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 .
Status of the claims
In Response to Non-Final received 15 October 2025 (referred to herein as Remarks) claim 36 is newly added and claims 16, 20, 23, and 27 are canceled. Claims 1, 2, 4-11, 17, 18, 24-26, 28-34, and 36 are currently pending and under consideration.
It is noted:
Pursuant to 37 C.F.R. 1.121(c) Applicant’s response to the Non-Final mailed 15 May 2025 is considered not compliant (see claim 1, line 2); however, in the interest of compact prosecution the examiner has provided this action. Applicant did not use underline in their amendments to the claims (e.g., “in a human subject”).
Withdrawn Rejections
In view of Applicant amending claim 1 to incorporate the subject is human (line 2) and includes a period without administration of the antibody construct (last 2 lines) all prior art rejections under 35 USC 102(a)(1) and 35 USC 103 rejections are hereby withdrawn.
The following rejections are necessitated by amendment.
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.
Claims 1, 2, 4-11, 17, 18, 24-26, 28-34, and 36 are rejected under 35 U.S.C. 103 as being unpatentable over Topp (see Topp et al., as cited on the PTO-892 mailed 05/15/2025), Hipp (see Hipp et al., as cited on the PTO-892 mailed 05/15/2025, specifically “U”), Kufer (U.S. Patent 9,340,621, as cited on the PTO-892 dated 23 February 2024), and Hipp2 (see Hipp et al., as cited on the PTO-892 mailed 05/15/2025, specifically “W”) as evidenced by Choi (see Choi et al., as cited on the PTO-892 mailed 05/15/2025) and Jackson Laboratory (see Jackson Laboratory as cited on the PTO-892 mailed 02/23/2024).
Topp announces a Phase I clinical study for a dose-escalation of administering a BCMAxCD3 (i.e., BI836909) antibody with continuous IV infusions for 4 weeks in 6 week cycles (i.e., 2 weeks with no administration) with dose escalation proceeding based on clinical findings during the first 2-4 weeks of cycle 1 allowing for up to 5 cycles of treatment and 10 cycles with ongoing clinical benefit in patients (i.e., human) with RRMM (see Topp Methods). In addition, Topp teaches the first four dose cohorts were safe and well tolerated in 9 patients (see Topp last 3 lines).
Hipp discloses the same BCMAxCD3 bispecific T cell engager, BI836909, taught by Topp has comparable cross-reactive binding to both BCMA and CD3 epsilon of human and macaque origin with picomolar and low nanomolar affinities respectively (see Hipp 8th para). The toxicity studies in cynomolgus monkeys demonstrated doses of 135µg/kg/day via continuous intravenous infusion up to 405µg/kg/day via daily subcutaneous injection for up to 28 days were both safe and effective (see Hipp 8th para). In addition, “these pre-clinical data demonstrate that BI836909 is highly potent, efficacious and BCMA-selective T cell redirecting agent and support clinical testing of BI836909 in multiple myeloma patients” (see Hipp 9th para). It is noted the BCMAxCD3 antibody construct, BI36909, is a BiTE® connected via a peptide linker as evidenced by Hipp2 (see Hipp2 Sup Figure 1a).
