treating of autoantibody-mediated membranous nephropathy with an antibody specific for CD38. Thus, it would have been obvious to one having ordinary skill in the art to modify the method rendered obvious by the cited references with the antibody of the patented claims to arrive to the present claims.
New rejection, necessitated by claim amendments: claims 1 – 8, 10 – 15, and 22 – 25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 5, 11, and 12 of U.S. Patent No. 8,088,896 in view of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2.
Patented claim 1 recites an isolated antibody or antigen-binding fragment thereof that binds to CD38, which comprises the three variable heavy chain complementarity determining regions (H-CDRs) and the three variable light-chain complementarity determining regions (L-CDRs) that are in the variable heavy chain and variable light chain pairs selected from: (i) SEQ ID NO: 18 and 48, (ii) SEQ ID NO: 20 and 50, (iii) SEQ ID NO: 21 and 51, (iv) SEQ ID NO: 22 and 52, and (v) SEQ ID NO: 25 and 55.
Patented SEQ ID NO: 21 discloses the CDRs of SEQ ID NOs: 1 – 3 of present claim 1 and the sequence of SEQ ID NO: 7 of present claim 10 with 100% identity, and patented SEQ ID NO: 51 discloses the CDRs of SEQ ID NOs: 4 – 6 and the sequence of SEQ ID NO: 8 of present claim 10 with 100% identity.
The main difference between the present claims and the patented claims is that the present claims recite the anti-CD38 antibody in a method to treat autoantibody-mediated membranous nephropathy with the limitations of present claim 1. However, DE WEERS and VAN DE DONK 2 disclose this difference. The teachings of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2, and how they relate to the claims, are set forth in the rejections under 35 U.S.C. 103 above.
Because the patented claims disclose an antibody specific for CD38, and DE WEERS and VAN DE DONK 2 disclose that the anti-CD38 antibody may be used in a method to treat autoantibody-mediated membranous nephropathy of present claim 1, it would have been obvious to one having ordinary skill in the art to use the patented claims’ anti-CD38 antibody to treat autoantibody-mediated membranous nephropathy as claimed.
New rejection, necessitated by claim amendments: 1 – 8, 10 – 15, and 22 – 25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 5, 11, and 12 of U.S. Patent No. 9,579,378 in view of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2.
Patented claim 1 recites a pharmaceutical composition comprising a combination of (i) an antibody specific for CD38 comprising an HCDR1 of sequence GFTFSSYYMN (SEQ ID NO: 1), HCDR2 of sequence GISGDPSNTYYADSVKG (SEQ ID NO: 2), HCDR3 of sequence DLPLVYTGFAY (SEQ ID NO: 3), LCDR1 of sequence SGDNLRHYYVY (SEQ ID NO: 4), LCDR2 of sequence GDSKRPS (SEQ ID NO: 5), and LCDR3 of sequence QTYTGGASL (SEQ ID NO: 6) and (ii) melphalan for the treatment of multiple myeloma.
Patented claim 2 recites that the antibody comprises a variable heavy chain of the sequence of SEQ ID NO: 7 and a variable light chain of the sequence of SEQ ID NO: 9.
Patented SEQ ID NO: 7 discloses the CDRs of SEQ ID NOs: 1 – 3 of present claim 1 and the sequence of SEQ ID NO: 7 of present claim 10 with 100% identity, and patented SEQ ID NO: 9 discloses the CDRs of SEQ ID NOs: 4 – 6 and the sequence of SEQ ID NO: 8 of present claim 10 with 100% identity.
The main difference between the present claims and the patented claims is that the present claims recite the anti-CD38 antibody in a method to treat autoantibody-mediated membranous nephropathy with the limitations of present claim 1. However, DE WEERS and VAN DE DONK 2 disclose this difference. The teachings of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2, and how they relate to the claims, are set forth in the rejections under 35 U.S.C. 103 above.
Because the patented claims disclose an antibody specific for CD38, and DE WEERS and VAN DE DONK 2 disclose that the anti-CD38 antibody may be used in a method to treat autoantibody-mediated membranous nephropathy of present claim 1, it would have been obvious to one having ordinary skill in the art to use the patented claims’ anti-CD38 antibody to treat autoantibody-mediated membranous nephropathy as claimed.
