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 Claims
Claims 1, 4-8, 10-15, 18, 24-26, 27, and 29 are amended. Claims 9, 16-17, 21, 34-39, 41-47, 52-105 are cancelled. Claims -----1-8, 10-15, 18-20, 22-33, 40, 48-50, 106-107 are currently pending and under examination.
Response to Remarks filed 01/23/2026
Applicant’s arguments and amendments regarding the 35 USC 112 rejection have been fully considered and are persuasive. Specifically deletion of the term “about” from the claims overcome the rejection. Therefore, the 35 USC 112 rejection is withdrawn.
Applicant’s arguments and amendments regarding the 35 USC 103 rejection have been fully considered and are not persuasive.
Specifically Applicant states:
“As explained in the present application, it was necessary to administer canonical
bispecific T cell engagers via cIV infusions due to their short half-life, despite the inconvenience of such an administration scheme for patients. The next generation of T cell engagers included half-life extending (HLE) moieties (such as Fc domains as recited in claim 1) to enable a longer dosing interval and to avoid the cIV infusions required by the first generation molecules. See paragraphs [0004] and [0042] of the specification. As HLE bispecific T cell engagers were designed to overcome the challenges of continuous infusion, one of ordinary skill in the art would not have started with a continuous infusion of an HLE bispecific T cell engager in formulating a dosing strategy.
The present invention is based, in part, on the surprising discovery that severity and
frequency of cytokine release syndrome (CRS) events in patients receiving HLE bispecific T cell engagers were reduced with a cIV priming dose strategy. The data in the application show that CRS events were associated with the peak serum levels (Cmax) following the first dose of an HLE bispecific T cell engager. See paragraph [0042] and Example 1. It was determined that by infusing the first dose of the HLE bispecific T cell engager continuously over an extended period of time, the serum concentration of the molecule slowly increases to the Cmax and avoids sharp spikes in peak serum levels, thereby decreasing severity of CRS events while at the same time allowing maintenance of higher levels of cumulative drug exposure to achieve efficacious doses as early as possible in the treatment cycle. See paragraph [0043]. This administration approach primes the T cells so that subsequent administration of higher therapeutic doses produces a reduced or minimal cytokine release and associated CRS events.”
However, Chaudry et al teach the infusion of a BiTE comprising a CD3 and Fc via continuous infusion. Therefore, one of ordinary skill in the art would have been motivated to begin a dose optimization strategy with a 24-hour continuous infusion priming dose. Additionally, Chen et al teach that a priming dose can reduce CRS. Therefore, one would be motivated to perform a 24-hour priming dose prior to a therapeutic dose. Therefore, the results of the instant application are an expected outcome of the dose strategy that would have been obvious to one of ordinary skill in the art at the time of effective filing.
Additionally, the amendment to claim 1 inserting “of 30 minutes to 90 minutes” is an obvious variant of the method of Chaudhary, Chen et al, and Carter et al that would be reached via routine optimization.
Lastly, Applicant's arguments are not found persuasive with respect to unexpected results, because the arguments of counsel cannot take the place of evidence in the record. As set forth in MPEP 716.01:
Objective evidence which must be factually supported by an appropriate affidavit or declaration to be of probative value includes evidence of unexpected results, commercial success, solution of a long-felt need, inoperability of the prior art, invention before the date of the reference, and allegations that the author(s) of the prior art derived the disclosed subject matter from the applicant. See, for example, In re De Blauwe, 736 F.2d 699, 705, 222 USPQ 191, 196 (Fed. Cir. 1984) ("It is well settled that unexpected results must. be established by factual evidence." See also In re Lindner, 457 F.2d 506, 508, 173 USPQ 356, 358 (CCPA 1972); Ex parte George, 21 USPQ2d 1058 (Bd. Pat. App. & Inter. 1991). The arguments of counsel cannot take the place of evidence in the record. In re Schulze, 346 F.2d 600, 602, 145 USPQ 716, 718 (CCPA 1965). Examples of attorney statements which are not evidence and which must be supported by an appropriate affidavit or declaration include statements regarding unexpected results, commercial success, solution of a long-felt need, inoperability of the prior art, invention before the date of the reference, and allegations that the author(s) of the prior art derived the disclosed subject matter from the applicant. See MPEP § 2145 generally for case law pertinent to the consideration of applicant's rebuttal arguments.
