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 .
Response to Arguments
Applicant's arguments filed 07/02/2026 have been fully considered but they are not persuasive. Arguments pertaining to any remaining rejections are addressed in this Office Action.
Status of the Claims & Amendments
This action is in response to papers filed 07/02/2026 in which claims 1, 11, and 13 were amended, no claims were canceled, and no new claims were added. All of the amendments have been thoroughly reviewed and entered.
Applicant has amended claim 1 to overcome the 35 USC § 103 rejection; the 35 USC § 103 rejections of claim 1 and dependent claims have not been overcome. Applicant' s arguments, see Pgs. 6 - 9, filed 07/02/2026, with respect to the 35 USC § 103 rejections have been fully considered but are not persuasive for the reasons discussed in this office action.
Any rejection or objection not reiterated herein has been overcome by amendment.
Election/Restrictions
Applicant’s election without traverse of Group I (i.e., claims 1-33, and 38 drawn to cells and a kit) in the reply filed on June 6, 2024, was previously acknowledged. With the cancellation of claims 2 - 10, the election of claims 1, 11-22, 25, 27-33, and 38 is made final. Additionally, Applicant’s election without traverse of Species: tumor antigen (claim 19), CD 19 (claims 21 and 22), and CAR (claim 25), was previously acknowledged and is made final.
Claims 23 - 24, 26, and 34 – 37 remain withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to nonelected groups, there being no allowable generic or linking claim.
Accordingly, claims 1, 11-22, 25, 27-33, and 38 are currently under consideration.
Information Disclosure Statement
The information disclosure statements (IDS) filed 9th Jan 2026, 8 Feb 2022, 19 Sept 2022, 7 Aug 2023, and the Third-Party submission filed 17 May 2022 have been considered.
Maintained Claim Interpretation
Regarding claim 1, the term, “ an antimorphic mutation” with respect to Fas is being interpreted as a Fas polypeptide that interacts with a wild-type Fas polypeptide, but blocks its signal transduction to downstream molecules and is the same as “dominant negative” (bridging Pgs. 24-25, specification).
Regarding the sequences disclosed, the following relationship between sequences is understood. Differences highlighted in bold:
1 50
US-17-214-436-12 MLGIWTLLPLVLTSVARLSSKSVNAQVTDINSKGLELRKTVTTVETQNLE
US-17-214-436-14 MLGIWTLLPLVLTSVARLSSKSVNAQVTDINSKGLELRKTVTTVETQNLE
US-17-214-436-10 MLGIWTLLPLVLTSVARLSSKSVNAQVTDINSKGLELRKTVTTVETQNLE
51 100
US-17-214-436-12 GLHHDGQFCHKPCPPGERKARDCTVNGDEPDCVPCQEGKEYTDKAHFSSK
US-17-214-436-14 GLHHDGQFCHKPCPPGERKARDCTVNGDEPDCVPCQEGKEYTDKAHFSSK
US-17-214-436-10 GLHHDGQFCHKPCPPGERKARDCTVNGDEPDCVPCQEGKEYTDKAHFSSK
101 150
US-17-214-436-12 CRRCRLCDEGHGLEVEINCTRTQNTKCRCKPNFFCNSTVCEHCDPCTKCE
US-17-214-436-14 CRRCRLCDEGHGLEVEINCTRTQNTKCRCKPNFFCNSTVCEHCDPCTKCE
US-17-214-436-10 CRRCRLCDEGHGLEVEINCTRTQNTKCRCKPNFFCNSTVCEHCDPCTKCE
151 200
US-17-214-436-12 HGIIKECTLTSNTKCKEEGSRSNLGWLCLLLLPIPLIVWVKRKEVQKTCR
US-17-214-436-14 HGIIKECTLTSNTKCKEEGSRSNLGWLCLLLLPIPLIVWVKRKEVQKTCR
US-17-214-436-10 HGIIKECTLTSNTKCKEEGSRSNLGWLCLLLLPIPLIVWVKRKEVQKTCR
201 250
US-17-214-436-12 KHRKENQGSHESPTLNPETVAINLSDVDLLKDITSDSENSNFRNEIQSLV
US-17-214-436-14 KHRKENQGSHESPTLNPETVAINLSDVDLSKYITTIAGVMTLSQVKGFVR
US-17-214-436-10 KHRKENQGSHESPTLNPETVAINLSDVDLSKYITTIAGVMTLSQVKGFVR
251 300
US-17-214-436-12 ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
US-17-214-436-14 KNGVNEAKIVEIKNDNVQDTAEQKVQLLRNWHQLHGKKEAYDTLIKDLKK
US-17-214-436-10 KNGVNEAKIDEIKNDNVQDTAEQKVQLLRNWHQLHGKKEAYDTLIKDLKK
301 335
US-17-214-436-12 ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
US-17-214-436-14 ANLCTLAEKIQTIILKDITSDSENSNFRNEIQSLV
US-17-214-436-10 ANLCTLAEKIQTIILKDITSDSENSNFRNEIQSLV
Maintained 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.