New rejection, necessitated by claim amendments: claims 1 – 8, 10 – 15, and 22 – 25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 5, 11, and 12 of U.S. Patent No. 9,486,547 in view of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2.
Patented claim 1 recites radioconjugate comprising an antibody specific for CD38.
Patented claim 6 recites that the antibody comprises a variable heavy chain of the sequence QVQLVESGGGLVQPGGSLRLSCAASGFTFSSYYMNWVRQAPGKGLEWVSGISGDPSNTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARDLPLVYTGFAYWGQGTLVTVSS (SEQ ID NO: 10) and
a variable light chain of the sequence DIELTQPPSVSVAPGQTARISCSGDNLRHYYWWYQQKPGQAPVLVIYGDSKRPSGIPERFS[ ]GSNSGNTATLTISGTQAEDEADYYCQTYTGGASLVFGGGTKLTVLGQ (SEQ ID NO: 11).
Patented SEQ ID NO: 10 discloses the CDRs of SEQ ID NOs: 1 – 3 of present claim 1 and the sequence of SEQ ID NO: 7 of present claim 10 with 100% identity, and patented SEQ ID NO: 11 discloses the CDRs of SEQ ID NOs: 4 – 6 and the sequence of SEQ ID NO: 8 of present claim 10 with 100% identity.
The main difference between the present claims and the patented claims is that the present claims recite the anti-CD38 antibody in a method to treat autoantibody-mediated membranous nephropathy with the limitations of present claim 1. However, DE WEERS and VAN DE DONK 2 disclose this difference. The teachings of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2, and how they relate to the claims, are set forth in the rejections under 35 U.S.C. 103 above.
Because the patented claims disclose an antibody specific for CD38, and DE WEERS and VAN DE DONK 2 disclose that the anti-CD38 antibody may be used in a method to treat autoantibody-mediated membranous nephropathy of present claim 1, it would have been obvious to one having ordinary skill in the art to use the patented claims’ anti-CD38 antibody to treat autoantibody-mediated membranous nephropathy as claimed.
Response to Arguments
On p. 9, last paragraph – 10, first paragraph, of the reply of 10/14/2025, Applicant argues that “[t]he claims of the '896 patent are directed to an antibody and the claims of the '547 patent are directed to radio-conjugates of an anti-CD38 antibody. The claims of the '378 patent are directed to methods of treating myeloma with drug combinations that comprise an anti-CD38 antibody in combination with melphalan. The claimed method for treatment of autoantibody-mediated membranous nephropathy in a subject in need thereof, the method comprising administering to the subject nine infusions of an antibody or antibody fragment specific for CD38 over six 28-day cycles is not the same invention or an obvious variant of the claims of those patents. Just as in the rejections discussed above, the claimed invention has unexpected results over the claims of the cited patents even if they are viewed with de Weers and Oleinika.”
Applicant’s argument is not persuasive because the patented claims disclose the anti-CD38 antibody of the present claims. Although it is not disclosed in a method for treatment of autoantibody-mediated membranous nephropathy of present claim 1, DE WEERS and VAN DE DONK 2 render the claimed method obvious for the reasons discussed in the 103 rejection above. Thus, it would have been obvious to modify DE WEERS and VAN DE DONK 2’s method with the patented anti-CD38 antibody.
New rejection, necessitated by claim amendments: claims 1 – 8, 10 – 15, and 22 – 25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 of U.S. Patent No. 9,289,490 in view of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2.
The patented claims disclose a method of treating comprising administering an antibody/fragment specific for CD38. Patented SEQ ID NOs: 10 and 11 (claim 4) disclose SEQ ID NOs: 7 and 8, respectively, of present claim 10 with 100% identity.
The main difference between the present claims and the patented claims is that the present claims recite the anti-CD38 antibody in a method to treat autoantibody-mediated membranous nephropathy with the limitations of present claim 1. However, DE WEERS and VAN DE DONK 2 disclose this difference. The teachings of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2, and how they relate to the claims, are set forth in the rejections under 35 U.S.C. 103 above.
Because the patented claims disclose an antibody specific for CD38, and DE WEERS and VAN DE DONK 2 disclose that the anti-CD38 antibody may be used in a method to treat autoantibody-mediated membranous nephropathy of present claim 1, it would have been obvious to one having ordinary skill in the art to use the patented claims’ anti-CD38 antibody to treat autoantibody-mediated membranous nephropathy as claimed.
