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 .
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 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.
Priority
The instant application, filed 03/14/2023, is a 371 filing of PCT/CN2021/121535, filed 09/29/2021, and claims foreign priority to PCT/CN2020/118988, filed 09/29/2020.
Status of Application, Amendments, and/or Claims
Applicant’s response of 01/07/2026 is acknowledged. Claims 1, 3-5, 9-10, 17, 34, and 65 are amended and claims 2, 6-8, 11-16, 18-33, 36-64, and 67-70 are cancelled. Claims 1, 3-5, 9-10, 17, 34-35, and 65-66 are currently pending and are examined on the merits herein.
Withdrawn Objections and Rejections
In the office action of 10/17/2025,
Claims 38 and 65-66 were rejected under 35 USC 112(b). The cancellation of claim 38 has rendered the rejections moot and the rejections are withdrawn.
Claim 23 was rejected under 35 USC 112(d). The cancellation of the claim has rendered the rejection moot and the rejection is withdrawn.
Claims 2, 34-35, 38, and 65-66 were rejected under 35 USC 112(a). The cancellation of claims 2 and 38 and amendment to claim 34 to remove limitation (b) has overcome the rejections and the rejections are withdrawn.
Claim 23 was rejected under 35 USC 112(a). The cancellation of the claim has rendered the rejection moot and the rejection is withdrawn.
Claims 1-5, 9-10, 34-35, 38, and 65-66 were rejected under 35 USC 102 (a)(1) as being anticipated by Kuhn. Applicant’s amendment to independent claim 1 to require that the domain comprise both a LTα and LTβ or variants thereof has overcome the rejections and the rejections are withdrawn.
Claims 1-5, 9-10, 34-35, 38, and 65-66 were rejected under 35 USC 102 (a)(1) as being anticipated by WO’346. Applicant’s amendment to independent claim 1 to require that the domain comprise both a LTα and LTβ or variants thereof has overcome the rejections and the rejections are withdrawn.
Claims 1-5, 9-10, 25, and 34-35 were rejected under 35 USC 102 (a)(1) as being anticipated by WO’395. Applicant’s amendment to independent claim 1 to require that the domain comprise both a LTα and LTβ or variants thereof has overcome the rejections and the rejections are withdrawn.
Claims 1, 10, 21, and 23 were rejected under 35 USC 103 over Kuhn in view of WO’644 and US’023. Applicant’s amendment to independent claim 1 to require that the domain comprise both a LTα and LTβ or variants thereof has overcome the rejections and the rejections are withdrawn.
Claims 1, 10, 18 and 20 were rejected under 35 USC 103 over WO’346 in view of Harrop. Applicant’s amendment to independent claim 1 to require that the domain comprise both a LTα and LTβ or variants thereof has overcome the rejections and the rejections are withdrawn.
Claims 1, 25, and 27 were rejected under 35 USC 103 over WO’395 in view of WO’981. Applicant’s amendment to independent claim 1 to require that the domain comprise both a LTα and LTβ or variants thereof has overcome the rejections and the rejections are withdrawn.
The following grounds of rejections are new or modified as necessitated by applicant’s amendment to the claims.
Nucleotide and/or Amino Acid Sequence Disclosures
The instant specification recites the following sequences without accompanying SEQ ID NOs:
Page 44, [00152] and pages 102-103, [0331]: (GSGGS)n, (GGGS)n, and (GGGGS)n
REQUIREMENTS FOR PATENT APPLICATIONS CONTAINING NUCLEOTIDE AND/OR AMINO ACID SEQUENCE DISCLOSURES
Items 1) and 2) provide general guidance related to requirements for sequence disclosures.