Kufer discloses the treatment of human tumor xenograft, NCI-H929, female NOD/SCID mice (i.e., multiple myeloma, a BCMA-positive neoplasm) with bispecific BCMA-98xCD3 or BCMA-34xCD3 by intravenous bolus (see instant claims 9 and 31) injection for 17 consecutive days (see Kufer col. 63-64, example 19; see instant claim 1). The animals were injected with 0.5 mg/kg/day which is 12.8 µg per day (see instant claim 1) given the average weight of female NOD mice at 15 weeks is 25.6±1.7g as evidenced by Jackson Laboratory (see Jackson Laboratory, in particular, weight table). It is noted, the elected species of BCMA binding domain (Seq ID Nos: 171-179) and CD3 binding domain (Seq ID Nos: 633-639, 641, and 642) recited in instant claims 12-14 part 18, 15, 17 part 18-19, 21, 22, and 24-26 corresponds to Kufer BCMA-34xCD3 (see Seq ID Nos: 337-340; see Non-Final dated 23 February 2024). Furthermore, Kufer BCMA-34xCD3 has a first and second domain in the format of a scFv and is connected via a glycine/serine linker (see Kufer Seq ID No. 340 aa 244-249, claim 6; see instant claims 11, 33, and 34). Animals that were administered BCMA-34xCD3 had significantly reduced tumor volumes starting on day 16 compared to controls (see Kufer figure 16 group 4). Kufer teaches a method of treating a BCMA positive neoplasm (i.e., MM) comprising administering a dose of 6.5-650µg/day (i.e., 12.8µg/day) of BCMA-34xCD3 (i.e., identical to instant Seq ID No: 171-179, 633-639, 641, and 642) intravenously for 17 consecutive days. Claim 1 is drawn to two cycles of administration wherein one cycle is at least 7 consecutive days followed by a period without administration; however, claim 1 does not specify any particular duration without administration. The specification defines “one cycle” as at least seven consecutive days (see specification pg. 10, 4th para). Therefore, the time between the last dose on day 7 to the dose on day 8 is within the scope of “a period of without administration of the antibody construct”. Despite the breadth of instant claim 1, Topp teaches 6 week cycles with 4 weeks of administration followed by 2 weeks without administration which is pertinent to instant claims 5 and 6 (see above).
Thus, a person of ordinary skill in the art would substitute the BCMAxCD3 bispecific T cell engager as taught by Topp (i.e., BI836909) for BCMA-34xCD3 taught by Kufer given these are art recognized equivalents for the same purpose (i.e., BCMAxCD3 bispecific T cell engager with similar structure) in the method of treating MM as taught by Topp. In addition, given BI836909 taught by both Topp and Hipp and BCMA-34xCD3 are bispecific antibodies directed to the same targets with the same antibody format the ordinary artisan would administer at up to 135µg/kg/day via continuous intravenous infusion as taught by Hipp as these doses were safe in cynomolgus monkeys. It is noted 135µg/kg/day is about 545.4 µg/day in female cynomolgus monkeys (average wt=4.04kg) as evidenced by Choi (see Choi pg. 49, 1st col). This is pertinent to claims 1, 2, 4-11, 17, 18, 24-26, 28-34, and 36.
Applicant's arguments filed 15 October 2025 have been fully considered but they are not persuasive. Applicant argues unexpected results administering AMG420 over a broad dosing range (see Remarks pg. 13, 2nd para).
First, in arguing allegedly unexpected results Applicant must compare the claimed subject matter with the closest prior art to be effective to rebut a prima facie case of obviousness. In re Burckel, 592 F.2d 1175, 201 USPQ 67 (CCPA 1979) (see MPEP § 716.02(e)). In the instant case comparison of BI836909 as taught by Topp, Hipp, or Hipp2.
Second, even if the allegedly unexpected results were in fact unexpected the objective evidence of nonobviousness must be commensurate in scope with the claims which the evidence is offered to support (see MPEP § 716.02(d)). In the instant case Applicant indicates the allegedly unexpected results are drawn to a particular bispecific structure (i.e., AMG420) which comprises a particular full length amino acid sequence (i.e., complete VH, VL, and linker between binding domains) was administered through continuous IV infusion with 4 weeks on/2 week off cycles for up to 5 cycles to multiple myeloma patients which are limitations not recited in instant claims. The language of claim 1 encompasses full length antibodies, BiTEs with any linker length, antibodies conjugated to secondary structures (e.g., drug, label), and antibodies with additional binding domain. Unexpected results observed with a BiTE structure would not be representative of the breadth of structures instantly claimed (see Mølhøj et al. (2006) CD19-/CD3-bispecific antibody of the BiTE class is far superior to tandem diabody with respect to redirected tumor cell lysis. Molecular Immunology Vol. 44, Iss. 8, pgs. 1935-1943, in particular abstract).