Response to Arguments
On p. 10, under the heading Obviousness-type Double Patenting over '490 in view of de Weers & Oleinika, Applicant argues that “[t]he claims of the '490 patent are directed to methods of treating myeloma with drug combinations that comprise an anti-CD38 antibody in combination with immunomodulatory imide drugs. The claimed method for treatment of autoantibody-mediated membranous nephropathy in a subject in need thereof, the method comprising administering to the subject nine infusions of an antibody or antibody fragment specific for CD38 over six 28-day cycles is not the same invention or an obvious variant of the claims of the '490 patent. Just as in the rejections discussed above, the claimed invention has unexpected results over the claims of the '490 patent even if they are viewed with de Weers and Oleinika.”
Applicant’s argument is not persuasive because the patented claims disclose the anti-CD38 antibody of the present claims. Although it is not disclosed in a method for treatment of autoantibody-mediated membranous nephropathy of present claim 1, DE WEERS and VAN DE DONK 2 render the claimed method obvious for the reasons discussed in the 103 rejection above. Thus, it would have been obvious to modify DE WEERS and VAN DE DONK 2’s method with the patented anti-CD38 antibody.
New rejection, necessitated by claim amendments: claims 1 – 8, 10 – 15, and 22 – 25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 – 8 of U.S. Patent No. 9,765,152 in view of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2.
Patented claim 1 recites a method for treating multiple myeloma or non-hodgkins lymphoma in a subject in need thereof, wherein said method comprises administering to the subject a therapeutically effective amount of a combination of: (i) bortezomib or carfilzomib, (ii) an antibody specific for CD38.
Patented claim 4 discloses that the antibody comprises a variable heavy chain of the sequence of SEQ ID NO: 10; and a variable light chain of the sequence of SEQ ID NO: 11.
Patented SEQ ID NO: 10 discloses the CDRs of present SEQ ID NOs: 1 – 3 of present claim 1 and present SEQ ID NO: 7 of present claim 10 with 100% identity.
Patented SEQ ID NO: 11 discloses the CDRs of present SEQ ID NO: 4 – 6 and present SEQ ID NO: 8 of present claim 10 with 100% identity.
The main difference between the present claims and the patented claims is that the present claims recite the anti-CD38 antibody in a method to treat autoantibody-mediated membranous nephropathy with the limitations of present claim 1. However, DE WEERS and VAN DE DONK 2 disclose this difference. The teachings of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2, and how they relate to the claims, are set forth in the rejections under 35 U.S.C. 103 above.
Because the patented claims disclose an antibody specific for CD38, and DE WEERS and VAN DE DONK 2 disclose that the anti-CD38 antibody may be used in a method to treat autoantibody-mediated membranous nephropathy of present claim 1, it would have been obvious to one having ordinary skill in the art to use the patented claims’ anti-CD38 antibody to treat autoantibody-mediated membranous nephropathy as claimed.
New rejection, necessitated by claim amendments: claims 1 – 8, 10 – 15, and 22 – 25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 4, and 5 of U.S. Patent No. 10,533,057 in view of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2.
Patented claim 1 recites a method for treatment of relapsed/refractory multiple myeloma in humans, said method comprising administering to a human patient in need an antibody specific for CD38.
Patented claim 4 recites that the antibody comprises a variable heavy chain of SEQ ID NO: 8 and a variable light chain of the sequence of SEQ ID NO: 9.
Patented SEQ ID NO: 8 discloses the CDRs of present SEQ ID NOs: 1 – 3 of present claim 1 and present SEQ ID NO: 7 of present claim 10 with 100% identity.
Patented SEQ ID NO: 9 discloses the CDRs of present SEQ ID NO: 4 – 6 of present claim 1 and present SEQ ID NO: 8 of present claim 10 with 100% identity.
The main difference between the present claims and the patented claims is that the present claims recite the anti-CD38 antibody in a method to treat autoantibody-mediated membranous nephropathy with the limitations of present claim 1. However, DE WEERS and VAN DE DONK 2 disclose this difference. The teachings of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2, and how they relate to the claims, are set forth in the rejections under 35 U.S.C. 103 above.
Because the patented claims disclose an antibody specific for CD38, and DE WEERS and VAN DE DONK 2 disclose that the anti-CD38 antibody may be used in a method to treat autoantibody-mediated membranous nephropathy of present claim 1, it would have been obvious to one having ordinary skill in the art to use the patented claims’ anti-CD38 antibody to treat autoantibody-mediated membranous nephropathy as claimed.
