DETAILED ACTION
Final Rejection
Notice of Pre-AIA or AIA Status
1. The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Election/Restrictions (Finalized)
2. As indicated in the non-final rejection office action dated 05/15/2025 the election of species was extended to anti-HBV siRNA to include amended claim limitation to an anti-HBV siRNA. Applicant’s election of Group III claims 27 and 72-80 with traverse between Group III and IV. Applicant’s argument on traverse between Groups III and IV were found persuasive on the ground that claims 27 and 34 have overlapping subject matter. Restriction for Group IV was withdrawn, and the Group III were rejoined with claims 34 and 81-84 and the claims 27, 34 and 72-84 read on the elected species anti-HBV siRNA.
The requirement for election of invention of the Group and a species anti-HBV siRNA was made FINAL in the office action dated 05/15/2025.
The election of species to the extent of interferon α (IFN α), pegylated interferon α (PEG- IFN α) is withdrawn in view of the prior art search results. The species anti-HBV siRNA, interferon α (IFN α), and pegylated interferon α (PEG- IFN α) are under examination in this office action.
Status of Claims
3. Claims 27, 34, 72-73, 75-78, 80-81 and 83-84 are pending as per amended claim listing filed on 07/22/2026.
4. Applicant has cancelled claims 1-26, 28-33, 35-71, 74, 79 and 82 as per the amended claim listing filed on 07/22/2026.
5. Amended claims 27, 34, 72-73, 75-78, 80-81 and 83-84 are under examination in this office action.
Priority
6. This application claims the benefit under 35 U.S.C. § 119(e) of the United States Provisional Application Serial No. 63/522,851, filed June 23, 2023.
Information Disclosure Statement
7. The information disclosure statement (IDS) submitted on 04/24/2025 is in compliance with the provisions of 37 CFR 1.97, accordingly, the information disclosure statement is being considered by the examiner.
Claim Interpretation (modified)
8. The claims in this application are given their broadest reasonable interpretation using the plain meaning of the claim language in light of the specification as it would be understood by one of ordinary skill in the art.
Claim 27. A method for treating a hepatitis B viral (HBV) infection in a subject with chronic hepatitis B (CHB), the method comprising:
a) determining a baseline HBV antibody concentration in a subject with CHB prior to administering an HBV surface antigen (HBsAg) to the subject;
b) administering the HBsAg to the subject;
c) determining a post-baseline HBV antibody concentration in the subject after being administered the HBsAg, and identifying the subject as a responder subject if the post-baseline HBV antibody concentration is greater than the baseline HBV antibody concentration; and
d) administering an HBV therapy to the responder subject wherein the responder subject is not administered the HBsAg after the subject is identified as a responder subject,
wherein the HBsAg comprises virus-like particles (VLPs) comprising HBV surface envelope proteins Pre-S1, Pre-S2 and S, and
wherein the HBV therapy comprises an anti-HBV siRNA and does not comprise the HBs Ag.
The instant amended claim 27 is interpreted to be directed to a method for treating a hepatitis B viral (HBV) infection in a subject with chronic hepatitis B (CHB), the method comprising:
a) determining a baseline HBV antibody concentration in a subject with CHB prior to administering an HBV surface antigen (HBsAg) to the subject;
b) administering the HBsAg to the subject;
c) determining a post-baseline HBV antibody concentration in the subject after being administered the HBsAg, and identifying the subject as a responder subject if the post-baseline HBV antibody concentration is greater than the baseline HBV antibody concentration; and
d) administering an HBV therapy to the responder subject wherein the responder subject is not administered the HBsAg after the subject is identified as a responder subject,
wherein the HBsAg comprises virus-like particles (VLPs) comprising HBV surface envelope proteins Pre-S1, Pre-S2 and S, and
wherein the HBV therapy comprises an anti-HBV siRNA and does not comprise the HBs Ag.
The instant claim 27 preamble recites a transitional phrase “comprising” which is open ended to include additional elements that are not the recited elements.
The claim 27 amendment introduced multiple “wherein” contingent clauses. The claim recites a negative limitation that “wherein the HBV therapy comprises an anti-HBV siRNA and does not comprise the HBs Ag”.
.