Third it is unclear which results Applicant has pointed to as unexpected. For example, is “no dose-limiting toxicities were seen up to 400µg/day” allegedly unexpected or rather that “9 out of 42 total patients had complete responses to AMG420 treatment” or both (see Remarks pg. 13, 2nd para). Complete responses were observed in 1 patient at 6.5µg/day, 1 patient at 100µg/day, 1 patient with MRD-negative complete response at 200 µg/day, and 5 patients at 400µg/day (see specification pg. 58, 1st full para); however, as stated above these results are not compared with the closest prior art (i.e., BI836909), nor is it clear what is unexpected.
Fourth, to establish unexpected results over a claimed range, Applicants should compare a sufficient number of tests both inside and outside the claimed range to show the criticality of the claimed range. In re Hill, 284 F.2d 955, 128 USPQ 197 (CCPA 1960) (see MPEP § 716.02(d)(II)). The instant claims are drawn to administering 6.5µg/day-650µg/day (see claim 1; see Remarks pg. 13, last para). In so far as Applicants may be pointing to DLT results as allegedly unexpected results Applicants show no dose-limiting toxicities (DLT) up to 400 µg/day but DLTs at 800 µg/day (see specification pg. 57, 2nd full para). Therefore, it is unclear at what dose does DLT become a factor. For example, are DLTs observed at 600 µg/day or 700 µg/day? Furthermore, it is also unclear as to what results Applicants are alleging are unexpected. For example, is a lack of DLT, the number of complete responses (CR), the number of partial responses (PR), or a combination thereof unexpected. Likewise are the results unexpected across all treatment groups or are there particular doses that were unexpected.
Fifth, to the extent Applicant is arguing that the dose of 5 µg/kg/day as taught by Hipp2 examiner notes that when scaled to a 90kg human this would equate to 450 µg/kg/day (see Musto, P. (2016) Average weight of American men increased 7 kilograms in 20 years, Health & Lifestyle, in particular 3rd para; see Hipp figure 6b, 7b, see Hipp2 pg. 2, 5th para).
Therefore, the 35 USC 103 rejection above is maintained.
Claims 1, 2, 4-11, 17, 18, 24-26, 28-34, and 36 are rejected under 35 U.S.C. 103 as being unpatentable over U.S. Patent No. 9,340,621 B2 (referred to herein as Kufer, as cited on the PTO-892 dated 23 February 2024) and Yuraszeck (as cited on the PTO-892 dated 23 February 2024), evidenced by Jackson Laboratory (see Jackson Laboratory as cited on the PTO-892 mailed 02/23/2024).
Kufer discloses the treatment of human tumor xenograft, NCI-H929, female NOD/SCID mice (i.e., multiple myeloma, a BCMA-positive neoplasm) with bispecific BCMA-98xCD3 or BCMA-34xCD3 by intravenous bolus (see instant claims 9 and 31) injection for 17 consecutive days (see Kufer col. 63-64, example 19; see instant claim 1). The animals were injected with 0.5 mg/kg/day which is 12.8 µg per day (see instant claim 1) given the average weight of female NOD mice at 15 weeks is 25.6±1.7 g as evidenced by Jackson Laboratory (see Jackson Laboratory, weight table). It is noted, the elected species of BCMA binding domain (Seq ID Nos: 171-179) and CD3 binding domain (Seq ID Nos: 633-639, 641, and 642) recited in instant claims 1, 17, 18, 24-26, and 36 corresponds to Kufer BCMA-34xCD3 (see Seq ID Nos: 337-340; see Non-Final dated 23 February 2024). Furthermore, Kufer BCMA-34xCD3 has a first and second domain in the format of a scFv and is connected via a glycine/serine linker (see Kufer Seq ID No. 340 aa 244-249, claim 6; see instant claims 11, 33, and 34). Animals that were administered BCMA-34xCD3 had significantly reduced tumor volumes starting on day 16 compared to controls (see Kufer figure 16 group 4).
