DETAILED ACTION
Notice of Pre-AIA or AIA Status
1. The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
2. Applicant’s reply filed on 5/26/2026 is acknowledged. Claims 1-7, 9-11, 13-14, 16-17, 19, 24, 29, 34, 37 and 39 are pending. Claims 8, 12, 15, 18, 20-23, 25-28, 30-33, 35-36 and 38 are canceled. Claims 19, 24, 29, 34, 37 and 39 are withdrawn. Claims 1, 2, 4, 6-7, 11, 13-14 and 17 have been amended.
3. Claims 1-7, 9-11, 13-14, 16 and 17 are under examination.
Information Disclosure Statement
4. The information disclosure statement (IDS) submitted on 5/26/2026 has been considered by the examiner.
Nucleotide and/or Amino Acid Sequence Disclosures
5. The submission of a substitute sequence listing including SEQ ID NOs: 254-271 and 250-253 present in the specification is acknowledged. However, applicant failed to provide a proper statement of no new matter. See 37 CFR 1.825(a)(4) or 1.825(b)(5).
Objections and Rejections Withdrawn
6. All claim objections and rejections except those maintained below are withdrawn in view of applicant’s amendments.
Rejections Maintained
Claim Rejections - 35 USC § 103
7. 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.
8. Claims 1-7, 9-11, 13-14, 16 and 17 remain rejected under 35 U.S.C. 103 as being unpatentable over Chuang et al. (WO 2018/177371A1, pub. date: Oct 4, 2018, IDS filed on 1/2/2025), in view of Kley et al. (WO 2017/077382A1, pub. date: 5/11/2017) and Cheung et al (US 2017/0210819A1, pub. date: 7/27/2017).
Regarding claims 1-5, Chuang et al. teaches a bispecific antibody (BsAb) comprising a first antigen binding site that binds to CD3 and a second antigen binding site that binds to a tumor antigen, in particular EGFR,
wherein the second antigen (EGFR) binding site is a Fab which comprises a VH-CH1 comprising SEQ ID NO: 76, and a VL-C[Symbol font/0x6B] comprising SEQ ID NO:75, or a scFv which comprises SEQ ID NO: 78,
wherein the first antigen (CD3) binding site is a Fab comprising a VL-C[Symbol font/0x6B] domain and a VH-CH1 domain, or a scFv (Example 1, [0069] and Fig. 3).
The amino acid sequences of SEQ ID NO: 76 and 75 comprise instant SEQ ID NO: 77 and 81, respectively, and are 100% identical to instant SEQ ID NO: 83 and 84 respectively, see sequence alignment below:
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723
700
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230
692
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354
685
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712
680
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227
712
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366
747
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Regarding claims 6, 9 and 10, Chuang et al. teaches a bispecific antibody anti-CD3 Fab/anti-EGFR scFv, wherein the anti-CD3 Fab comprises VHCH1 and VLC[Symbol font/0x6B], and the anti-EGFR scFv is linked to CH1 of the anti-CD3 FAB via a peptide linker (Fig. 3(B), [0069], [00129]).
Regarding amended claim 7, Chuang teaches an anti-EGFR scFv comprises SEQ ID NO: 77 ([00136], Table 6). The amino acid sequence of SEQ ID NO: 77 comprises instant SEQ ID NO:258, see sequence alignment below:
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468
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Regarding claim 13 and 16, Chuang et al. teaches a bispecific antibody anti-CD3 scFv/anti-EGFR FAB, wherein the anti-EGFR Fab comprises VHCH1 and VLC[Symbol font/0x6B], the anti-CD3 scFv is linked to CH1 of the anti-EGFR FAB via a peptide linker, wherein the peptide linker is at least 5 amino acids in length ([00129] and Fig. 3(A), and [0052]).
Regarding claim 14, Chuang et al. teaches a bispecific antibody anti-CD3 scFv/anti-EGFR FAB, wherein the anti-EGFR Fab comprises a VH-CH1 comprising SEQ ID NO: 76, and a VL-C[Symbol font/0x6B] comprising SEQ ID NO:75. The amino acid sequences of SEQ ID NO: 76 and 75 are 100% identical to instant SEQ ID NO: 83 and 84 respectively (see sequence alignment above).
Regarding claim 17, Chuang et al. teaches a bispecific antibody anti-CD3 scFv/anti-EGFR scFv (Fig. 3 (C)).
