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 .
Claims 17-20, 22-24, 26-27, 29-33, 37-38, and 40-44, of record 10/28/2025, are pending and subject to prosecution. Claims 17-18, 20, 22-24, 26-27, 32-33, and 37 are amended. Claims 21, 34-36, and 39 are cancelled. Claims 40-44 are newly added.
Declaration of Dr. Todo
A declaration under 37 CFR 1.132 was submitted on 10/28/2025 as part of the response.
The declaration asserts unexpected results in the form of reduced bevacizumab concentration in serum and increased intratumoral administration of bevacizumab through intratumoral administration of the claimed virus as compared to the systemic administration of bevacizumab taught by Karrasch et al. (Declaration, page 2-5). Lower levels of bevacizumab in serum is believed to reduce the risk of side effects from therapy (Declaration, page 5-6).
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). See MPEP 716.02. While the data in fig. A-1, A-2, B-1, and B-2 clearly show higher intratumoral and lower serum concentrations of bevacizumab with administration of the claimed virus versus systemic bevacizumab administration, these results are not unexpected. Armed oncolytic viruses have been rationally designed in order to selectively express anti-cancer agents within tumors and minimize systemic effects (See Seymour et al., page 360, col. 2, ¶1 and fig. 2). Further, Liikanen et al. demonstrated that an oncolytic adenovirus expressing trastuzumab produced significantly higher intratumoral and lower blood levels of the antibody versus systemic trastuzumab administration (See fig. 4B-D). One of ordinary skill in the art could therefore reasonably expect other oncolytic virus-encoded antibodies, such as HSV-encoded bevacizumab, to show similar results due to the shared tropism and action of these viruses.
Status of Prior Rejections/Response to Arguments
RE: Objection to claims 17, 24, and 39:
The cancellation of claim 39 renders the rejection thereto moot.
The amendment to claims 17 and 24 are effective to obviate the objection. The objection is withdrawn.
RE: Rejection of claims 17-24, 26-27, and 29-39 under 35 U.S.C. 112(b):
The cancellation of claims 21, 34-36, and 39 renders the rejection thereto moot.
The amendment to claim 17 is effective to obviate the rejection. The rejection is withdrawn.
RE: Rejection of claims 17, 19-24, 27, 29-30, 32, and 34 under 35 U.S.C. 103 over Karrasch et al. (US 20090317456 A1) in view of de Gruijl et al. (Expert Opinion on Biological Therapy, 2015), Todo (Cell Adhesion & Migration, 2008), and Armstrong et al. (US 2013309226 A1):
RE: Rejection of claims 17-24, 27, 29-30, and 32-34 under 35 U.S.C. 103 over Karrasch et al. (US 20090317456 A1) in view of de Gruijl et al. (Expert Opinion on Biological Therapy, 2015), Todo (Cell Adhesion & Migration, 2008), and Armstrong et al. (US 2013309226 A1), further in view of Hawkins-Daarud et al. (Frontiers in Oncology, 2013):
RE: Rejection of claims 17, 19-24, 26-27, 29-30, 32, and 34 under 35 U.S.C. 103 over Karrasch et al. (US 20090317456 A1) in view of de Gruijl et al. (Expert Opinion on Biological Therapy, 2015), Todo (Cell Adhesion & Migration, 2008), and Armstrong et al. (US 2013309226 A1, further in view of Goins et al. (Cold Spring Harbor Protocols, 2011):
RE: Rejection of claims 17, 19-24, 27, 29-32, and 34 under 35 U.S.C. 103 over Karrasch et al. (US 20090317456 A1) in view of de Gruijl et al. (Expert Opinion on Biological Therapy, 2015), Todo (Cell Adhesion & Migration, 2008), and Armstrong et al. (US 2013309226 A1), further in view of Markert et al. (Molecular Therapy, 2009):
RE: Rejection of claims 17, 19-24, 27, 29-30, 32, 34, and 39 under 35 U.S.C. 103 over Karrasch et al. (US 20090317456 A1) in view of de Gruijl et al. (Expert Opinion on Biological Therapy, 2015), Todo (Cell Adhesion & Migration, 2008), and Armstrong et al. (US 2013309226 A1), further in view of He et al. (Thrombosis Research, 2011):
RE: Rejection of claims 17, 19-20, 27, 29-30, 32, and 36 under 35 U.S.C. 103 over Karrasch et al. (US 20090317456 A1) in view of Todo (Cell Adhesion & Migration, 2008) and Hauswirth et al. (US 20060193830 A1):
The cancellation of claims 21, 34-36, and 39 renders the rejections thereto moot.