Yuraszeck discloses the preclinical properties of blinatumomab, a CD19 and CD3 BiTE® (bispecific T-cell engagers), have been well characterized and blinatumomab is considered representative of the general characteristics of BiTE® (see Yuraszeck pg. 636, 2nd col. 2nd paragraph). Yuraszeck discloses blinatumomab has been approved to treating acute lymphoblastic leukemia (ALL), in a 4 week on and 2 week off schedule and step wise dosing in the first cycle starting with 9 µg/day continuous intravenous injection (cIV) for 7 days then 28 µg/day cIV for three weeks followed by 28 µg/day cIV for 4 weeks for subsequent cycles (see Yuraszeck pg. 641, 2nd col. 2nd paragraph, Table 2). Furthermore, six out of seven listed clinical trials for blinatumomab had flat dosing at various doses (e.g., 5 µg/m2, 15 µg/m2, 30 µg/m2, 112 µg/d) with 4 weeks on and 2 weeks off across repeated cycles with positive outcomes (see Yuraszeck Table 2). Yuraszeck teaches flat dosing has practical advantages over body surface area (BSA) based dosing such as better compliance and reduced risks of medical errors (see Yuraszeck pg. 639, 1st col. 2nd paragraph). It is noted that step dosing during the first cycle was more advantageous over flat dosing in regards to mitigating adverse events (see Yuraszeck pg. 639, 1st col. 2nd paragraph). Moreover, pretreatment with glucocorticoids could blunt the increase in cytokine levels with minimal impact on proliferation of killing of ALL cells, and thus are coadministered with other BiTE® constructs (see Yuraszeck pg. 637, 2nd col. 1st paragraph). Yuraszeck also discloses a similar BiTE®, AMG 420, directed to BCMA and CD3 being developed for myeloid and plasma cell antigens (see Yuraszeck pg. 637, 1st col. 2nd paragraph, Table 1).
Therefore, a person of ordinary skill in the art would have substituted the treatment protocol of MM in mice as taught by Kufer with treatment of MM in humans using the dosing protocol set forth for blinatumomab as taught by Yuraszeck given the following: i. Kufer discloses the BCMA-CD3 BiTE is effective in treating a preclinical model of MM, ii. Yuraszeck teaches blinatumomab is generalizable across the BiTE antibody class, iii. Yuraszeck teaches the cyclic administration using continuous IV administration with periods of administration followed by periods without administration at doses in the range of 0.5-30µg/m2 or 112µg/d of the blinatumomab BiTE, and iv. Kufer teaches a skilled person knows how to modify or adapt certain parameters of this study, (e.g., dose, timelines) while still arriving at a meaningful and reproducible result (see Kufer col. 13 last para). Thus, given the preclinical success of the BCMAxCD3 BiTE taught by Kufer and potency of this class of antibody in humans as taught by Yuraszeck the ordinary artisan would substitute the dose taught by Kufer with the lower doses taught by Yuraszeck. There is a reasonable expectation of success given the generalization of blinatumomab across the antibody class and its own success at these doses. Furthermore, Yuraszeck discloses alternative BiTEs directed to different targets (i.e., AMG211 and AMG330) had starting doses of 52µg/d and 0.5 µg/d (see Yuraszeck pg. 637, 2nd col. last para).
Regarding claims 27-30 and 36, Kufer teaches a skilled person knows how to modify or adapt certain parameters of this study, (e.g., dose, timelines) while still arriving at a meaningful and reproducible result (see Kufer col. 13 last para). Yuraszeck teaches therapy using BiTE® antibodies with cyclic treatment comprising periods with and without treatment. Specifically, Yuraszeck teaches a six weeks cycle with 4 weeks of administration and 2 weeks without administration; thereby, arriving at the presently claimed invention (i.e., a period with or without administration of 1wk-1month).
Applicant's Remarks filed 15 October 2025 have been fully considered but they are not persuasive. Applicants have argued that “a person of ordinary skill in the art would expect a dosing regimen for a BCMAxCD3 BiTE® molecule to treat a BCMA positive neoplasm (such as multiple myeloma) to be different from that for a CD19xCD3 BiTE® to treat ALL” (see Remarks para spanning pgs. 15-16).