Accordingly, while the arguments of counsel about the unexpected properties are noted, they were not found persuasive as no affidavit or declaration including statements regarding the expectations of one of ordinary skill has been submitted. In order to demonstrate that the claimed invention yields unexpected results, Applicant is encouraged to provide evidence of such in the form of an affidavit or declaration, or clearly point out such evidence in the specification as originally filed.
Additionally with respect to Applicant’s assertion that “the present invention is based, in part, on the surprising discovery that severity and frequency of cytokine release syndrome (CRS) events in patients receiving HLE bispecific T cell engagers were reduced with a cIV priming dose strategy,” it appears that the data discussed by Applicant is not sufficient to overcome the rejection of the claims under 35 U.S.C. 103. For instance Examples 3 and 4 detail experiments where a bispecific T cell engager priming dose was administered for 4 or 7 days, respectively; however the priming dose of claim 1 is administered over 1 to 7 days. Furthermore Example 4 details an experiment where a priming dose is 1000 μg/kg or 5000 μg/kg; however the claims are drawn to any priming dose and any bolus dose. As such Applicant’s evidence of surprising results is not commensurate in scope with the claims, and as such the 35 USC 103 rejection is maintained.
Rejections Maintained- Nonfinal 10/23/2025
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.
Claim(s) 1-8, 10-15, 18-20, 22-33, 40, 50-51, 106-107 are rejected under 35 U.S.C. 103 as being unpatentable over Chaudhary (WO2019067805; published 04/04/2019), Chen et al. (Clin Transl Sci, 12: 600-608, 2019), and Carter et al. (US PG PUB 2018/0177873, publication date: 06/28/2018).
Chaudhary teach a method of administering a bispecific T-cell engaging (BiTE) molecule to a patient over a 24 hour infusion (Chaudhary, pg. 256, paragraph 00485-00486). Chaudhary teach the BiTE has a first domain that binds to a target cancer cell and a second domain that binds to human CD3 and an Fc domain (Chaudhary et al, pg. 125, Table 13, SEQ ID NO:3545-3830 and 7458-7721).
Therefore, Chaudhary teach a method of administering a therapeutic dose of a BiTE via continuous IV infusion over 1 day wherein the BiTE has a first binding domain that binds to a target cancer cell and a second binding domain that binds to human CD3, and an FC domain. Chaudhary does not teach a method of administering a priming dose of a BiTE via continuous IV infusion over 1 day to 7 days and a subsequent therapeutic dose by bolus IV infusion wherein the BiTE has a first antigen that binds to a target cancer cell and a second binding domain that binds to human CD3 and an FC domain. These deficiencies are remedied by Chen et al. and Carter et al.
Chen et al. teach that “T-cell–engaging bispecific antibodies (T-BsAbs) are an important class of antibody therapeutics in immuno-oncology. T-BsAbs simultaneously bind to CD3 on T cells and a tumor-associated antigen on tumor cells, activate T cells, and redirect T cells’ cytotoxicity against tumor cells. Cytokine release syndrome (CRS), a common dose-limiting adverse event forT-BsAbs, is associated with T-cell activation. A ‘priming’ dose strategy (i.e., a lower initial dose followed by a higher maintenance dose) has been implemented in the clinic to mitigate CRS and to achieve efficacious doses with T-BsAbs.” See Abstract. Based upon these teachings, one of ordinary skill in the art would have been motivated to administer a bispecific antibody that binds to a tumor antigen and CD3 in a regimen that comprises a prime dose followed by a maintenance, i.e., therapeutic, dose, as such as method would be expected to mitigate CRS, thereby improving the safety profile of the administered bispecific antibody.
Carter et al. teach that bispecific antibodies may be administered to humans via intravenous administration as a bolus or by continuous infusion over a period of time, see [0674].