37 CFR 1.821(c) requires that patent applications which contain disclosures of nucleotide and/or amino acid sequences that fall within the definitions of 37 CFR 1.821(a) must contain a "Sequence Listing," as a separate part of the disclosure, which presents the nucleotide and/or amino acid sequences and associated information using the symbols and format in accordance with the requirements of 37 CFR 1.821 - 1.825. This "Sequence Listing" part of the disclosure may be submitted:
In accordance with 37 CFR 1.821(c)(1) via the USPTO patent electronic filing system (see Section I.1 of the Legal Framework for Patent Electronic System (https://www.uspto.gov/PatentLegalFramework), hereinafter "Legal Framework") as an ASCII text file, together with an incorporation-by-reference of the material in the ASCII text file in a separate paragraph of the specification as required by 37 CFR 1.823(b)(1) identifying:
the name of the ASCII text file;
ii) the date of creation; and
iii) the size of the ASCII text file in bytes;
In accordance with 37 CFR 1.821(c)(1) on read-only optical disc(s) as permitted by 37 CFR 1.52(e)(1)(ii), labeled according to 37 CFR 1.52(e)(5), with an incorporation-by-reference of the material in the ASCII text file according to 37 CFR 1.52(e)(8) and 37 CFR 1.823(b)(1) in a separate paragraph of the specification identifying:
the name of the ASCII text file;
the date of creation; and
the size of the ASCII text file in bytes;
In accordance with 37 CFR 1.821(c)(2) via the USPTO patent electronic filing system as a PDF file (not recommended); or
In accordance with 37 CFR 1.821(c)(3) on physical sheets of paper (not recommended).
When a “Sequence Listing” has been submitted as a PDF file as in 1(c) above (37 CFR 1.821(c)(2)) or on physical sheets of paper as in 1(d) above (37 CFR 1.821(c)(3)), 37 CFR 1.821(e)(1) requires a computer readable form (CRF) of the “Sequence Listing” in accordance with the requirements of 37 CFR 1.824.
If the "Sequence Listing" required by 37 CFR 1.821(c) is filed via the USPTO patent electronic filing system as a PDF, then 37 CFR 1.821(e)(1)(ii) or 1.821(e)(2)(ii) requires submission of a statement that the "Sequence Listing" content of the PDF copy and the CRF copy (the ASCII text file copy) are identical.
If the "Sequence Listing" required by 37 CFR 1.821(c) is filed on paper or read-only optical disc, then 37 CFR 1.821(e)(1)(ii) or 1.821(e)(2)(ii) requires submission of a statement that the "Sequence Listing" content of the paper or read-only optical disc copy and the CRF are identical.
Specific deficiencies and the required response to this Office Action are as follows:
Specific deficiency – Nucleotide and/or amino acid sequences appearing in the specification are not identified by sequence identifiers in accordance with 37 CFR 1.821(d).
Required response – Applicant must provide:
A substitute specification in compliance with 37 CFR 1.52, 1.121(b)(3) and 1.125 inserting the required sequence identifiers, consisting of:
A copy of the previously-submitted specification, with deletions shown with strikethrough or brackets and insertions shown with underlining (marked-up version);
A copy of the amended specification without markings (clean version); and
A statement that the substitute specification contains no new matter.
Claim Rejections - 35 USC § 112(d)
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.
Claims 9-10 are 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.
Claims 9 and 10 depend on the CAR-T cell of claim 1 and recite that the second antigen is a receptor or ligand expressed on the cell that can interact with the T cell and that the second antigen is selected from the recited group, respectively. As amended, claim 1 recites that the domain that is capable of binding to a second antigen comprises both LTα or a variant thereof and LTβ or a variant thereof.
As claim 1 already requires the domain to be LTα and LTβ or a variants thereof, which inherently bind a receptor, the recitation of claim 9 does not further limit the claim upon which it depend. Additionally, because claim 9 also encompasses an embodiment in which the second antigen is a ligand, the claim is also broader than the claim upon which it depends.
Claim 10 recites that the second antigen is selected from the group recited. Claim 1 requires that the domain that is capable of binding to the second antigen be LTα and LTβ. LTα and LTβ, however, do not bind to all of the ligands/receptors recited in claim 10. As claim 10 encompasses additional second antigens to which the second domain can be capable of binding, claim 10 is broader than the claim upon which it depends. It is also noted that the receptor to which LTα and LTβ bind is inherent to the structure of LTα and LTβ and, as such, the embodiment in which the second antigen is LTβR fails to limit the claim upon which it depends.
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.
Claim Rejections - 35 USC § 103
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, 3-5, 9-10, 17, 34-35, and 65-66 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2020/097346 A1 (McGinnes, K., et al) 14 May 2020.
WO’346 teaches strategies to co-express a co-stimulatory polypeptide and an anti-GPC3 chimeric antigen receptor (CAR) for use in cell-based immunotherapy. Modulation of costimulatory pathways may be achieved by expressing, or overexpressing, in hematopoietic cells, including hematopoietic stem cells or immune cells such as T cells or NK cells, one or more costimulatory polypeptides. In some instances, hematopoietic cells that co-express one or more co-stimulatory polypeptides and an anti-GPC3 CAR would be expected to exhibit superior bioactivities, for example, cell proliferation, activation, e.g., increased cytokine production, e.g., IL-2 or IFN-γ production, cytotoxicity, and/or in vivo anti-tumor activity (page 1, line 32 – page 2, line 7).