Regarding claim 1, Chuang et al. does not teach that the anti-CD3 Fab comprises a VH of instant SEQ ID NO:15, and a VL of instant SEQ ID NO:20.
Regarding amended claim 7, Chuang et al. does not teach that the anti-CD3 Fab comprises a VHCH1 of instant SEQ ID NO:23, a VLCK of instant SEQ ID NO:24.
Regarding amended claim 11, Chuang et al. does not teach that the anti-CD3 Fab comprises a VLCK of instant SEQ ID NO:24.
Regarding claims 1, 7 and 11, Kley et al. teaches a chimeric protein comprising a targeting moiety directed against CD3 expressed on T cells, wherein the targeting moiety is an anti-CD3 antibody, and the anti-CD3 antibody is OKT3 or otelixizumab or fragment thereof (page 68-69). Kley et al. teaches that otelixizumab comprises a heavy chain comprising SEQ ID NO: 195 and a light chain comprising SEQ ID NO: 196 (page 69). The amino acid sequence SEQ ID NO: 195 comprises instant SEQ ID NO: 15 and 23, and the amino acid sequence SEQ ID NO: 196 comprises instant SEQ ID NO: 20 and 24, see sequence alignment below:
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786
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698
801
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Cheung et al. teaches making bispecific antibody comprising a first antigen binding site that binds to CD3 and as second antigen binding site that binds to a tumor antigen, wherein the first antigen binding site that binds to CD3 comprises a VH and a VL of antibody otelixizumab, mOKT3 or huOKT3 ([0068], [0142] and [0034]).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have used the VH (or VHCH1) and VL (or VLCL) of otelixizumab to make the bispecific anti-CD3/anti-EGFR antibody of Chuang in view of Kley and Cheung. One of ordinary skill in the art would have been motivated to do so because Kley et al. teaches that otelixizumab can be used in making chimeric protein targeting CD3 expressed on T cells and Cheung teaches that otelixizumab can be used to make bispecific antibody comprising a first antigen binding site that binds to CD3 and a second antigen binding site that binds to a tumor antigen. One of ordinary skill in the art would have had a reasonable expectation of success because Kley et al. discloses the sequences of heavy and light chains of otelixizumab and Cheung et al. teaches that otelixizumab can be used to make bispecific antibodies that target T cells and tumor antigens.
Regarding amended claim 11, Chuang et al. does not teaches instant SEQ ID NO; 231.
Chuang et al. teaches a bispecific antibody anti-CD3 Fab/anti-EGFR scFv, wherein the anti-CD3 Fab comprises VHCH1 and VLC[Symbol font/0x6B], and the anti-EGFR scFv is linked to CH1 of the anti-CD3 FAB via a peptide linker (Fig. 3(B), [0069], [00129]). Chuang teaches SEQ ID NO:77 which comprises anti-EGFR scFv and a peptide linker at the N-terminus ([00136], Table 6). Cheung et al. teaches making bispecific antibody comprising a first antigen binding site that binds to CD3 and as second antigen binding site that binds to a tumor antigen, wherein the first antigen binding site that binds to CD3 comprises a VH and a VL of antibody otelixizumab, mOKT3 or huOKT3 ([0068], [0142] and [0034]). Kley et al. teaches that otelixizumab comprises a heavy chain comprising SEQ ID NO: 195 and a light chain comprising SEQ ID NO: 196 (page 69). The amino acid sequence SEQ ID NOs: 195 and 196 comprise instant SEQ ID NO: 23 and 24, respectively.