Claim(s) 1, 11-22, 25, 27-29, 32-33, and 38 remain rejected under 35 U.S.C. 103 as being unpatentable over Pule (GB1810070.1, corresponding to US 20210363217 with a priority filing date: 06/19/2018) in view of Wang (Wang, L., et al. The Fas–FADD death domain complex structure reveals the basis of DISC assembly and disease mutations. Nat Struct Mol Biol 17, 1324–1329 (2010)), as previously discussed and reiterated below.
Regarding claim 1, Pule teaches a cell which comprises:
(i) an engineered intracellular binding polypeptide which is capable of modulating an
intracellular signalling pathway; and
(ii) a chimeric antigen receptor (CAR) or a transgenic T cell receptor (TCR) (Pg. 2, 2nd para).
Pule’s recitation (ii) reads on instant claim 1(a) and Pule recitation (i) broadly reads on instant claim 1(b). Specifically, Pule teaches an embodiment wherein the engineered intracellular binding polypeptide:
(i) reduces or prevents an interaction between its target polypeptide and a second
polypeptide;
(ii) sequesters and/or facilitates degradation of its target polypeptide; or
(iii) activates its target polypeptide (Pule claim 12).
The intracellular signalling pathway in Pule’s claim 1 is an apoptosis, self-renewal, cell survival or cell activation pathway (claim 15). Pule further teaches that various modifications and variations of the described methods and system of the invention will be apparent to those skilled in the art (lines 11-12, Pg. 47).
See comparison of Pule’s invention with instant claim 1:
Pule (GB1810070.1) pg. 2 recitation
Instant Claim 1 recitation
Thus, in a first aspect the present invention provides a cell which comprises:
(i) an engineered intracellular binding polypeptide which is capable of modulating an intracellular signalling pathway; and
(ii) a chimeric antigen receptor (CAR) or a transgenic T cell receptor (TCR).
A cell comprising:
(a) an antigen-recognizing receptor that binds to an antigen, and
(b) a Fas polypeptide comprising an antimorphic mutation that acts antagonistically to a wild type Fas polypeptide wherein the Fas polypeptide comprises the amino acid sequence set forth in SEQ ID NO:12 or SEQ ID NO: 14.
Pule does not name the intracellular binding polypeptide a Fas polypeptide comprising an antimorphic mutation of Fas, but Pule teaches the intracellular binding polypeptide functions by inhibiting /reducing the activity of the pro-apoptotic protein Fas (lines 16-20, Pg. 10); i.e., acts antagonistically to a wild type Fas polypeptide, as recited in the amendment. See following recitation from Pule bridging pgs. 1 and 2:
Thus, the intracellular binding polypeptide may improve the ability of the engineered immune cell to function in a hostile microenvironment by reducing its susceptibility to apoptosis, increasing the level of self-renewal and/or cell survival and/or increasing levels of cell activation (e.g. following antigen binding to a CAR or transgenic TCR).