WO’346 demonstrates that expressing tumor necrosis factor (TNF) superfamily costimulatory peptides CD70, LIGHT, and OX40L in T cells in combination with an anti-GPC3 CAR with a 4-1BB costimulatory domain enhances the activity of the T cell relative to anti-GPC3 CAR alone. In the presented experiments, T cells were transduced with virus encoding an anti-GPC3 CAR polypeptide with a 41BB costimulatory domain (GPC3-CAR-4-1BB; SEQ ID NO: 1) or virus encoding GPC3-CAR-4-1BB and CD70 (SEQ ID NO: 34), LIGHT (SEQ ID NO: 43), or OX40L (SEQ ID NO: 47) separated by a P2A ribosomal skip sequence (page 73, lines 14-21). WO’346 further teaches that LIGHT is also known as HVEML and is ligand of HVEM (page 19, lines 20-37).
WO’346 further discloses that the CAR comprises a CD8α signal sequence, an extracellular antigen binding domain that binds GCP3, a CD8 hinge domain, a CD8 transmembrane domain, and an intracellular domain comprising a 4-1BB costimulatory domain and a CD3ζ cytoplasmic signaling domain (page 44, Table 1 – line 13).
WO’346 tested T cells co-expressing the anti-GPC3 CAR with a 4-1BB costimulatory domain and TNF superfamily member polypeptides CD70, LIGHT, or OX40L in tumor xenograft models in mice and demonstrated enhanced activity (page 78, Example 8). WO’346 studied subcutaneous human hepatocellular carcinoma (HCC) xenograft models established mice. The xenografts were established by subcutaneous injection of Hep G2, Hep 3b, or JHH7 HCC cells. Treatment with GPC3 CAR-T cells was initiated when tumor volumes reached approximately 100 mm3 Mice were randomized into treatment groups of 5 mice each, based on tumor volume, and treated with T cells expressing the GPC3 CAR alone or in combination with CD70, LIGHT, or OX40L at a dose of 5x105 CAR+ cells intravenously (pages 78-79, Example 8). As WO’346 teaches the administration of the CAR+ T cells to mice, the T cells would have necessarily had to been in the form of a composition comprising pharmaceutically acceptable excipient, such as a vehicle.
WO’346 further teaches alternative co-stimulatory polypeptides and teaches that the co-stimulatory polypeptide can be a member of the B7/CD28 superfamily, a member of the TNF superfamily, or a ligand thereof (page 88, claim 1). WO’346 further teaches that the co-stimulatory peptide is a member of the B7/CD28 superfamily or ligands thereof selected from a group that includes CD28, CD80, CD86, ICOS, ICOSL, B7-H3, and B7-H4 (page 88, claim 3). WO’346 further teaches that the co-stimulatory polypeptide can be a member of the TNF superfamily or a ligand thereof, selected from a group including 4-1BB, 4-1BBL, CD27, CD30, CD30L, CD40, CD40L, GITR, GITRL, HVEM, LIGHT, OX40, OX40L, and LTβR (page 88, claim 3).
WO’346 further teaches that the costimulatory polypeptide may include members of the TNF superfamily or ligands thereof, including TNF-beta, which is LTα, and LTβ (page 2, line 22; page 10, line 30 – page 11, line 8; page 38, line 14).
WO’346 teaches that LTα (TNF-beta) is a member of the TNF superfamily involved in the regulation of cell survival, proliferation, differentiation, and apoptosis. The amino acid sequence of an exemplary human TNF-beta is provided as SEQ ID NO: 45 (page 20, lines 19-26), which is identical to instant SEQ ID NO: 7, as shown in the alignment below:
PNG
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288
588
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Greyscale
WO’346 teaches that LTβ has a sequence of SEQ ID NO: 66 (page 27, lines 36-41), which is identical to instant SEQ ID NO: 10 as shown in the ABSS alignment below:
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346
581
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Greyscale
WO’346 further teaches that LTBR, or TNFRSF3, is a cell surface receptor that binds to the lymphotoxin membrane form which is a complex of LTα and LTβ. It plays a role in apoptosis, lipid metabolism, and the development and organization of lymphoid tissue and transformed cells (page 23, lines 25-29). WO’346 teaches that LTα and LTβ form heterotrimers which anchor LTα to the cell surface, is involved in the formation of secondary lymphoid organs, and mediates a large variety of inflammatory, immunostimulatory, and antiviral responses (page 27, lines 29-34).