It would have been obvious to one of ordinary skill in the art to have made a bispecific antibody comprising anti-CD3 Fab/anti-EGFR scFv, wherein the anti-CD3 Fab comprises VHCH1 and VLC[Symbol font/0x6B] of otelixizumab, and the anti-EGFR scFv is linked to the CH1 of the anti-CD3 Fab via a peptide linker (Fig. 3(B), [0069], [00129]) in view of Kley and Cheung. One of ordinary skill in the art would have been motivated to do so because Chuang et al. teaches a bispecific antibody anti-CD3 Fab/anti-EGFR scFv, wherein the anti-CD3 Fab comprises VHCH1 and VLC[Symbol font/0x6B], and the anti-EGFR scFv is linked to CH1 of the anti-CD3 FAB via a peptide linker (Fig. 3(B), [0069], [00129]), Kley et al. teaches that otelixizumab can be used in making chimeric protein targeting CD3 expressed on T cells and Cheung teaches that otelixizumab can be used to make bispecific antibody comprising a first antigen binding site that binds to CD3 and a second antigen binding site that binds to a tumor antigen. One of ordinary skill in the art would have had a reasonable expectation of success because Kley et al. discloses the sequences of heavy and light chains of otelixizumab, Chuang et al. teaches the sequence of anti-EGFR scFv and peptide linker (SEQ ID NO:77), and Cheung et al. teaches that otelixizumab can be used to make bispecific antibodies that target T cells and tumor antigens.
By linking the VHCH1 of otelixizumab to the anti-EGFR scFv via a peptide linker (SEQ ID NO:77 taught by Chuang), one would have arrived a polypeptide having a sequence that is 100% identical to instant SEQ ID NO:231, see sequence alignment below:
Alignment between the amino acid sequence of instant SEQ ID NO:231 and VHCH1 of otelixizumab:
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Alignment between the amino acid sequence of instant SEQ ID NO:231 and SEQ ID NO:77 of Chuang
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Regarding amended claim 14, Chuang et al. does not teach anti-CD3 scFv comprises instant SEQ ID NO:251.
Chuang et al. teaches a bispecific antibody anti-CD3 scFv/anti-EGFR FAB, wherein the anti-EGFR Fab comprises a VH-CH1 comprising SEQ ID NO: 76, and a VL-C[Symbol font/0x6B] comprising SEQ ID NO:75. The amino acid sequences of SEQ ID NO: 76 and 75 are 100% identical to instant SEQ ID NO: 83 and 84 respectively (see sequence alignment above). Chuang et al. teaches making scFv by linking a VH and a VL of an antibody via a peptide (GGGGS)3 (see SEQ ID NO:77)
Kley teaches the heavy and light chain amino acid sequence of Otelixizumab.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention and one would have been motivated to have used the VH and VL of otelixizumab and a linker (GGGGS)3 to make an anti-CD3 scFv in view of Kley and Cheung. One of ordinary skill in the art would have been motivated to do so because Chuang et al. teaches a bispecific antibody anti-CD3 scFv/anti-EGFR FAB, and a linker of (GGGGS)3 for linking VH and VL to produce a scFv, and Cheung teaches that otelixizumab can be used to make bispecific antibody comprising a first antigen binding site that binds to CD3 and a second antigen binding site that binds to a tumor antigen. One of ordinary skill in the art would have had a reasonable expectation of success because Kley et al. discloses the sequences of heavy and light chains of otelixizumab and Cheung et al. teaches that otelixizumab can be used to make bispecific antibodies that target T cells and tumor antigens.
The amino acid sequence of anti-CD3 scFv of otelixizumab comprises a VH of SEQ ID NO:195, a linker (GGGGS)3 and a VL of SEQ ID NO:196 would be 100% identical to instant SEQ ID NO:251.
Applicant’s Arguments
The instant application provides experimental data showing superior features of the claimed bi-specific antibody, comprising an anti-CD3 binding moiety derived from CTA.03 (the elected species) as compared with bi-specific antibodies having an anti-CD3 binding moiety derived from CTA.01. An outline of such experimental data is provided below:
" Armed-T cells displaying the anti-CTA03Fab/anti-CD 19 or anti-EGFR bi-specific antibodies as claimed exhibited higher cytotoxicity against CD19-expressing Raji cells or EGFR-expressing HT29 cells relative to armed-T cells displaying the control anti-CTAO1Fab/anti-TAA bi-specific antibodies. Example 6 and FIGs.13A and 13B.
" Armed T cells displaying anti-CTA03Fab/anti-EGFR armed-T cells exhibited higher cytotoxicity against EGFR-expressing HT29 and HCT116 cell lines relative to armed-T cells displaying the control anti-CTAO1Fab/anti-TAA bi- specific antibodies. Example 6 and FIGs. 14A and 14B.
" Mice treated with armed immune cells displaying the exemplary CTA03Fab/CTAT02scFv bi-specific antibody as claimed exhibited longer
survival rate relative to mice treated with armed immune cells displaying the control CTAO1Fab/CTAT02scFv bi-specific antibody. Example 7 and FIG. 16B.