Claim 34. A method for treating an HBV infection in a subject with chronic hepatitis B, the method comprising:
administering an HBV therapy to the subject wherein the subject has been determined to have a post-baseline HBV antibody concentration after being administered an HBV surface antigen (HBsAg) that is greater than a baseline HBV antibody concentration prior to being administered the HBsAg,
wherein the method does not comprise administering to the subject the HBsAg after it has been determined for the subject that the post-baseline HBV antibody concentration is greater than the baseline HBV antibody concentration,
wherein the HBsAg comprises virus-like particles (VLPs) comprising HBV surface envelope proteins Pre-S 1, Pre-S2 and S, and
wherein the HBV therapy comprises an anti-HBV siRNA and does not comprise the HBsAg.
The instant claim 34 preamble recites a transitional phrase “comprising” which is open ended to include additional elements that are not the recited elements.
The instant claim 34 amendment introduced a “wherein” contingent clause and also include transitional phrase “comprise” multiple sites, for reciting additional claim limitations.
The claim recites a negative limitation wherein the HBV therapy comprises an anti-HBV siRNA and does not comprise the HBsAg.
Claim 76. The method of claim 27, wherein the HBV therapy further comprises an interferon alfa (IFNα) or pegylated interferon alfa (PEG-IFNα).
Claim 83. The method of claim 81, wherein the HBV therapy further comprises an interferon alfa (IFNα) or pegylated interferon alfa (PEG-IFNα).
The instant claims 76, and 83 as above, recites a “wherein” clause to include “the HBV therapy”, however further introduces a transitional phrase “comprises” which is open ended to comprise additional or alternative elements directed to anti-HBV therapy.
Withdrawn Claim Rejections - 35 USC § 112
9. Withdrawn rejection of claims 27, 34, 72-73, 75-78, 80-81 and 83-84 under 35 U.S.C. 112(a) written description requirement in view of applicant’s amendment to the claims filed on 07/22/2026.
10. Withdrawn rejection of claims 27, 34, 72-73, 75-78, 80-81 and 83-84 under 35 U.S.C. 112(b) as being indefinite in view of applicant’s amendment to the claims filed on 07/22/2026.
Claim Rejections - 35 USC § 102 (maintained)
11. 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 the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 27 and 34 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Chen 2021 (Clinical Trial NCT04749368 first posted 02/11/2021, see PDF printout, BRII Biosciences Limited, Vir Biotechnology, Inc, and VBI Vaccines Inc) as evidenced by Ma et al 2021 (JHEP Reports 2021 (3) p. 1-11), Ji et al 2025 (Gastroenterology 2025;169:136–149).
Chen 2021 (Clinical Trial NCT04749368) anticipated instant claims 27 and 34 by disclosing a Phase-2 clinical trial to investigate the safety and efficacy of BRII-835 and BRII-179 combination therapy treating adult participants with chronic Hepatitis B Virus (HBV) infection. Chen 2021 (Clinical Trial NCT04749368) further disclosed that the experimental Cohort A were treated via subcutaneous injection with BRII-835 (VIR-2218), experimental Cohort B were treated with BRII-835 (VIR-2218) for 32 weeks, BRII-179 (VBI-2601) with IFN-α up to Week 40, and experimental Cohort C received BRII-835 (VIR-2218) and BRII-179 (VBI-2601) up to Week 40 (See, Clinical Trial NCT04749368, attached PDF printout).
Ma et al 2021 provides evidence BRII-179 is an HBV VLP comprising large (L), middle (M), and small (S) envelope proteins (VLP reads on comprising Pre-S1, Pre-S2, and S envelope proteins of HBV) (See, Ma et al 2021, page 2, col 1 para 3). A recently initiated clinical study (NCT04749368) is evaluating the combination of HBV-specific small-interfering RNA and BRII-179, with the aim of reducing immunosuppressive viral antigen levels via gene silencing before stimulating HBV-specific immunity with multi-doses of BRII-179 (See, Ma et al 2021, page 10 col 2 last para). Ji et al 2025 provides evidence an HBV-targeting siRNA (elebsiran) (BRII-835) (See, page 137, col 1 para 3).
In the clinical trial NCT04749368 determining a bassline HBV antibody concentration in a subject prior to administering the VLP (HBs Ag), identification of responders following administration of the VLP based on increase in antibody titers to HBs Ag and subsequent administration of BRII-835 (an anti-HBV siRNA) are disclosed in the study protocol.