One of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to develop a method for administering a therapeutic dose of a bispecific T-cell engaging molecule to a patient diagnosed with cancer, comprising administering to the patient an initiation cycle of the bispecific T-cell engaging molecule, said initiation cycle comprising: administering a priming dose of the bispecific T-cell engaging molecule by continuous intravenous infusion over a period of 1 day to 7 days; and administering after the priming dose a therapeutic dose of the bispecific T-cell engaging molecule by a bolus intravenous infusion, wherein the bispecific T-cell engaging molecule comprises a first domain that specifically binds to a target cancer cell antigen, a second domain that specifically binds to human CD3, and an Fc domain. One of ordinary skill in the art would have been motivated to do so, because Chaudhary teach a method of administering a therapeutic dose of a BiTE via continuous IV infusion over 1 day wherein the BiTE has a first binding domain that binds to a target cancer cell and a second binding domain that binds to human CD3, and an Fc domain. Furthermore based upon the teachings of Chen et al., one of ordinary skill in the art would have been motivated to administer a bispecific antibody that binds to a tumor antigen and CD3 in a regimen that comprises a prime dose followed by a maintenance, i.e., therapeutic, dose, as such as method would be expected to mitigate CRS, thereby improving the safety profile of the administered bispecific antibody. Also Carter et al. teach that bispecific antibodies may be administered to humans via intravenous administration as a bolus or by continuous infusion over a period of time.
It is noted that the courts have stated where the claimed ranges “overlap or lie inside the ranges disclosed by the prior art” and even when the claimed ranges and prior art ranges do not overlap but are close enough that one skilled in the art would have expected them to have similar properties, a prima facie case of obviousness exists (see In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976); In re Woodruff, 919 F.2d 1575, 16 USPQ2d 1934 (Fed. Cir. 1990); Titanium Metals Corp. of America v. Banner, 778 F2d 775. 227 USPQ 773 (Fed. Cir. 1985) (see MPEP 2144.05.01).
The courts have also found that “where 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 re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955). See MPEP 2144.05 II.
Therefore, the claimed ranges merely represent an obvious variant and/or routine optimization of the values of the cited prior art, and as such the invention of Chaudhary, Chen et al., and Carter et al. meets the limitations of a method for administering a therapeutic dose of a bispecific T-cell engaging molecule to a patient diagnosed with cancer, comprising administering to the patient an initiation cycle of the bispecific T-cell engaging molecule, said initiation cycle comprising: administering a priming dose of the bispecific T-cell engaging molecule by continuous intravenous infusion over a period of 1 day to 7 days; and administering after the priming dose a therapeutic dose of the bispecific T-cell engaging molecule by a bolus intravenous infusion, wherein the bispecific T-cell engaging molecule comprises a first domain that specifically binds to a target cancer cell antigen, a second domain that specifically binds to human CD3, and an Fc domain.
Claims 2-8, 10-15, 18-20, 22-30, 50, and 51 merely represent an obvious variant and/or routine optimization of the values of the cited prior art.
Regarding claim 31, Chaudhary teach a PSMA (prostate cancer antigen) BiTE (Table 9, pg. 104), a BCMA BiTE (Table 9, pg. 102), a CLDN18.2 BiTE (Table 9, pg. 105), and a DLL3 BiTE (Table 9, pg. 103).
Therefore the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective filing date of the invention, as evidenced by the references.
Claim(s) 32 and 33 are rejected under 35 U.S.C. 103 as being unpatentable over Chaudhary (WO2019067805; published 04/04/2019), Chen et al. (Clin Transl Sci, 12: 600-608, 2019), and Carter et al. (US PG PUB 2018/0177873, publication date: 06/28/2018), as applied to claims 1-8, 10-15, 18-20, 22-33, 40, 50-51, 106-107, and further in view of Anderson et al. (US PB PUB 2016/0347840, publication date: 12/01/2016).
The teachings of Chaudhary, Chen et al., and Carter et al. are detailed above. These references do not teach the bispecific antibody structure of claim 32 or the treatment of a patient diagnosed with prostate cancer by administering a bispecific molecule that binds PSMA. This is remedied by Anderson et al.
At [0147], Anderson et al. teaches dual variable domain immunoglobulin (DVD-Ig) bispecific molecules, and these molecules meet the limitations of the bispecific antibody structure of claim 32. Furthermore at [0005], Anderson et al. teach that PSMA is overexpressed in prostate cancer.