New rejection, necessitated by claim amendments: claims 1 – 8, 10 – 15, and 22 – 25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, and 4 of U.S. Patent No. 10,308,722 in view of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2.
Patented claim 1 recites a method for treating multiple myeloma or non-hodgkins lymphoma in a subject in need thereof, wherein said method comprises administering to the subject a therapeutically effective amount of a combination of: (i) thalidomide, lenalidomide or pomalidomide, (ii) an antibody specific for CD38.
Patented claim 4 recites that the antibody comprises a variable heavy chain of the sequence of SEQ ID NO: 10; and a variable light chain of the sequence of SEQ ID NO: 11.
Patented SEQ ID NO: 10 discloses the CDRs of present SEQ ID NOs: 1 – 3 of present claim 1 and present SEQ ID NO: 7 of present claim 10 with 100% identity.
Patented SEQ ID NO: 11 discloses the CDRs of present SEQ ID NO: 4 – 6 of present claim 1 and present SEQ ID NO: 8 of present claim 10 with 100% identity.
The main difference between the present claims and the patented claims is that the present claims recite the anti-CD38 antibody in a method to treat autoantibody-mediated membranous nephropathy with the limitations of present claim 1. However, DE WEERS and VAN DE DONK 2 disclose this difference. The teachings of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2, and how they relate to the claims, are set forth in the rejections under 35 U.S.C. 103 above.
Because the patented claims disclose an antibody specific for CD38, and DE WEERS and VAN DE DONK 2 disclose that the anti-CD38 antibody may be used in a method to treat autoantibody-mediated membranous nephropathy of present claim 1, it would have been obvious to one having ordinary skill in the art to use the patented claims’ anti-CD38 antibody to treat autoantibody-mediated membranous nephropathy as claimed.
New rejection, necessitated by claim amendments: claims 1 – 8, 10 – 15, and 22 – 25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4, 9 – 11, 13 – 15, and 19 and 4 of U.S. Patent No. 10,184,005 in view of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2.
Patented claim 1 recites a method of inducing specific killing of tumor cells that express CD38, comprising the step of contacting said cells with a sufficient amount of an isolated anti-CD38 antibody or antigen-binding fragment thereof, which comprises the three variable heavy chain complementarity determining regions (H-CDRs) and the three variable light-chain complementarity determining regions (L-CDRs) that are in the variable heavy chain and variable light chain pairs selected from: (i) SEQ ID NO: 18 and 48, (ii) SEQ ID NO: 20 and 50, (iii) SEQ ID NO: 21 and 51, (iv) SEQ ID NO: 22 and 52, and (v) SEQ ID NO: 25 and 55, wherein said antibody or antigen-binding fragment thereof binds CD38 and has the ability to mediate killing of a CD38+ target cell.
Patented SEQ ID NO: 21 discloses the CDRs of present SEQ ID NOs: 1 – 3 of present claim 1 and present SEQ ID NO: 7 of present claim 10 with 100% identity.
Patented SEQ ID NO: 51 discloses the CDRs of present SEQ ID NO: 4 – 6 of present claim 1 and present SEQ ID NO: 8 of present claim 10 with 100% identity.
The main difference between the present claims and the patented claims is that the present claims recite the anti-CD38 antibody in a method to treat autoantibody-mediated membranous nephropathy with the limitations of present claim 1. However, DE WEERS and VAN DE DONK 2 disclose this difference. The teachings of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2, and how they relate to the claims, are set forth in the rejections under 35 U.S.C. 103 above.
Because the patented claims disclose an antibody specific for CD38, and DE WEERS and VAN DE DONK 2 disclose that the anti-CD38 antibody may be used in a method to treat autoantibody-mediated membranous nephropathy of present claim 1, it would have been obvious to one having ordinary skill in the art to use the patented claims’ anti-CD38 antibody to treat autoantibody-mediated membranous nephropathy as claimed.