Thus, Pule teaches an invention that provides a solution to modulate the ability of engineered immune cells to function efficiently in adoptive immunotherapy of cancer by allowing the cell that comprises the engineered polypeptide to reduce its susceptibility to apoptosis (lines 6-7 and 19-24 on Pg. 1 and lines bridging pgs. 1 - 2).
Regarding the limitation wherein the Fas polypeptide comprises the amino acid sequence set forth in SEQ ID NO: 12 or SEQ ID NO: 14 of claim 1, Pule teaches that the Fas protein is human Fas (SEQ ID NO: 7, Uniprot accession number P25445, lines 20-21, Pg. 11). Pule further teaches the sequence of the cytoplasmic domain of Fas (SEQ ID NO: 8). See sequence below of Fas with the sequence of the intracellular (cytoplasmic) domain underlined, both as disclosed by Pule (SEQ ID NO: 7 and 8 respectively):
MLGIWTLLPLVLTSVARLSSKSVNAQVTDINSKGLELRKTVTTVETQNLEGLHHDGQFCHKPCPPGERKARDCTVNGDEPDCVPCQEGKEYTDKAHFSSKCRRCRLCDEGHGLEVEINCTRTQNTKCRCKPNFFCNSTVCEHCDPCTKCEHGIIKECTLTSNTKCKEEGSRSNLGWLCLLLLPIPLIVWVKRKEVQKTCRKHRKENQGSHESPTLNPETVAINLSDVDLSKYITTIAGVMTLSQVKGFVRKNGVNEAKIDEIKNDNVQDTAEQKVQLLRNWHQLHGKKEAYDTLIKDLKKANLCTLAEKIQTIILKDITSDSENSNFRNEIQSLV. This sequence is the same as instant SEQ ID NO: 10 disclosed; i.e., wild-type Fas.
Regarding claim 11, Pule further teaches that the intracellular binding polypeptide enhances cell persistence of the immunoresponsive cell (improve the ability of engineered immune cells to proliferate, survive and/or engraft in a microenvironment; lines 20-23, Pg. 1).
Regarding claim 12, Pule further teaches that the antigen-recognizing receptor is expressed from a vector (lines 1-2, Pg. 31).
Regarding claim 13, Pule further teaches that the exogenous intracellular binding polypeptide is expressed from a vector (lines 24-27, Pg. 37).
Regarding claim 14, Pule further teaches that the cell is an immunoresponsive cell (cytolytic immune Cell, lines 11-12, Pg. 44).
Regarding claims 15 and 16, Pule further teaches that the cell is a cell of the lymphoid lineage like Natural Killer (NK) cell (NK cells, belonging to the group of innate lymphoid cells, lines 19 - 24, Pg. 29).
Regarding claim 17, Pule further teaches that the cell is a T cell (lines 15-16, Pg. 44).
Regarding claim 18, Pule further teaches that the T cell of claim 17 is a cytotoxic T lymphocyte (CTL) cell (Cytolytic T cells (TC cells, or CTLs), line 7, Pg. 29).
Regarding claims 19 and 20, Pule further teaches that the antigen is a tumor antigen (tumour associated antigens (TAA), Table 1 and lines 14-16, Pg. 31).
Regarding claim 21, Pule further teaches that the tumor antigen is selected from a group of antigens that includes CD19 (Table 1, Pg. 31).
Regarding claim 22, Pule further teaches that the antigen is CD19 (Table 1, Pg. 31).
Regarding claim 25, Pule further teaches that the antigen-recognizing receptor is a chimeric antigen receptor (CAR) (lines 24-27, Pg. 37).
Regarding claim 27, Pule further teaches that the CAR comprises an extracellular antigen-binding domain, a transmembrane domain, and an intracellular signaling domain (lines 12-13, Pg. 30).
Regarding claim 28, Pule further teaches that the intracellular signaling domain further comprises at least one co-stimulatory signaling region (comprise additional co-stimulatory signaling, lines 12-13, Pg. 33).
Regarding claim 29, Pule further teaches that the at least one co-stimulatory signaling region comprises a CD28 polypeptide (lines 12-13, Pg. 33).