One of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to combine the teachings of Chaudhary, Chen et al., and Carter et al. with those of Anderson to arrive at a method of administering a bispecific T-cell engaging (BiTE) molecule to a patient over a 24 hour infusion wherein the BiTE has a first domain that binds to a target cancer cell and a second domain that binds to human CD3 and an Fc domain, wherein the BiTE molecule is in DVD-Ig format and wherein said BiTE comprises an anti-PSMA moiety that may be used in the treatment of prostate cancer. One of ordinary skill in the art would have been motivated to do so, because Chaudhary, Chen et al., and Carter et al. teach a method of administering a bispecific T-cell engaging (BiTE) molecule to a patient over a 24 hour infusion wherein the BiTE has a first domain that binds to a target cancer cell and a second domain that binds to human CD3 and an Fc domain, and wherein the BiTE molecule is administered as a priming dose followed by a therapeutic dose. Furthermore Anderson et al. teaches dual variable domain immunoglobulin (DVD-Ig) bispecific molecules, and these molecules meet the limitations of the bispecific antibody structure of claim 32. Also at [0005], Anderson et al. teach that PSMA is overexpressed in prostate cancer. Based upon these teachings, one of ordinary skill in the art would have had ample motivation to modify the invention of Chaudhary, Chen et al., and Carter et al. to comprise a BiTE molecule in DVD-Ig format, wherein the binding domain that binds to a tumor antigen is anti-PSMA, because the resultant BiTE molecule would reasonably be expected to treat patients that have been diagnosed with PSMA-expressing prostate cancer.
Therefore the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective filing date of the invention, as evidenced by the references.
Claim(s) 40 is rejected under 35 U.S.C. 103 as being unpatentable over Chaudhary (WO2019067805; published 04/04/2019), Chen et al. (Clin Transl Sci, 12: 600-608, 2019), and Carter et al. (US PG PUB 2018/0177873, publication date: 06/28/2018), as applied to claims 1-8, 10-15, 18-20, 22-33, 40, 50-51, 106-107, and further in view of Armitage et al. (US PB PUB 20140161828, publication date: 06/12/2014).
The teachings of Chaudhary, Chen et al., and Carter et al. are detailed above. These references do not teach the treatment of a patient diagnosed with multiple myeloma by administering a bispecific molecule that binds BCMA. This is remedied by Armitage et al.
At [0061], Armitage et al. teach that BCMA is expressed on multiple myeloma cells.
One of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to combine the teachings of Chaudhary, Chen et al., and Carter et al. with those of Armitage et al. to arrive at a method of administering a bispecific T-cell engaging (BiTE) molecule to a patient over a 24 hour infusion wherein the BiTE has a first domain that binds to a target cancer cell and a second domain that binds to human CD3 and an Fc domain, wherein the BiTE molecule is in DVD-Ig format and wherein said BiTE comprises an anti-BCMA moiety that may be used in the treatment of multiple myeloma. One of ordinary skill in the art would have been motivated to do so, because Chaudhary, Chen et al., and Carter et al. teach a method of administering a bispecific T-cell engaging (BiTE) molecule to a patient over a 24 hour infusion wherein the BiTE has a first domain that binds to a target cancer cell and a second domain that binds to human CD3 and an Fc domain, and wherein the BiTE molecule is administered as a priming dose followed by a therapeutic dose. Furthermore Armitage et al. teach that BCMA is expressed on multiple myeloma cells. Based upon these teachings, one of ordinary skill in the art would have had ample motivation to modify the invention of Chaudhary, Chen et al., and Carter et al. to comprise a BiTE molecule, wherein the binding domain that binds to a tumor antigen is anti-BCMA, because the resultant BiTE molecule would reasonably be expected to treat patients that have been diagnosed with BCMA-expressing multiple myeloma.
Therefore the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective filing date of the invention, as evidenced by the references.
Claim(s) 48 is rejected under 35 U.S.C. 103 as being unpatentable over Chaudhary (WO2019067805; published 04/04/2019), Chen et al. (Clin Transl Sci, 12: 600-608, 2019), and Carter et al. (US PG PUB 2018/0177873, publication date: 06/28/2018), as applied to claims 1-8, 10-15, 18-20, 22-33, 40, 50-51, 106-107, and further in view of Kannan (WO2014153063; published 09/25/2014).
The teachings of Chaudhary, Chen et al., and Carter et al. are detailed above. These references do not teach an Fc domain of SEQ ID: 132. This is remedied by Kannan.