As previously stated in the Non-Final mailed 15 May 2025 (referred to herein as Non-Final2, see pg. 13, 1st para) and Final mailed 28 August, 2024 (referred to herein as Final1, see pg. 7 last para) Yuraszeck discloses, “the preclinical properties of blinatumomab, the first and only approved BiTE® antibody construct, have been well characterized and are representative of the general characteristics of BiTE® antibody constructs” (see Yuraszeck pg. 636, 2nd col. last para). Therefore, Yuraszeck invites a person of ordinary skill in the art to use the dosing regimen (i.e., continuous IV fusion, multiple cycles, periods without administration) of blinatumomab as guidance for preclinical studies. Applicant has provided no evidence to support the contrary. In fact, Applicant’s assertion that differences in tumor targets is sufficient to disqualify blinatumomab as generalizable to alternative BiTE® antibody constructs as suggested by Yuraszeck is contradicted by the state of the art at the time of filing. For example, the use continuous IV infusion (i.e., a general characteristic of BiTE® antibody constructs) as taught by Yuraszeck is drawn to the overall structure of the antibody, not the particular target antigens (see Sedykh et al. Bispecific antibodies: design, therapy, perspective. Drug Design, Development and Therapy. Vol. 12, pgs. 195-208). Specifically,
“The single stranded structure of blinatumomab allows easy protein expression in monomeric form in significant amounts and provides broad therapeutic potential for use in lymphoma and leukemia. Unfortunately, this feature is the reason continuous intravenous administration of the drug is required” (see Sedykh pg. 197, 1st col. 2nd para).
In addition, 5 years before the effective filing date of the instant application Frankel and Baeuerle disclose 3 additional BiTE® antibody constructs each targeting CD3 and a different antigen (i.e., EpCAM, CEA, and PSMA) each with different expression patterns in clinical development for different cancers utilizing the same cyclic administration (i.e., periods of administration followed by periods without administration) Yuraszeck discloses is generalizable (see Frankel and Baeuerle as cited on the PTO-892 mailed 08/28/2024, in particular pg. 386 Table 1). Therefore, Applicant’s assertion that the dosing scheme for a BCMAxCD3 BiTE® cannot be developed from the dosing scheme of a well characterized CD19xCD3 BiTE® because the target tumor antigens are different is not accurate.
It is noted Applicant’s assertion is also in contrast to Applicant’s own teachings in the instant specification,
“The first generation of BiTE® antibody constructs (see WO 99/54440 and WO 2005/040220) was brought into the clinic as AMG 103 (blinatumomab, anti- CD19 x anti-CD3) and AMG 110 (solitomab, anti-EpCAM x anti-CD3). Blinatumomab, which is approved for patients with ALL, is administered via continuous intravenous infusion, with a lower initial dose in the first period of administration and a higher dose in the remaining treatment, during the first cycle and in all subsequent cycles. In a comparison of step dosing versus constant (flat) dosing as a means to reach the target dose of blinatumomab, step dosing was found to be more effective at mitigating adverse events. In view of the positive efficacy signal and favorable safety profile, a similar administration scheme has hence been used for solitomab which was also administered with increasing doses in each cycle.” (see specification pg. 2, 3rd para).
Applicant also argues unexpected results (see Remarks pg. 16, last para).
First, in arguing allegedly unexpected results Applicant must compare the claimed subject matter with the closest prior art to be effective to rebut a prima facie case of obviousness. In re Burckel, 592 F.2d 1175, 201 USPQ 67 (CCPA 1979) (see MPEP § 716.02(e)). In the instant case comparison with blinatumomab.