Response to Arguments
On p. 7, under the heading Obviousness-type Double Patenting over each of'152,'057,'722,&'005 in view of de Weers and Oleinika, Applicant argues that “[t]he claims of the '152 patent are directed to methods of treating myeloma with drug combinations that comprise an anti-CD38 antibody in combination with protease inhibitors. The claims of the '057 patent are directed to methods of treating myeloma with an anti-CD38 antibody. The claims of the '722 patent are directed to methods of treating myeloma with drug combinations that comprise an anti-CD38 antibody in combination with immunomodulatory imide drugs. The claims of the '005 patent are directed to a "method of inducing specific killing of tumor cells." The claimed method for treatment of autoantibody-mediated membranous nephropathy in a subject in need thereof, the method comprising administering to the subject nine infusions of an antibody or antibody fragment specific for CD38 over six 28-day cycles is not the same invention or an obvious variant of the claims of those patents. Just as in the rejections discussed above, the claimed invention has unexpected results over the claims of the cited patents even if they are viewed with de Weers and Oleinika.”
Applicant’s argument is not persuasive because the patented claims disclose the anti-CD38 antibody of the present claims. Although it is not disclosed in a method for treatment of autoantibody-mediated membranous nephropathy of present claim 1, DE WEERS and VAN DE DONK 2 render the claimed method obvious for the reasons discussed in the 103 rejection above. Thus, it would have been obvious to modify DE WEERS and VAN DE DONK 2’s method with the patented anti-CD38 antibody.
New rejection, necessitated by claim amendments: claims 1 – 8, 10 – 15, and 22 – 25 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3, 7, 11, and 17 – 31 of U.S. Application No. 17/298,156 in view of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2.
Copending claim 1 recites an antibody/fragment specific for CD38.
Copending claims 22, 23, and 31 each recites the anti-CD38 antibody comprises a variable heavy chain domain comprising the amino acid sequence of SEQ ID NO: 7 and a variable light chain domain comprising the amino acid sequence of SEQ ID NO: 8.
Copending SEQ ID NO: 7 discloses the CDRs of present SEQ ID NOs: 1 – 3 of present claim 1 and present SEQ ID NO: 7 of present claim 10 with 100% identity.
Copending SEQ ID NO: 8 discloses the CDRs of present SEQ ID NO: 4 – 6 of present claim 1 and present SEQ ID NO: 8 of present claim 10 with 100% identity.
The main difference between the present claims and the patented claims is that the present claims recite the anti-CD38 antibody in a method to treat autoantibody-mediated membranous nephropathy with the limitations of present claim 1. However, DE WEERS and VAN DE DONK 2 disclose this difference. The teachings of DE WEERS, TESAR, OLEINIKA, and VAN DE DONK 2, and how they relate to the claims, are set forth in the rejections under 35 U.S.C. 103 above.
Because the patented claims disclose an antibody specific for CD38, and DE WEERS and VAN DE DONK 2 disclose that the anti-CD38 antibody may be used in a method to treat autoantibody-mediated membranous nephropathy of present claim 1, it would have been obvious to one having ordinary skill in the art to use the patented claims’ anti-CD38 antibody to treat autoantibody-mediated membranous nephropathy as claimed.
This is a provisional nonstatutory double patenting rejection.
Response to Arguments
On p. 8, under the heading Obviousness-type Double Patenting over '156 in view of de Weers and Oleinika, Applicant argues that “[t]he claims of the '156 patent are directed to lyophilized compositions of an anti-CD38 antibody. The claimed method for treatment of autoantibody-mediated membranous nephropathy in a subject in need thereof, the method comprising administering to the subject nine infusions of an antibody or antibody fragment specific for CD38 over six 28-day cycles is not the same invention or an obvious variant of the claims of those patents. Just as in the rejections discussed above, the claimed invention has unexpected results over the claims of the cited patents even if they are viewed with de Weers and Oleinika.”
Applicant’s argument is not persuasive because the patented claims disclose the anti-CD38 antibody of the present claims. Although it is not disclosed in a method for treatment of autoantibody-mediated membranous nephropathy of present claim 1, DE WEERS and VAN DE DONK 2 render the claimed method obvious for the reasons discussed in the 103 rejection above. Thus, it would have been obvious to modify DE WEERS and VAN DE DONK 2’s method with the patented anti-CD38 antibody.
Conclusion
Claims 1 – 8, 10 – 15, and 22 – 25 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.
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/ESTELLA M. GUSTILO/Examiner, Art Unit 1646
/GREGORY S EMCH/Supervisory Patent Examiner, Art Unit 1678