In sum, the experimental data outlined above show superior features associated with the claimed bi-specific antibody, having the specific anti-CD3 binding moiety derived from CTA.03 as defined in independent claim 1, as compared with a control bi-specific antibody having the anti- CD3 moiety derived from CTA.01 (OKT3 as indicated in the instant application. See, e.g., page 64, lines 1-2).
Chuang discloses bi-specific antibodies comprising an anti-CD3 binding moiety derived from reference antibody CTA.02, which, according to Wu as noted in the Office Action, is a murine version of the OKT3 antibody. Accordingly, the data provided in the instant application discussed above show unexpected superior bioactivities of the claimed bi-specific antibody over Chuang, the closest prior art.
Kley discloses an anti-CD3 antibody relating to CTA.03 but does not provide any insight as to bioactivities of bi-specific antibodies comprising such an anti-CD3 antibody in the context of armed immune cells displaying such.
Cheung is cited for disclosing making bi-specific antibodies comprising an anti-CD3 binding moiety from otelixizumab, mouse OKT3, or human OKT3 but provides no insight that would make a skilled person in the art to believe that a bi-specific antibody having an anti-CD3 binding moiety from otelixizumab would exhibit the superior results reported in the instant application over those from OKT3.
Taken together, the claimed bi-specific antibody exhibited superior features over Chuang, the closest prior art cited in the Office Action and such superior features cannot be predicted based on disclosures of Chuang, Kley, and Cheung. As set forth in MPEP § 2145, an applicant can rely on evidence showing that the claimed invention yields unexpectedly improved properties or properties not present in the prior art to rebut an obviousness rejection. Further, the law is well settled that "[w]hen unexpected results are used as evidence of nonobviousness, the results must be shown to be unexpected compared with the closest prior art;" emphasis added. See Pfizer v. Apotex, 480 F.3d 1348, 1370 (Fed. Cir., 2007). Pursuant to the well-settled law, the unexpected superior features exhibited by the claimed bi-specific antibody render the amended claims not obvious over Chuang in view of Kley and Cheung.
Response to Arguments
Applicant’s arguments have been considered but are not persuasive.
MPEP (MPEP 716.02) states that any differences between the claimed invention and the prior art may be expected to result in some differences in properties. The issue is whether the properties differ to such an extent that the difference is really unexpected. In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
Applicant’s Fig. 13A discloses the bispecific antibody CTA03Fab/CTAT02scFv is more cytotoxic than CTA02Fab/CTA02scFv
Applicant’s Fig. 13B discloses the bispecific antibody CTA03scFv/CTAT03Fab is more cytotoxic than CTA02scFv/CTAT03Fab
Applicant’s Fig. 14A-B disclose the bispecific antibody CTA03Fab/CTAT03scFv is more cytotoxic than CTA01Fab/CTA03scFv shown.
Applicant’s Fig. 16A-B disclose the bispecific antibody CTA03Fab/CTAT02scFv is more cytotoxic than CTA01Fab/CTA02scFv shown in Fig. 16A-B.
However these results are not unexpected because the prior art has recognized that even if bispecific antibodies target the same tumor antigen and both use a CD3 binding arm, a bispecific antibody built from an antigen binding domain of otelixizumab (CTA03) could reasonably be expected to behave differently from one built from an antigen binding domain of OKT3 (CTA02). This is because different anti-CD3 antibodies bind to different CD3 epitope (a different region of CD3), have different binding affinity (may differ substantially), have different T-cell activation strength (could be weaker or stronger), and produce a different cytokine profile. Jacobs et al. (Cancer Immunol Immunother, 1997, 44: 557-264) shows that bispecific antibody T3/OC1 (MOV18xOKT3) was less efficient than OC/TR (MOV18xαCD3) and T3/OC2 (MOV18xTR66) bs-mAbs, which are raised with different anti-CD3 specificities, in retargeting (Fig. 1) (page 259, column 1, under Results). Therefore, one would have expected a difference in cytotoxicity (either stronger or weaker) when the anti-CD3 binding arm is different.
Furthermore, MPEP 716.02(d) states “Whether the unexpected results are the result of unexpectedly improved results or a property not taught by the prior art, the "objective evidence of nonobviousness must be commensurate in scope with the claims which the evidence is offered to support."