The applicant asserts that the prior art references do not teach or suggest the unexpected results of increased intratumoral concentration and decreased serum concentration of bevacizumab when administered via the claimed virus versus systemically (Applicant Remarks, page 9-11 and Declaration, page 2-6).
This argument is not found persuasive for the reasons stated above with regard to the Declaration. The rejections are maintained in modified form to address the amendments to the claims.
New/Maintained Objections/Rejections
Claim 37 is objected to because of the following informalities:
In line 3 of claim 37, the word “sequence” should be inserted after “polynucleotide”.
Appropriate correction is required.
Claim Interpretation
Claim 17 recites the limitation “(a) a DNA encoding a polypeptide constituting an antibody heavy chain that comprises an amino acid sequence of SEQ ID NO: 30… wherein the two DNAs of (a) together encode the heavy and light chains of an antivascular endothelial cell growth factor… antibody”. While the phrase “an amino acid sequence of SEQ ID NO: 30” reads on any sequence comprising two or more contiguous amino acids present in instant SEQ ID NO 30, the claim is interpreted as requiring a sequence derived from SEQ ID NO 30 that is long enough to be recognizable as and to function as an anti-VEGF antibody heavy chain.
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.
Claims 17, 19-20, 22-24, 27, 29-30, and 32 are rejected under 35 U.S.C. 103 as being unpatentable over Karrasch et al. (US 20090317456 A1), of record, in view of de Gruijl et al. (Expert Opinion on Biological Therapy, 2015), of record ,Todo (Cell Adhesion & Migration, 2008), of record, and Armstrong et al. (US 2013309226 A1), of record.
Regarding claims 17, 19-20, 22-24, and 27: Karrasch et al. teach the combined administration of an oncolytic virus and an antiangiogenic agent for treating cancer (See Abstract). The virus is preferably HSV-1 or HSV-2 (which read on “oncolytic herpes simplex virus”) (See ¶0131-0132). The HSV can be attenuated by a deletion to prevent γ134.5 gene expression (which reads on “a deletion or inactivation of a γ34.5 gene”) (See ¶0135 and 0141). The antiangiogenic agent is preferably a VEGF pathway-targeting molecule, such as an anti-VEGF antibody or fragment thereof or a soluble VEGF receptor (See ¶0153-0155). The anti-VEGF antibody can be bevacizumab (See ¶0160-0161). Karrasch et al. do not teach the oncolytic virus as expressing the antiangiogenic agent or the antiangiogenic agent as encoded by instant SEQ ID NOs 30-31.
De Gruijl et al. review the arming of oncolytic viruses to increase the immune response (See Abstract). Multiple types of oncolytic viruses have been modified to express antibodies or antibody fragments (See page 966, col. 1, full ¶2 and col. 2, 1 and page 967, col. 1, ¶1-2).
Todo teaches that HSV can be armed with antiangiogenic factors (See Abstract and page 211, col. 1, ¶1). The HSV genome allows the insertion of large and/or multiple transgenes (See page 208, col. 2, full ¶1).