Kannan et al discloses an FC domain with 100% sequence identity to SEQ ID: 132 (Kannan, SEQ ID: 44).
One of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to combine the teachings of Chaudhary, Chen et al., and Carter et al. with those of Kannon to arrive at a method of administering a bispecific T-cell engaging (BiTE) molecule to a patient over a 24 hour infusion wherein the BiTE has a first domain that binds to a target cancer cell and a second domain that binds to human CD3 and an Fc domain of SEQ ID: 132. One of ordinary skill in the art would have been motivated to do so, because Chaudhary, Chen et al., and Carter et al. teach a method of administering a bispecific T-cell engaging (BiTE) molecule to a patient over a 24 hour infusion wherein the BiTE has a first domain that binds to a target cancer cell and a second domain that binds to human CD3 and an Fc domain, and wherein the BiTE molecule is administered as a priming dose followed by a therapeutic dose. Furthermore based upon the teachings of Kannon, one of ordinary skill in the art would have been motivated to add and FC domain of SEQ ID: 132 to the BiTE in order to improve cancer treatment activity. As such one of ordinary skill in the art would have been motivated to modify the invention of Chaudhary, Chen et al., and Carter et al. to further include and FC domain of SEQ ID: 132, because there would have been a reasonable expectation that the resultant invention which comprises a BiTE with a functional FC domain, is effective in treating cancer.
Therefore the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective filing date of the invention, as evidenced by the references.
Claim(s) 49 is rejected under 35 U.S.C. 103 as being unpatentable over Chaudhary (WO2019067805; published 04/04/2019), Chen et al. (Clin Transl Sci, 12: 600-608, 2019), and Carter et al. (US PG PUB 2018/0177873, publication date: 06/28/2018), as applied to claims 1-8, 10-15, 18-20, 22-33, 40, 50-51, 106-107, and further in view of Weiss et al (WO2016166360; published 10/20/2016).
The teachings of Chaudhary, Chen et al., and Carter et al. are detailed above. These references do not teach an Fc domain of SEQ ID: 140. This is remedied by Weiss et al.
Weiss et al discloses an FC domain with 100% sequence identity to SEQ ID: 140 (Weiss et al, SEQ ID: 414).
One of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to combine the teachings of Chaudhary, Chen et al., and Carter et al. with those of Weiss et al to arrive at a method of administering a bispecific T-cell engaging (BiTE) molecule to a patient over a 24 hour infusion wherein the BiTE has a first domain that binds to a target cancer cell and a second domain that binds to human CD3 and an Fc domain of SEQ ID: 140. One of ordinary skill in the art would have been motivated to do so, because Chaudhary, Chen et al., and Carter et al. teaches a method of administering a bispecific T-cell engaging (BiTE) molecule to a patient over a 24 hour infusion wherein the BiTE has a first domain that binds to a target cancer cell and a second domain that binds to human CD3 and an Fc domain, and wherein the BiTE molecule is administered as a priming dose followed by a therapeutic dose. Furthermore based upon the teachings of Weiss et al, one of ordinary skill in the art would have been motivated to add and FC domain of SEQ ID: 140 to the BiTE in order to improve cancer treatment activity. As such one of ordinary skill in the art would have been motivated to modify the invention of Chaudhary, Chen et al., and Carter et al. to further include and FC domain of SEQ ID: 140, because there would have been a reasonable expectation that the resultant invention which comprises a BiTE with a functional FC domain, is effective in treating cancer.
Therefore the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective filing date of the invention, as evidenced by the references.
Claim(s) 106 is rejected under 35 U.S.C. 103 as being unpatentable over Chaudhary (WO2019067805; published 04/04/2019), Chen et al. (Clin Transl Sci, 12: 600-608, 2019), and Carter et al. (US PG PUB 2018/0177873, publication date: 06/28/2018), as applied to claims 1-8, 10-15, 18-20, 22-33, 40, 50-51, 106-107, and further in view of Sahin et al. (US PB PUB 20150157711, publication date: 12/01/2016).
The teachings of Chaudhary, Chen et al., and Carter et al. are detailed above. These references do not teach the treatment of a patient diagnosed with gastric or esophageal cancer by administering a bispecific molecule that binds CLDN18.2. This is remedied by Sahin et al.