Regarding claim 32, Pule further teaches a composition comprising an effective amount of a cell of claim 1 (a pharmaceutical composition comprising an engineered cell, lines 5-6, Pg. 38).
Regarding claim 33, Pule further teaches that the composition further comprises a pharmaceutically acceptable excipient (lines 13-14, Pg. 38).
Regarding claim 38, Pule further teaches a kit comprising a cell of claim 1 (lines 26-27, Pg. 34).
Pule does not teach or suggest that the antimorphic Fas polypeptide comprises SEQ ID NO:12 or SEQ ID NO: 14 as recited in claim 1 or how to arrive at such sequences.
However, before the effective filing date of instant application, Wang had taught several mutations within the Fas cytoplasmic (death domain) complex (title, abstract). Wang taught such mutations from autoimmune lymphoproliferative syndrome (ALPS) patients (abstract) and further tested some of these mutations for their function; i.e., abrogation of mutant Fas’s ability to signal apoptosis (Fas mutants engineered to disrupt the Fas–FADD complex also act as dominant negatives, D260V almost completely abrogated apoptosis; line 4 and lines 8-9 below Fig 4, left-side column, Pg. 1328).
e.g., the D260V modification in the cytoplasmic death domain prevents the binding between the dominant negative Fas polypeptide and a FADD polypeptide (Fas mutants engineered to disrupt the Fas–FADD complex also act as dominant negatives, D260V almost completely abrogated apoptosis; line 4 and line 8-9 below Fig 4, left-side column, Pg. 1328). Wang taught that the point mutations in human Fas are structure-based point mutations or mutations obtained from ALPS patients (Fig. 2b, and Fig. 2b legend). The location of the point mutation disclosed by Wang (line 8 below Fig 4, left-side column, Pg. 1328) is bolded in Pule’s sequence above. Wang further teaches the sequence of the death domain of Fas (Fig. 2b, and Fig. 2b legend). By alignment, this position of the sequence is identical to instant sequence. Wang further teaches that the dominant negative Fas polypeptide comprises a point mutation at position 260 of a human Fas consisting of the amino acid sequence set forth in instant SEQ ID NO: 10 (Fas mutants engineered to disrupt the Fas–FADD complex also act as dominant negatives, lines 4 and 8 below Fig 4, left-side column, Pg. 1328).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention, seeking long-lived immunoresponsive cell in vivo for adoptive immunotherapy (a goal of Pule), to combine the teachings of Wang with the teachings of Pule because Wang provides the teachings to make an antimorphic mutant of Fas and Pule provides the motivation to seek out peptides that will abrogate Fas-mediated apoptotic signaling (among other teachings) in therapeutic approaches. It would have been prima facie obvious for the skilled artisan to follow the teachings of Wang and make modifications in the cytoplasmic domain of Fas because of the known benefit of such modifications taught by Wang. Thus, given the teachings of the cited references and the level of skill of the ordinary skilled artisan, one of ordinary skill in the art would have been motivated to modify the cytoplasmic domain of Pule as taught by Wang. One of ordinary skill in the art would have reasonable expectation of success because both references focus on the intracellular binding polypeptide of Fas as essential to making an antimorphic Fas. See MPEP 2143 I (G).
Thus, one of ordinary skill in the art seeking to modify human Fas, would take the sequence of human Fas taught by Pule (SEQ ID NO: 7 and 8 combined), and modify the amino acid at position 260 because Wang teaches that a D260V mutation at this position abrogates apoptosis. By alignment, it is seen that modifying a D to a V in combined SEQ ID NO: 7 and 8 of Pule one would obtain the sequence of SEQ ID NO: 14 as shown here:
In the alignment above, Qy is combination of SEQ ID NO: 7 and 8 of Pule) and Db is SEQ ID NO: 14 of the instant application the boxed region is the position indicated by Wang (D260V) as being responsible for abrogating apoptosis.
Thus, one would obtain the cell of claim 1, wherein the dominant negative Fas polypeptide comprises the amino acid sequence set forth in SEQ ID NO: 14, as recited.
SEQ ID NO: 12 is not considered here because it has been recited as being optional; i.e., or.