Claim Rejections - 35 USC § 103 (maintained)
12. 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.
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.
13. Claims 27, 34, 76, 78, and 80 are rejected under 35 U.S.C. 103 as being unpatentable over Ma et al 2021 (JHEP Reports 2021 (3) p. 1-11), and further in view of Hoa et al 2009 (Antimicrob Agents Chemother. 2009 Dec;53(12):5134-40), Chen 2021 (Clinical Trial NCT04749368 first posted 02/11/2021, see PDF printout, BRII Biosciences Limited, Vir Biotechnology, Inc, and VBI Vaccines Inc), Sepp-Lorenzino et al 2018 (WO2018195165A1 published 10/15/2018), Hui et al 2022 (Clin Mol Hepatol. 2022 Feb 17;28(3):408–424), and as evidenced by Ji et al 2025 (Gastroenterology 2025;169:136–149).
Claim 27: Ma et al 2021 is in the art and teaches instant claim 27 by disclosing a clinical trial directed to a therapeutic vaccine BRI-179 restores HBV-specific immune responses in responder patients with chronic HBV (See, See, Ma et al 2021, abstract). Ma et al 2021 discloses a method for treating a hepatitis B viral (HBV) infection in a responder subject with chronic hepatitis B (CHB). Ma et al 2021 teaches therapeutic vaccine BRII-179 restores HBV-specific B cell (antibody/humoral) and T cell (cellular immune response) immune responses in patients with chronic HBV in a phase Ib/IIa study. Functional cure of chronic HBV infection (CHB) without life-long treatment requires the restoration of defective HBV-specific humoral and cellular immunity. Therapeutic vaccines based on the major structural and non-structural proteins have been tested in patients with CHB but have shown scarce immunogenicity. BRII-179, also known as VBI-2601, is a novel formulation comprised of all 3 HBV surface envelope proteins (Pre-S1, Pre-S2, and S). Safety, antiviral activity, and immunogenicity of BRII-179 admixed with co-adjuvant interferon (IFN)-α were assessed in patients with CHB. Ma et al 2021 indicated further clinical evaluation of BRII-179 in combination with other therapies (See, Ma et al 2021, abstract, p.2, col 1, col 2 Patients and methods), the method comprising:
(a) determining a baseline HBV antibody concentration in a subject with CHB prior to administering an HBV surface antigen (HBsAg) to the subject requiring a visit for clinical evaluation, full laboratory evaluation (See, p.2 col 2, para 1);
( b) administering the HBsAg to the subject, the HBsAg in the form of BRII-179, also known as VBI-2601, is a novel formulation comprised of all 3 HBV surface envelope proteins (Pre-S1, Pre-S2, and S) (See, p.2 col 1, para 3; abstract)
(c) determining a post-baseline HBV antibody concentration in the subject after being administered the HBsAg, by disclosing positive anti-HBs response was defined at any post-baseline visit with either (i) post-baseline anti-HBs ≥ 2 IU/L if anti-HBs antibody was undetectable at baseline or (ii) post-baseline anti-HBs ≥ 5 times the baseline anti-HBs if baseline anti-HBs was ≥ 2 IU/L. Antibodies to Pre-S1 (anti-Pre-S1) and Pre-S2 (anti-Pre-S2) were measured at baseline and all subsequent visits using a customized ELISA protocol (See, p.2 col 2, para 3; abstract) and identifying the subject as a responder subject if the post-baseline HBV antibody concentration is greater than the baseline HBV antibody concentration. Ma et al 2021 teaches BRII-179, also known as VBI-2601, is a virus-like particle (VLP)-based immunotherapeutic derived from the prophylactic Sci-B-Vac® vaccine …… was used previously in a therapeutic setting in patients with CHB and showed signs of efficacy, i.e., restoration of anti-HBs to >10 mIU/ml in the vaccinated groups, a higher HBeAg seroconversion frequency, and suppression of HBV DNA to <4 log copies/ml in the anti-HBs responders compared to non-responder. The anti-HBs responders had a significantly higher HBeAg seroconversion rate and more frequent HBV DNA suppression than anti-HBs non-responders, demonstrating the functional relevance of anti-HBs seroconversion. However, the peak antibody titers in most antibody responders were observed after 3 or 4 doses of vaccination (at weeks 12 or 16), indicating that the antibody response was attenuated in the highly tolerant patients compared to healthy individuals in whom the protective titer (≥10 mIU/ml) was generally reached after the second dose. (See, page 2 col 1 para 3 and page 9 col 1 discussion para 2, and col 2 para 1 for “responders” and “non-responders”; abstract, p. 7, table 3-columns on antibody response, T-cell response can also be considered a response to identify responders); and
(d) Ma et al 2021 teaches administering anti-HBV therapy IFN-α to the responder subject by disclosing study design treatment group and responders BRII-179 20 ug+ IFN-α +NA (See, p.2 col 2, para 2 on Study design; abstract; p. 7, table 3-columns on Treatment and associated legends). Ma et al 2021 further shows express motivation by disclosing that a recently initiated clinical study (NCT04749368) is evaluating the combination of HBV-specific small-interfering RNA and BRII-179, with the aim of reducing immunosuppressive viral antigen levels via gene silencing before stimulating HBV-specific immunity with multi-doses of BRII-179 (See, Ma et al 2021, page 10, col 2 last para on conclusion).