While WO’346 does not exemplify a CAR-T cell comprising LTα and LTβ, it would have been prima facie obvious to one of ordinary skill in the art prior to the effective filing date of the claimed invention to use LTα and LTβ as the co-stimulatory polypeptides in the CAR-T cells disclosed by WO’346 based on the teachings of WO’346 as a whole. It would have been obvious to use LTα and LTβ as WO’346 teaches the ligands for use as co-stimulatory polypeptides in CAR T cells and teaches that LTα and LTβ form a complex that interacts with the cell surface receptor LTBR and plays a role in apoptosis, lipid metabolism, the development and organization of lymphoid tissues, transformation of cells, and mediates a large variety of inflammatory and immunostimulatory responses. An ordinarily skilled artisan would have had a reasonable expectation of success as WO’346 explicitly discloses the use of LTα and LTβ for use as co-stimulatory polypeptides in CAR-T cells.
This conclusion of obviousness is further supported by KSR (E) obvious to try. In this case, WO’346 teaches a finite number of co-stimulatory polypeptides for inclusion in CAR-T cells including LTα and LTβ. As such, one of ordinary skill in the art could have pursued these known, potential solutions, with a reasonable expectation of success. See MPEP 2143.
While WO’346 does not explicitly disclose that the LTα and LTβ polypeptides in the CAR T cells are capable of binding to a second antigen expressed on the surface of a cell that can interact with a T cell as recited in claim 1, or the limitations recited in claim 3-5 and 9, the LTα and LTβ polypeptides are capable of performing the functions as claimed as evidenced by the instant disclosure and; therefore, meet the recited limitations.
Additionally, the claimed functions are inherent properties of the LTα and LTβ polypeptides expressed in the CAR T cells disclosed by WO’346.
MPEP 2112 (I) states that "[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. IRECO Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). MPEP 2112 (II) states that there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the time of invention, but only that the subject matter is in fact inherent in the prior art reference. Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003).
Response to Arguments
Applicant’s arguments in the response filed 01/07/2026 have been fully considered in so far as they apply to the rejections of the instant office action, but were not persuasive.
With regards to WO’346, referenced by applicant in the response as “McGinness”, applicant argues that there was no motivation to substitute the CD70, LIGHT, or OX40L in the constructs of WO’346. Applicant further argues that in table 2, WO’346 discloses that co-expressing certain costimulatory polypeptides will lead to either enhanced or reduced IL-2 secretion and proliferation of CAR-T cells. Applicant argues that, therefore, without any testing data on LTα and LTβ domains, a person of ordinary skill in the art would not have been motivated to substitute CD70, LIGHT, or OX40L in the constructs tested with LTα and LTβ domains with a reasonable expectation of success.
These arguments, however, are not persuasive.
Explicit motivation in the prior art is not required in order establish a prima facie case of obviousness. MPEP 2143 provides 7 exemplary rationales that may be used to support a conclusion of obviousness, KSR (A)-(G), only one of which requires that there be some teaching, suggestion, or motivation in the prior art.
In the instant office action, the conclusion of obviousness is supported by specific teachings of WO’346 as well as KSR(E) obvious to try, a rationale that does not require explicit motivation in the art in order to establish a prima facie case of obviousness. See MPEP 2143. As discussed in the rejection of the instant office action, WO’346 teaches a finite number of costimulatory polypeptides for inclusion in CAR-T cells including LTα and LTβ polypeptides. As such, it would have been obvious for an ordinarily skilled artisan to pursue these costimulatory polypeptides with a reasonable expectation of success.
Furthermore, even if WO’346 does not provide testing data using LTα and LTβ polypeptides, conclusive proof of efficacy is not required in order to establish obviousness, for which the requirement is a reasonable expectation of success. MPEP 2143.02 (I) states that “conclusive proof of efficacy is not required to show a reasonable expectation of success” and reasoning that "the expectation of success need only be reasonable, not absolute”.