Thus, Pule in view of Wang make obvious instant claims 1, 11-22, 25, 27-29, 32-33, and 38.
Claims 30 and 31 remain rejected under 35 U.S.C. 103 as being unpatentable over Pule (GB1810070.1, filing date: 06/19/2018) and Wang (Wang, L., et al. The Fas–FADD death domain complex structure reveals the basis of DISC assembly and disease mutations. Nat Struct Mol Biol 17, 1324–1329 (2010)) as applied to claims 1, 11-22, 25, 27-29, 32-33, and 38 above, and in view of Adusumilli (US 20180273601, published 2018-09-27), as previously discussed and reiterated below.
Regarding claims 30 and 31, the cell of claim 1 is discussed above.
Pule does not teach or suggest that the cell further comprises a suicide gene and the suicide gene is inducible Caspase 9 Suicide gene.
However, Adusumilli teaches immune cells which (a) recombinantly express a chimeric antigen receptor (CAR), and a dominant negative form of an inhibitor of a cell mediated immune response of the immune cell, and (b) an exogenous dominant negative immune checkpoint polypeptide (paragraph (0014]) as a means of improved adoptive immunotherapy (paragraph [0218]). Adusumilli also teaches that further modifications can be introduced to the immune cells of the invention such as, the cells can be modified to address immunological complications and/or targeting by the CAR to healthy tissues that express the same target antigens as the tumor cells. For example, a suicide gene can be introduced into the cells to provide for depletion of the cells when desired (paragraph [0079]) and thus eliminate any undesired effects of an engineered adoptive immune cell. Adusumilli further teaches a specific embodiment wherein the suicide gene is an inducible Caspase 9 Suicide gene (last line of paragraph [0015]).
It would have been obvious to one of ordinary skill in the art, seeking long-lived immunoresponsive cell in vivo for adoptive immunotherapy (a goal of Pule), to combine the teachings of Adusumilli with the teachings of Pule because Adusumilli provide the teachings to deplete rogue immunoresponsive cells and Pule seek to use engineered immunoresponsive cells in therapeutic approaches. It would have been prima facie obvious for the skilled artisan to follow the teachings of Adusumilli and make further modifications in the immunoresponsive cell of Pule because of the known benefit of such modifications disclosed by Adusumilli. Thus, given the teachings of the cited references and the level of skill of the ordinary skilled artisan, one of ordinary skill in the art would have been motivated to combine prior art elements according to known methods to yield predictable results (introduce the suicide gene of Adusumilli into the engineered immunoresponsive cell of Pule). See MPEP 2143 I.(A) and (G).
Thus, Pule and Wang in view of Adusumilli make obvious instant claims 30 and 31.
Therefore the invention as a whole would have been prima facie obvious to one ordinary skill in the art before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains.
Response to Arguments
Applicant’s arguments, see Pgs. 5 - 7, filed 7-02-2026, with respect to rejections under 35 USC § 103 have been fully considered but they are not persuasive for the reasons discussed below.
First, see Pg. 5, Applicant summarizes the USC § 103 rejection presented in the Final Office Action (FOA). Then, Applicant cites case law of Univ. of Strathclyde v. Clear-Vu Lighting LLC, 17 F.4th 155, 160 (Fed. Cir. 2021., to argue that Examiner has not satisfied the burden of demonstrating motivation to modify Pule’s teachings with Wang to arrive at the claimed invention.
Next, Applicants state in Pgs. 6-7:
1) the primary reference of Pule requires the use of an intracellular binding polypeptide to bind to a target (Fas) to inhibit its pro-apoptotic role. Accordingly, Wang's dominant negative polypeptide (comprising a point mutation) could not substitute in for an intracellular binding polypeptide.
Next, Applicants state in Pgs. 7:
2) unexpected results are seen in T cells modified with Fas DNR exhibited enhanced survival relative to control - modified T cells as late as 6 months following transfer; and provide citation to para [0280] of specification.
Applicants arguments are not persuasive because:
Obviousness rejection requires at first: 1. Determining the scope and contents of the prior art.