The final activity of a bispecific antibody depends on many design variables: including binding specificity and affinity of both arms, linker length, and molecular format. Wu et al. (Pharmacol Ther., 2018, 182: 161-175) teaches “Multiple factors can affect the potency of a particular T-BsAb, including the antigen itself, binding epitope, antibody affinities, and the specific format used” (page 8, under subheading 3.2. Factors that affect the potency of therapeutic T-BsAb) (note: T-BsAb stands for T cell engaging bispecific antibody see title). Wu et al. teaches “Different formats differ in molecular size, stability, flexibility, compactness, ease of production, valency of antigen binding, mode of interaction with target cells and effector cells, as well as pharmacokinetics” (page 11, under subheading 3.2.3. Formats of T-BsAbs).
Double Patenting
9. 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.
10. Claims 1-7, 9-11, 13-14, 16 and 17 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-24 of copending Application No. 18/682,632 (reference application), in view of Chuang et al. (WO 2018/177371A1, pub. date: Oct 4, 2018, IDS filed on 1/2/2025). Although the claims at issue are not identical, they are not patentably distinct from each other.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
The claims of copending application disclose a bi-specific antibody specific to CD3 and a tumor associated antigen (TAA), wherein the bi-specific antibody comprises a first antigen binding fragment that binds human CD3, wherein the first antigen binding fragment comprises a first heavy chain that comprises a first heavy chain variable region (VH) and a first light chain that comprises a first light chain variable region (VL) of a first reference antibody, wherein the first heavy chain and the first light chain comprise the same VH and VL as the reference antibody,
wherein the first reference antibody is CTA.02, CTA.03, CTA.04, or CTA.05
wherein the bi- specific antibody comprises a second antigen binding fragment that binds the TAA, which is CD20, CD19, EGFR, HER2, PSMA, CEA, EpCAM, FAP, PD-L1, CD38, CD33, cMET, CD47, TRAIL-R2, mesothelin, or GD2.
The claims of copending application does not disclose that the second antigen EGFR binding fragment comprises instant SEQ ID NOs: 77 and 81, 83 and 84.
The teachings of Chuang et al have been set forth above.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have used the VH and VL of the anti-EGFR antibody of Chuang to make the bispecific anti-CD3/anti-EGFR antibody of the copending application. One of ordinary skill in the art would have been motivated to do so with a reasonable expectation of success because Chuang et al. teaches making bispecific anti-CD3/anti-EGFR antibody.
Applicant’s Arguments
As set forth under MPEP 804(I)(B)(1)(b)(i): If a provisional nonstatutory double patenting rejection is the only rejection remaining in an application having the earlier patent term filing date, the examiner should withdraw the rejection in the application having the earlier patent term filing date and permit that application to issue as a patent, thereby converting the provisional nonstatutory double patenting rejection in the other application into a nonstatutory double patenting rejection upon issuance of the patent.
Here, the instant application has the patent term filing date of March 23, 2021, which is earlier than that of the '632 application, i.e., August 10, 2022.
Pursuant to MPEP 804(I)(B)(1)(b)(i), Applicant respectfully requests that the Examiner withdraw the double patenting rejection over the '632 Application when it is the only rejection remaining in the instant application.
Response to Arguments
The rejection is maintained because it is not the only rejection remaining at this time.
New Grounds of Objection and Rejection
Claim Objections
11. Claim 1 is objected to for missing the word “first” before “reference antibody” in line 7.
Claim Rejections - 35 USC § 112
12. The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
13. Claim 11 is rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Claim 11 has been amended to depend on claim 10. Claim 10 requires the first polypeptide to comprise the first light chain, and a second peptide to comprise the first heavy chain. However, claim 11 defines first polypeptide as comprising SEQ ID NO:231 (which is VH-CH1) and the second peptide as comprising SEQ ID NO:24 (which is VL-C[Symbol font/0x6B]).
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Conclusion
14. No claims are 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).
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.
15. Any inquiry concerning this communication or earlier communications from the examiner should be directed to HONG SANG whose telephone number is (571)272-8145. The examiner can normally be reached Monday-Friday 8am-5pm.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Gregory Emch can be reached at 571-272-8149. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/HONG SANG/Primary Examiner, Art Unit 1646
Prosecution Insights