Hoa et al 2009 is in the art and discloses a randomized controlled study investigating viral suppression and serological response following pre-S1/pre-S2/S vaccine therapy combined with lamivudine treatment in HBeAg-positive patients with chronic hepatitis B and teaches identification of responders by disclosing anti-HBs responders showed significantly higher HBeAg seroconversion rates, greater suppression of HBV DNA levels, and a lower median reduction in HBV DNA levels than those of anti-HBs non-responders. Thus the concept of identification of responders and non-responders for combination treatment comprising the vaccine and antiviral (anti-HBV) for CHB patients is taught by Hoa et al 2009 (See, abstract, see methods, results, discussion , figures, entire article).
Chen 2021 (Clinical Trial NCT04749368) further discloses the Phase-2 clinical trial NCT04749368 to investigate the safety and efficacy of BRII-835 and BRII-179 combination therapy treating adult participants with chronic Hepatitis B Virus (HBV) infection. Chen 2021 disclosed that the experimental Cohort A were treated via subcutaneous injection with BRII-835 (VIR-2218), experimental Cohort B were treated with BRII-835 (VIR-2218) for 32 weeks, BRII-179 (VBI-2601) with IFN-α up to Week 40, and experimental Cohort C received BRII-835 (VIR-2218) and BRII-179 (VBI-2601) up to Week 40 (See, Clinical Trial NCT04749368, attached PDF printout).
Sepp-Lorenzino et al 2018 (WO2018195165A1) is in the art and discloses methods for the treatment of a subject having a Hepatitis B virus (HBV) infection, e.g., a chronic HBV infection, using a combination of an RNAi agent that targets HBV and an HBV vaccine. It is disclosed a RNAi agent and an HBV vaccine for use in treatment of HBV infection, comprising sequentially administering to the subject having an HBV infection: a) an RNAi agent that inhibits expression of at least three HBV transcripts, wherein the RNAi agent forms a double stranded region; b) a protein-based vaccine comprising a first HBV core antigen (HBcAg) polypeptide, and a first HBV surface antigen (HBsAg) polypeptide; and c) a nucleic acid-based vaccine comprising an expression vector construct encoding a second HBcAg polypeptide, and/or a second HBsAg polypeptide, wherein the second HBcAg polypeptide, and/or the second HBsAg polypeptide, shares at least one epitope with at least one of the first HBcAg polypeptide, and/or the first HBsAg polypeptide (See, abstract, entire WO2018195165A1).
Hui et al 2022 is in the art and teaches RNA interference as a novel treatment strategy for chronic hepatitis B infection. RNA interference (RNAi) by small-interfering RNA (siRNA) and anti-sense oligonucleotide (ASO) has been studied as a novel treatment strategy for CHB. RNAi targets post-transcriptional messenger RNAs and pregenomic RNAs to reduce hepatitis B virus (HBV) antigen production and viral replication. By reducing viral antigens, host immune reconstitution against HBV may also be attained. Phase I/II trials on siRNAs have demonstrated them to be safe and well-tolerated. siRNA is effective when given in monthly doses with different total number of doses according to different trial design, and can lead to sustainable dose-dependent mean HBsAg reduction by 2–2.5 log (See, abstract, entire article).