In this regard, and regarding argument 1), Pule had taught the need to engineer immune cells such that it has reduced susceptibility to apoptosis, increased the level of self-renewal and/or cell survival and/or increased levels of cell activation (summary). A means to achieve that was an engineered intracellular binding polypeptide which is capable of modulating an intracellular signalling pathway. One signalling pathway taught by Pule is FAS/FADD (DISC) mediated pro-apoptotic signalling (Figure 3).
Thus, Pule suggest abrogating the apoptotic function of Fas within the context of an immune cell.
The secondary reference of Wang teaches a dominant negative mutation in Fas (D260V) that achieves the function Pule is hoping to achieve with their intracellular peptide.
The second requirement in an obviousness rejection is: 2. Ascertaining the differences between the prior art and the claims at issue.
The combination of the two references discussed then eliminates any difference between instant application and the combination of references because as per the third requirement in an obviousness rejection: 3. Level of skill of the ordinary artisan, the ordinary skilled artisan knows that a peptide that abrogates apoptosis caused by Fas may be substituted with a dominant negative/antimorphic mutation in Fas itself. Thus the principle of operation of Pule's long-lasting immune cell is improved upon by a dominant negative/antimorphic mutation provided by Wang. Any or all of taught embodiments or components in the prior art are available for further consideration by skilled artisans as they see fit. See MPEP 2114 II.
Regarding 2), unexpected results, "To be particularly probative, evidence of unexpected results must establish that there is a difference between the results obtained and those of the closest prior art, and that the difference would not have been expected by one of ordinary skill in the art at the time of the invention." Bristol-Myers Squibb Co. v. Teva Pharm. USA, Inc., 752 F.3d 967, 977 (Fed. Cir. 2014).
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." (emphasis added). See MPEP §716.02. "It is not enough to show that results are obtained which differ from those obtained in the prior art: that difference must be shown to be an unexpected difference". ( original emphasis). In re Klosak, 455 F.2d 1077, 1080 (CCPA 1972).
Applicants cite to a paragraph that states > “6 months” survival. However, without any numbers of sample size, it is impossible to compare this metric with the prior art. Since the references used in instant rejection do not show enhanced survival relative to control (not studied), we turn to the art of Shannon as cited in the prior art section, for use as the closest prior art.
Shannon teaches T cells expressing Fas-4-1BB fusion proteins improve survival of T cells (Fig. 24 B). See comparison of instant survival on the left and that demonstrated by Shannon on the right.
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Since no unexpectedly superior results are seen in instant study compared to the prior art, Applicants arguments are not dispositive.
In view of the foregoing, the rejection of claim 1 over Pule in view of Wang is maintained.
Withdrawn Double Patenting
The nonstatutory double patenting rejection of claims 1, 11-22, 25, 27-33, and 38 as being unpatentable over copending Application No. US 17/858,320, corresponding to US 20230058774 (referred to as ‘320) has been withdrawn on account of amendments made to the copending application.
Maintained Relevant Prior Art
Shannon (WO 2018/170475 Al , of record as 3rd party IDS submission) teach immunomodulatory fusion proteins containing an extracellular binding domain and an intracellular signaling domain, wherein binding of a target can generate a modulatory signal in a host cell, such as a T cell (abstract). On pg. 8, last para, an embodiment is presented wherein the extracellular component comprises an extracellular portion of a CD95 (Fas) and the intracellular portion is another protein. On pg. 41, Shannon disclose: For example, dominant negative fusion proteins are included within the scope of the disclosure. Example 25 shows immunotherapy with T cells expressing Fas-4-1BB fusion proteins improve survival.
Conclusion
No claims are allowed.
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.
Correspondence
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SHABANA MEYERING, Ph.D. whose telephone number is (703)756-4603. The examiner can normally be reached M - F: 9am to 5pm EST.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Ram Shukla can be reached on (571) 272-0735. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/SHABANA S MEYERING/Examiner, Art Unit 1635
/RAM R SHUKLA/Supervisory Patent Examiner, Art Unit 1635
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