Armstrong et al. teach VEGF-targeting heavy and light chains forming the VEGF-targeting monoclonal antibody bevacizumab for treating cancer (See ¶0077 and 0089 and fig. 9). Armstrong et al. teach a paired anti-VEGF heavy and light chain wherein the heavy chain sequence is 99.5% identical (which reads on “at least 90% homologous”, “at least 95% homologous”, and “at least 99% homologous”) to instant SEQ ID NO 30 (See ¶0027, SEQ ID NO 11 and alignment below (first 120 bp displayed)).
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The light chain is identical (which reads on “at least 90% homologous”, “at least 95% homologous”, and “at least 99% homologous”) to instant SEQ ID NO 31 (See ¶0027, SEQ ID NO 12 and alignment below (first 120 bp displayed)).
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It would have been obvious to one having ordinary skill in the art prior to the effective filing date of the claimed invention to modify the method of Karrasch et al. to have the anti-VEGF agent expressed by the oncolytic virus. One would be motivated to make this modification because de Gruijl et al. teach that expression via oncolytic viruses may focus the therapeutic effects of antibodies on the tumor microenvironment (See page 966, col. 1, full ¶1). There would be a reasonable expectation of success in doing so because de Gruijl et al. teach that other oncolytic viruses can be modified to express antibodies or fragments thereof (See 966, col. 1, full ¶2 and col. 2, ¶1 and page 967, col. 1, ¶1-2) and because Todo teaches that HSV can be armed with antiangiogenic factors and has a genome that allows insertion of large transgenes (See page 208, col. 2, full ¶1).
It also would have been obvious to one having ordinary skill in the art prior to the effective filing date of the claimed invention to modify method of Karrasch et al. to have the virus comprise the anti-VEGF heavy and light chains taught by Armstrong et al. for targeting VEGF. One would be motivated to make this modification because Armstrong et al. teach bevacizumab as a VEGF-binding antibody that can be used for treating cancer in a human subject (See ¶0077 and 0089) and because Karrasch et al. teach that bevacizumab can be used in conjunction with oncolytic HSV (See ¶0160-0161). There would be a reasonable expectation of success in making this modification because the virus could be readily modified to express the sequences taught by Armstrong et al.
While the prior art references do not expressly teach the expression of only one exogenous antibody from cells infected with oncolytic HSV, the examples of armed oncolytic viruses taught by de Gruijl et al. encode no more than one antibody or antibody fragment (See table 1). This suggests that a single antibody-encoding transgene would be obvious for use with an oncolytic viral vector and would read on “the anti-VEGF antibody is the only exogenous antibody that is expressed by a cell infected with the oncolytic HSV”.
Regarding claims 29-30 and 32: Following the discussion of claims 17, 19-20, 22-24, and 27, Karrasch et al. teach that the virus can be administered by direct intralesional injection (which reads on “administering… locally and directly to tumor tissue in a subject”) and that a therapeutically effective amount of virus and antiangiogenic agent can be administered to a patient for treating a tumorigenic disease (See ¶0242). The tumorigenic disease can be medulloblastoma, melanoma, prostate carcinoma (which reads on “prostate cancer”), head and neck cancer, esophageal cancer, renal cell carcinoma (which reads on “kidney cancer”), pancreatic cancer, breast cancer, lung cancer, colon cancer, gastric cancer, ovarian cancer, bladder cancer, sarcoma, squamous cell carcinoma (which reads on “squamous cell cancer”), liver cancer (which reads on “hepatocellular carcinoma”), and mesothelioma (See ¶0245). The virus and antiangiogenic agent can be combined with chemotherapy and/or radiotherapy (which reads on “radiation therapy”) (See ¶0249).
Claims 17-20, 22-24, 27, 29-30, and 32-33 are rejected under 35 U.S.C. 103 as being unpatentable over Karrasch et al. (US 20090317456 A1), of record, in view of de Gruijl et al. (Expert Opinion on Biological Therapy, 2015), of record, Todo (Cell Adhesion & Migration, 2008), of record, and Armstrong et al. (US 2013309226 A1), of record, further in view of Hawkins-Daarud et al. (Frontiers in Oncology, 2013), of record.