At [0012], Sahin et al. teach that CLDN18.2 is expressed on gastric cancer cells and esophageal cancer cells.
One of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to combine the teachings of Chaudhary, Chen et al., and Carter et al. with those of Sahin et al. to arrive at a method of administering a bispecific T-cell engaging (BiTE) molecule to a patient over a 24 hour infusion wherein the BiTE has a first domain that binds to a target cancer cell and a second domain that binds to human CD3 and an Fc domain, wherein the BiTE molecule is in DVD-Ig format and wherein said BiTE comprises an anti-CLDN18.2 moiety that may be used in the treatment of gastric or esophageal cancer. One of ordinary skill in the art would have been motivated to do so, because Chaudhary, Chen et al., and Carter et al. teach a method of administering a bispecific T-cell engaging (BiTE) molecule to a patient over a 24 hour infusion wherein the BiTE has a first domain that binds to a target cancer cell and a second domain that binds to human CD3 and an Fc domain, and wherein the BiTE molecule is administered as a priming dose followed by a therapeutic dose. Furthermore Sahin et al. teach that CLDN18.2 is expressed on gastric cancer cells and esophageal cancer cells. Based upon these teachings, one of ordinary skill in the art would have had ample motivation to modify the invention of Chaudhary, Chen et al., and Carter et al. to comprise a BiTE molecule, wherein the binding domain that binds to a tumor antigen is anti-CLDN18.2, because the resultant BiTE molecule would reasonably be expected to treat patients that have been diagnosed with CLDN18.2-expressing gastric or esophageal cancer cells.
Therefore the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective filing date of the invention, as evidenced by the references.
Claim(s) 107 is rejected under 35 U.S.C. 103 as being unpatentable over Chaudhary (WO2019067805; published 04/04/2019), Chen et al. (Clin Transl Sci, 12: 600-608, 2019), and Carter et al. (US PG PUB 2018/0177873, publication date: 06/28/2018), as applied to claims 1-8, 10-15, 18-20, 22-33, 40, 50-51, 106-107, and further in view of Thompson et al. (WO 2018140831, international publication date: 08/02/2018), document available at https://patentscope.wipo.int/search/en/search.jsf.
The teachings of Chaudhary, Chen et al., and Carter et al. are detailed above. These references do not teach the treatment of a patient diagnosed with small cell lung cancer by administering a bispecific molecule that binds DLL3. This is remedied by Thompson et al.
At [0704], Thompson et al. teach that DLL3 is a tumor antigen for small cell lung cancer.
One of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to combine the teachings of Chaudhary, Chen et al., and Carter et al. with those of Thompson et al. to arrive at a method of administering a bispecific T-cell engaging (BiTE) molecule to a patient over a 24 hour infusion wherein the BiTE has a first domain that binds to a target cancer cell and a second domain that binds to human CD3 and an Fc domain, wherein the BiTE molecule is in DVD-Ig format and wherein said BiTE comprises an anti-DLL3 moiety that may be used in the treatment of small cell lung cancer. One of ordinary skill in the art would have been motivated to do so, because Chaudhary, Chen et al., and Carter et al. teach a method of administering a bispecific T-cell engaging (BiTE) molecule to a patient over a 24 hour infusion wherein the BiTE has a first domain that binds to a target cancer cell and a second domain that binds to human CD3 and an Fc domain, and wherein the BiTE molecule is administered as a priming dose followed by a therapeutic dose. Furthermore Thompson et al. teach that DLL3 is a tumor antigen for small cell lung cancer. Based upon these teachings, one of ordinary skill in the art would have had ample motivation to modify the invention of Chaudhary, Chen et al., and Carter et al. to comprise a BiTE molecule, wherein the binding domain that binds to a tumor antigen is anti-DLL3, because the resultant BiTE molecule would reasonably be expected to treat patients that have been diagnosed with DLL3-expressing small cell lung cancer cells.
Therefore the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective filing date of the invention, as evidenced by the references.
Conclusion
THIS ACTION IS MADE FINAL. 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.
No claims are allowed.
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/J.K.D./Examiner, Art Unit 1642
/NELSON B MOSELEY II/Primary Examiner, Art Unit 1642
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