Regarding the results presented by WO’346 Table 2, while the results do demonstrate varying IL-2 and proliferation activity using different costimulatory polypeptides with different CARs, such teachings do not criticize, discredit, or otherwise discourage the use of LTα and LTβ polypeptides as co-stimulatory polypeptides for use with CAR-T cells. Additionally, even if different CAR T cells respond differently to the inclusion of different costimulatory polypeptides, the instant claims do not require any specific CAR nor do the instant claims require any specific outcomes aside from the general treatment of a disease or disorder. As such, it would have been obvious to try the co-stimulatory polypeptides disclosed by WO’346 in a given CAR T cell with a reasonable expectation of success.
Applicant argues that the inventors of the instant application extensively tested LTα/β and show that the domain works better than LIGHT citing examples 4-5.
Examples 4-5 of the instant specification studied CAR T cells armored with LTα/β and/or LIGHT in vivo. In the example, CARs targeting GPC2 protein were tested. While the examples do not clarify the structure of the CAR, it appears that the CAR comprised an anti-GPC2 sdAb, a 4-1BB costimulatory domain and a CD3z intracellular signaling domain.
Example 4 discloses that, while proliferation in peripheral blood was comparable between LTα/β and LIGHT armored CAR T cells, a notable difference was observed between the two TALEs, as shown in Fig. 6 (page 128, [0402]). The example concludes that CAR T cells armored with LTα/β or LIGHT TALEs can strikingly boost in vivo proliferation in both peripheral blood, organs, and tumors (page 128, [00403]). Fig. 6 shows that the average proliferation in the tumor is higher in LTα/β compared to LIGHT expressing CAR T cells, however, it is noted that there is overlap in the results and, on average, both perform better than control CAR T cells without the added costimulatory domain.
Example 5 demonstrates that CAR-T cells armored with LTα/β and/or light showed superior anti-tumor efficacy compared to conventional CAR-T cells. The example also discloses that CAR-T cells armored with LIGHT showed partial efficacy in 2/4 (50%) of mice while LTα/β showed efficacy in 4/4 (100%) of mice (page 128-129).
Example 6 discloses that CAR T cells armored with LTα/β and/or LIGHT are well tolerated in vivo (page 129).
The examples presented by applicant demonstrate that the inclusion of either LTα/β or LIGHT in the anti-GPC2 CAR T cells tested improved efficacy and were well tolerated. While the examples suggest that LTα/β may be more effective with the particular CAR T cells tested compared to LIGHT, MPEP 716.02 states that “A difference of degree is not as persuasive as a difference in kind – i.e., if the range produces ‘"a new property dissimilar to the known property,’" rather than producing a predictable result but to an unexpected extent.”
Furthermore, even if the results were unexpected, the studies and results are not commensurate with the entire scope of the instantly claimed invention.
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." In other words, the showing of unexpected results must be reviewed to see if the results occur over the entire claimed range.”
The instantly claimed invention encompasses a CAR T cell comprising a CAR with an extracellular binding domain capable of binding to any antigen, any transmembrane domain, and any intracellular domain. Additionally, based on the use of “comprising” language in the claim, the CAR may also encompass any additional structures including any costimulatory domain within the CAR structure. The examples of the instant disclosure, however, only demonstrate and compare the use of the LTα/β with LIGHT with a specific anti-GPC2 CAR T cell. As discussed by applicant in the response, Table 2 presented by WO’346 suggests that the CAR T cell used with the co-stimulatory polypeptide, particularly the costimulatory domain in the CAR T cells, may impact the efficacy of the co-stimulatory polypeptide. For instance, applicant points to CD40L in table 2. When the domain was included in a CAR with a 4-1BB costimulatory domain, IL-2 and proliferation were lower than when the domain was used in a CAR with a CD28 costimulatory domain, indicating that efficacy of the CAR T cell is not only impacted by the costimulatory polypeptide that is included, but also by the structure of the CAR.
Additionally, the instant claims encompass the treatment of any disease or disorder in a subject; however, the examples referenced demonstrate improved anti-tumor activity in a single neuroblastoma tumor model (Examples 4-5, pages 126-127). The examples do not demonstrate that such results would occur over the entire scope of the claimed invention in which any disease or disorder is treated.
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 extension fee 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to AUDREY L BUTTICE whose telephone number is (571)270-5049. The examiner can normally be reached M-Th 8:00-4:00.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Joanne Hama can be reached on 571-272-2911. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/AUDREY L BUTTICE/Examiner, Art Unit 1647
/SCARLETT Y GOON/Supervisory Patent Examiner
Art Unit 1693