The teachings of Karrasch et al., de Gruijl et al., Todo, and Armstrong et al. are set forth in the rejection above and are incorporated herein in their entirety.
Regarding claims 18 and 33: Following the discussion of claims 17, 19-20, 22-24, 27, 29-30, and 32, Karrasch et al., modified by de Gruijl et al., Todo, and Armstrong et al., render obvious the administration of an oncolytic HSV encoding the anti-VEGF antibody bevacizumab for treating tumors but do not expressly teach the armed virus as inducing less swelling than the same virus without the bevacizumab transgene.
Hawkins-Daarud et al. teach that bevacizumab inhibits angiogenesis and repairs vascular leakage (which reads on “swelling”) associated with new blood vessels (See page 6, col. 1, full ¶2).
It would have been obvious to one having ordinary skill in the art prior to the effective filing date of the claimed invention that an oncolytic virus expressing bevacizumab would be reasonably expected to reduce interstitial fluid compared to an identical virus that did not express bevacizumab, due to the antibody’s ability to normalize pre-existing vasculature and vessel permeability as taught by Hawkins-Daarud (See page 6, col. 1, full ¶2). Thus, a virus encoding bevacizumab, as rendered obvious by the combination of Karrasch et al., de Gruijl et al., Todo, and Armstrong et al. would be expected to lower fluid leakage from local blood vessels, thereby resulting in reduced edema and less peritumoral swelling.
Claims 17, 19-20, 22-24, 26-27, 29-30, and 32 are rejected under 35 U.S.C. 103 as being unpatentable over Karrasch et al. (US 20090317456 A1), of record, in view of de Gruijl et al. (Expert Opinion on Biological Therapy, 2015), of record, Todo (Cell Adhesion & Migration, 2008), of record, and Armstrong et al. (US 2013309226 A1), of record, further in view of Goins et al. (Cold Spring Harbor Protocols, 2011), of record.
The teachings of Karrasch et al., de Gruijl et al., Todo, and Armstrong et al. are set forth in the rejection above and are incorporated herein in their entirety.
Regarding claim 26: Following the discussion of claims 17, 19-20, 22-24, 27, 29-30, and 32, Karrasch et al., modified by de Gruijl et al., Todo, and Armstrong et al., render obvious the administration of an oncolytic HSV encoding the anti-VEGF antibody bevacizumab for treating tumors but do not expressly teach the insertion of the transgene in place of a non-essential gene.
Goins et al. teach methods for constructing recombinant HSV vectors for gene transfer (See Abstract). Goins et al. teach the insertion of a therapeutic transgene at the site of a deleted HSV gene of interest, such as UL41 (which reads on “a non-essential gene”) (See fig. 1).
It would have been obvious to one having ordinary skill in the art prior to the effective filing date of the claimed invention to modify the method of Karrasch et al., modified by de Gruijl et al., Todo, and Armstrong et al., to comprise the method of Goins et al. for inserting the antibody transgene into HSV. One would be motivated to make this modification because Goins et al. teach the UL41 locus as a viable site for transgene insertion (See fig. 1). There would be a reasonable expectation of success in doing so because such a modification could be readily performed.
Claims 17, 19-20, 22-24, 27, and 29-32 are rejected under 35 U.S.C. 103 as being unpatentable over Karrasch et al. (US 20090317456 A1), of record, in view of de Gruijl et al. (Expert Opinion on Biological Therapy, 2015), of record, Todo (Cell Adhesion & Migration, 2008), of record, and Armstrong et al. (US 2013309226 A1), of record, further in view of further in view of Markert et al. (Molecular Therapy, 2009), of record.
The teachings of Karrasch et al., de Gruijl et al., Todo, and Armstrong et al. are set forth in the rejection above and are incorporated herein in their entirety.