Second, even if the allegedly unexpected results were in fact unexpected the objective evidence of nonobviousness must be commensurate in scope with the claims which the evidence is offered to support (see MPEP § 716.02(d)). In the instant case Applicant indicates the allegedly unexpected results are drawn to a particular bispecific structure (i.e., AMG420) which comprises a particular full length amino acid sequence (i.e., complete VH, VL, and linker between binding domains) was administered through continuous IV infusion with 4 weeks on/2 week off cycles for up to 5 cycles to multiple myeloma patients which are limitations not recited in instant claims. The language of claim 1 encompasses full length antibodies, BiTEs with any linker length, antibodies conjugated to secondary structures (e.g., drug, label), and antibodies with additional binding domain. Unexpected results observed with a BiTE structure would not be representative of the breadth of structures instantly claimed (see Mølhøj et al. (2006) CD19-/CD3-bispecific antibody of the BiTE class is far superior to tandem diabody with respect to redirected tumor cell lysis. Molecular Immunology Vol. 44, Iss. 8, pgs. 1935-1943, in particular abstract).
Third it is unclear which results Applicant has pointed to as unexpected. For example, is “no dose-limiting toxicities were seen up to 400µg/day” allegedly unexpected or rather that “9 out of 42 total patients had complete responses to AMG420 treatment” or both (see Remarks pg. 13, 2nd para). Complete responses were observed in 1 patient at 6.5µg/day, 1 patient at 100µg/day, 1 patient with MRD-negative complete response at 200 µg/day, and 5 patients at 400µg/day (see specification pg. 58, 1st full para); however, as stated above these results are not compared with the closest prior art (i.e., BI836909), nor is it clear what is unexpected.
Fourth, to establish unexpected results over a claimed range, Applicants should compare a sufficient number of tests both inside and outside the claimed range to show the criticality of the claimed range. In re Hill, 284 F.2d 955, 128 USPQ 197 (CCPA 1960) (see MPEP § 716.02(d)(II)). The instant claims are drawn to administering 6.5µg/day-650µg/day (see claim 1; see Remarks pg. 13, last para). In so far as Applicants may be pointing to DLT results as allegedly unexpected results Applicants show no dose-limiting toxicities (DLT) up to 400 µg/day but DLTs at 800 µg/day (see specification pg. 57, 2nd full para). Therefore, it is unclear at what dose does DLT become a factor. For example, are DLTs observed at 600 µg/day or 700 µg/day? Furthermore, it is also unclear as to what results Applicants are alleging are unexpected. For example, is a lack of DLT, the number of complete responses (CR), the number of partial responses (PR), or a combination thereof unexpected. Likewise are the results unexpected across all treatment groups or are there particular doses that were unexpected.
Therefore, the 35 U.S.C. 103 rejection set forth above is maintained.
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, 2, 4-11, 17, 18, 24-26, 28-34, and 36 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 15 of U.S. Patent No. 9,598,500 B2 published 21 March 2017 (referred herein as ‘500 patent), Topp, Hipp, and Kufer as evidenced by Hipp2.
Claims 1, 2, 4-11, 17, 18, 24-26, 28-34, and 36 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 15 of U.S. Patent No. 9,340,621 B2 published 17 May 2016 (referred herein as ‘621 patent), Topp, Hipp, and Kufer as evidenced by Hipp2.
Claims 1, 2, 4-11, 17, 18, 24-26, 28-34, and 36 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 13 of U.S. Patent No. 9,150,664 B2 published 6 October 2015 (referred herein as ‘664 patent), Topp, Hipp, and Kufer as evidenced by Hipp2.
Claims 1, 2, 4-11, 17, 18, 24-26, 28-34, and 36 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 12 of U.S. Patent No. 11,419,933 B2 published 23 August 2022 (referred herein as ‘933 patent), Topp, Hipp, and Kufer as evidenced by Hipp2.
Claims 1, 2, 4-11, 17, 18, 24-26, 28-34, and 36 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 11 of U.S. Patent No. 10,752,694 B2 published 25 August 2020 (referred herein as ‘694 patent), Topp, Hipp, and Kufer as evidenced by Hipp2.
Claims 1, 2, 4-11, 17, 18, 24-26, 28-34, and 36 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 9, 10, and 17 of U.S. Patent No. 10,301,391 B2 published 28 May 2019 (referred herein as ‘391 patent), Topp, Hipp, and Kufer as evidenced by Hipp2.