Regarding claim 31: Following the discussion of claims 17, 19-20, 22-24, 27, 29-30, and 32, Karrasch et al., modified by de Gruijl et al., Todo, and Armstrong et al., render obvious the administration of an oncolytic HSV encoding the anti-VEGF antibody bevacizumab for treating tumors but do not expressly teach direct injection of the virus to a brain tumor during surgery.
Markert et al. teach the administration of oncolytic HSV directly to malignant gliomas (which read on “brain tumor”) by stereotactic injection, which requires surgical incision of the scalp and drilling into the skull, thereby reading on “injection during… surgery” (See page 206, col. 1, ¶1).
It would have been obvious to one having ordinary skill in the art prior to the effective filing date of the claimed invention to modify the method of Karrasch et al., modified by de Gruijl et al., Todo, and Armstrong et al., to comprise stereotactic injection into brain tumors, as taught by Markert et al. One would be motivated to make this modification because stereotactic injection was recognized as being suitable for delivering oncolytic virus directly to a brain tumor and because the virus could be readily administered by stereotactic injection.
Claims 17, 19-20, 27, 29-30, and 32 are rejected under 35 U.S.C. 103 as being unpatentable over Karrasch et al. (US 20090317456 A1), of record, in view of Todo (Cell Adhesion & Migration, 2008), of record, and Hauswirth et al. (US 20060193830 A1), of record.
Regarding claims 17, 19-20, and 27: Karrasch et al. teach the combined administration of an oncolytic virus and an antiangiogenic agent for treating cancer (See Abstract). The virus is preferably HSV-1 or HSV-2 (which read on “oncolytic herpes simplex virus”) (See ¶0131-0132). The HSV can be attenuated by a deletion to prevent γ134.5 gene expression (which reads on “a deletion or inactivation of a γ34.5 gene”) (See ¶0135). The antiangiogenic agent is preferably a VEGF pathway-targeting molecule, such as an anti-VEGF antibody or fragment thereof or a soluble VEGF receptor, such as VEGFR-1/FLT-1 (See ¶0153-0155).
Karrasch et al. do not teach the oncolytic virus as expressing the antiangiogenic agent or the antiangiogenic agent as encoded by instant SEQ ID NO 26.
Todo teaches that HSV can be armed with antiangiogenic factors (See Abstract and page 211, col. 1, ¶1). The HSV genome allows the insertion of large and/or multiple transgenes (See page 208, col. 2, full ¶1).
Hauswirth et al. teach an AAV vector that encodes a soluble FLT1 polypeptide (which reads on “soluble VEGF receptor”) having a nucleotide sequence identical to instant SEQ ID NO 26 (See ¶0010 and 0124, SEQ ID NO 26, and alignment below (first 120 bp displayed)).
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It would have been obvious to one having ordinary skill in the art to modify the method of Karrasch et al. to include a soluble FLT1 polypeptide, such as that taught by Hauswirth et al., for targeting VEGF. One would be motivated to make this modification because Hauswirth et al. teach that virus-mediated gene transfer enables local delivery of therapeutic proteins (See ¶0008). There would be a reasonable expectation of success in making this modification because Hauswirth et al. teach that the soluble FLT1 polypeptide can be expressed from a viral vector and because Todo teaches that HSV can be armed with antiangiogenic factors and has a genome that allows insertion of large transgenes (See page 208, col. 2, full ¶1 and page 211, col. 1, ¶1).
Regarding claims 29-30, 32, and 36: Following the discussion of claims 17, 19-20, and 27, Karrasch et al. teach that the virus can be administered by direct intralesional injection (which reads on “administering… locally and directly to tumor tissue in a subject”) and that a therapeutically effective amount of virus and antiangiogenic agent can be administered to a patient for treating a tumorigenic disease (See ¶0242). The tumorigenic disease can be medulloblastoma, melanoma, prostate carcinoma (which reads on “prostate cancer”), head and neck cancer, esophageal cancer, renal cell carcinoma (which reads on “kidney cancer”), pancreatic cancer, breast cancer, lung cancer, colon cancer, gastric cancer, ovarian cancer, bladder cancer, sarcoma, squamous cell carcinoma (which reads on “squamous cell cancer”), liver cancer (which reads on “hepatocellular carcinoma”), and mesothelioma (See ¶0245). The virus and antiangiogenic agent can be combined with chemotherapy and/or radiotherapy (which reads on “radiation therapy”) (See ¶0249).
Claims 41-44 are rejected under 35 U.S.C. 103 as being unpatentable over Karrasch et al. (US 20090317456 A1), of record, in view of Todo (Cell Adhesion & Migration, 2008), of record, and Hauswirth et al. (US 20060193830 A1), of record.
Regarding claims 41 and 43-44: Karrasch et al. teach the combined administration of an oncolytic virus and an antiangiogenic agent for treating cancer (See Abstract). The virus is preferably HSV-1 or HSV-2 (which read on “oncolytic herpes simplex virus”) (See ¶0131-0132). The HSV can be attenuated by a deletion to prevent γ134.5 gene expression (which reads on “a deletion or inactivation of a γ34.5 gene”) (See ¶0135). The antiangiogenic agent is preferably a VEGF pathway-targeting molecule, such as an anti-VEGF antibody or fragment thereof or a soluble VEGF receptor, such as VEGFR-1/FLT-1 (See ¶0153-0155). Karrasch et al. do not teach the oncolytic virus as expressing the antiangiogenic agent or the antiangiogenic agent as encoded by instant SEQ ID NO 26.
Todo teaches that HSV can be armed with antiangiogenic factors (See Abstract and page 211, col. 1, ¶1). The HSV genome allows the insertion of large and/or multiple transgenes (See page 208, col. 2, full ¶1).
Hauswirth et al. teach an AAV vector that encodes a soluble FLT1 polypeptide (which reads on “soluble VEGF receptor”) having a nucleotide sequence identical (which reads on “at least 95% homology”) to instant SEQ ID NO 26 (See ¶0010 and 0124, SEQ ID NO 26, and alignment below (first 120 bp displayed)).
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It would have been obvious to one having ordinary skill in the art to modify the method of Karrasch et al. to include a soluble FLT1 polypeptide, such as that taught by Hauswirth et al., for targeting VEGF. One would be motivated to make this modification because Hauswirth et al. teach that virus-mediated gene transfer enables local delivery of therapeutic proteins (See ¶0008). There would be a reasonable expectation of success in making this modification because Hauswirth et al. teach that the soluble FLT1 polypeptide can be expressed from a viral vector and because Todo teaches that HSV can be armed with antiangiogenic factors and has a genome that allows insertion of large transgenes (See page 208, col. 2, full ¶1 and page 211, col. 1, ¶1). Oncolytic HSV modified to express such a polypeptide would read on “wherein a cell infected with the oncolytic HSV does not express an exogenous antibody”.
Regarding claim 42: Following the discussion of claims 41 and 43-44, Karrasch et al. teach that the virus can be administered by direct intralesional injection (which reads on “administering… locally and directly to tumor tissue in a subject”) and that a therapeutically effective amount of virus and antiangiogenic agent can be administered to a patient for treating a tumorigenic disease (See ¶0242).
Allowable Subject Matter
Claims 37-38 and 40 are allowed.
The following is a statement of reasons for the indication of allowable subject matter:
An oncolytic HSV encoding an anti-VEGF scFv comprising instant SEQ ID NO 22 appears to be free of the prior art.
Conclusion
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.
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/J.S.S./Examiner, Art Unit 1633
/CHRISTOPHER M BABIC/Supervisory Patent Examiner, Art Unit 1633