Claims 1, 2, 4-11, 17, 18, 24-26, 28-34, and 36 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 10, 18, 26, 29, 30, 31, and 40 of copending Application No. 18/026,505 (referred herein as ‘505 application) Topp, Hipp, and Kufer as evidenced by Hipp2.
Claims 1, 2, 4-11, 17, 18, 24-26, 28-34, and 36 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, and 31-33 of copending Application No. 16/482,603 (referred herein as ‘603 application) Topp, Hipp, and Kufer as evidenced by Hipp2.
The teachings of Topp, Hipp, Kufer, and as evidenced by Hipp2 are set forth above.
Therefore, a person of ordinary skill in the art would substitute the nucleic acids encoding (i.e., ‘500 patent), amino acids sequences (i.e., ‘621 patent, ‘644 patent, ‘694 patent, ‘391 patent), a pharmaceutical composition (i.e., ‘933 patent, co-pending ‘603), or a method for administering to a patient with cancer (i.e., co-pending ‘505) comprising a BCMAxCD3 bispecific T-cell engager claimed in the U.S. Patents and co-pending applications for BI836909 in a method of treating RRMM comprising administering 135µg/kg/day in continuous intravenous in up to at least 5 cycles of 4 weeks of administration and 2 weeks with no administration.
Applicant's arguments filed 15 October 2025 have been fully considered but they are not persuasive. Applicant argues for the same reasons set forth in the Remarks regarding the 35 USC 103 rejection the double patenting rejections are also non-obvious (see Remarks pg. 19, last para).
Therefore, the above double patenting rejections are hereby maintained for the reasons set forth above.
Claims 1, 2, 4-11, 24, and 25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 15 of U.S. Patent No. 9,598,500 B2 published 21 March 2017 (referred herein as ‘500 patent) and Yuraszeck.
Claims 1, 2, 4-11, 17, 18, and 24-26 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 15 of U.S. Patent No. 9,340,621 B2 published 17 May 2016 (referred herein as ‘621 patent) and Yuraszeck.
Claims 1, 2, 4-11, 24, and 25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 13 of U.S. Patent No. 9,150,664 B2 published 6 October 2015 (referred herein as ‘664 patent) and Yuraszeck.
Claims 1, 2, 4-11, 17, 18, and 24-26 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 12 of U.S. Patent No. 11,419,933 B2 published 23 August 2022 (referred herein as ‘933 patent) and Yuraszeck.
Claims 1, 2, 4-11, 17, 18, and 24-26 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 11 of U.S. Patent No. 10,752,694 B2 published 25 August 2020 (referred herein as ‘694 patent) and Yuraszeck.
Claims 1, 2, 4-11, and 24-25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 9, 10, and 17 of U.S. Patent No. 10,301,391 B2 published 28 May 2019 (referred herein as ‘391 patent) and Yuraszeck.
Claims 1, 2, 4-11, 17, 18, and 24-26 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 10, 18, 26, 29, 30, 31, and 40 of copending Application No. 18/026,505 (referred herein as ‘505 application) in view of Yuraszeck and US Patent ‘621 (referred herein as Kufer).
Claims 1, 2, 4-11, 17, 18, and 24-26 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, and 31-33 of copending Application No. 16/482,603 (referred herein as ‘603 application) in view of Yuraszeck and Kufer.
Applicant's arguments filed 26 February 2025 have been fully considered but they are not persuasive.
Applicants argue that for the reasons stated in above in 35 U.S.C. 103 rejection over Kufer and Yuraszeck applies to the rejections for nonstatutory double patenting (see Remarks pg. 19, last para, pg. 20, 1st para).
For the reasons stated above the nonstatutory double patenting rejections are maintained.
Conclusion
No claim allowed.
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).
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/H.A.P./ Examiner, Art Unit 1644 /DANIEL E KOLKER/Supervisory Patent Examiner, Art Unit 1645