It would have been obvious to an artisan of ordinary skill in the art before the effective filing date of the claimed invention to modify the prior teachings of Ma et al 2021 with the teachings of Hoa et al 2009, Chen et al 2021, Sepp-Lorenzino et al 2018 and Hui et al 2022 on anti-HBV siRNA to arrive at the invention of claim 27. Based on the combined teachings applied to render obvious the claim 27, as recited supra, it is obvious that CHB subjects/patients are immunologically exhausted and requires restimulation or awakening of the immune system to HBV antigens. Having identified the immune responders to HBs Ag it would be obvious to not repeatedly stimulate the subjects only with HBs Ag (VLP), however additionally comprise the anti-HBV si RNA therapy to target the HBV replication by targeting HBV mRNA transcription and lower the HBV production. Combination therapies known in the art would be obvious to practice e.g. anti-HBV siRNA. The motivation based on the applied prior art teachings for the combination therapy would be to comprise anti-HBV therapy siRNA to target a HBV mRNA translation by targeting the HBV mRNAs by administering specific siRNA therapy targeting the HBV to mitigate exhaustion of the subject’s or patients’ immune system to overcome HBV replication engaging immune system and better allow engagement of already exhausted (CHB patients) immune system to better respond to the administered HBs Ag (VLP) vaccination or immunization for better outcome of treatment in CHB patients and for commercial success. One of the ordinary skills in the art would have a reasonable expectation of success given the disclosures of the prior art teachings as applied to claim 27 and as recited supra. This is analogous to some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the invention as claimed in claim 27. See KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 415-421, 82 USPQ2d 1385, 1395-97 (2007) (see MPEP § 2143, example of rationales, A-G).
Claim 34. Ma et al 2021 teaches instant claim 34 by disclosing a clinical trial directed to a therapeutic vaccine BRI-179 restores HBV-specific immune responses in responder patients with chronic HBV (See, Ma et al 2021, abstract, entire research paper) by disclosing the limitations of claim 34 a method for treating an HBV infection in a subject with chronic hepatitis B, the method comprising: a) administering an HBV therapy to the subject wherein it has been determined that a post-baseline HBV antibody concentration in the subject after being administered an HBsAg is greater than a baseline HBV antibody concentration in the subject prior to being administered the HBsAg (See, Ma et al 2021, abstract, entire research paper, and applied anticipatory teachings to claim 27 as recited above). The additional teachings of Ma et al 2021 with the teachings of Chen et al 2021, Sepp-Lorenzino et al 2018 and Hui et al 2022 on anti-HBV siRNA as applied to claim 27 are incorporated here in entirety to render obvious instant claim 34. The claim 34 does not explicitly recite identification of a responder subject, however, the claim limitation requires the subject to have a higher post-baseline HBV Ab concentration after HBs Ag administration as compared to a baseline HBV Ab concentration prior to HBs Ag administration.
It would have been obvious to an artisan of ordinary skill in the art before the effective filing date of the claimed invention to modify the prior teachings of Ma et al 2021 with the teachings of Hoa et al 2009, Chen et al 2021, Sepp-Lorenzino et al 2018 and Hui et al 2022 on anti-HBV siRNA to arrive at the invention of claim 34. Based on the combined teachings applied to render obvious the claim 34, as recited supra, it is obvious that CHB subjects/patients are immunologically exhausted and requires restimulation or awakening of the immune system to HBV antigens. Having identified the immune responders to HBs Ag it would be obvious to not repeatedly stimulate the subjects only with HBs Ag (VLP), however additionally comprise the anti-HBV si RNA therapy to target the HBV replication by targeting HBV mRNA transcription and lower the HBV production. Combination therapies known in the art would be obvious to practice e.g. anti-HBV siRNA. The motivation based on the applied prior art teachings for the combination therapy would be to comprise anti-HBV therapy siRNA to target a HBV mRNA translation by targeting the HBV mRNAs by administering specific siRNA therapy targeting the HBV to mitigate exhaustion of the subject’s or patients’ immune system to overcome HBV replication engaging immune system and better allow engagement of already exhausted (CHB patients) immune system to better respond to the administered HBs Ag (VLP) vaccination or immunization for better outcome of treatment in CHB patients and for commercial success. One of the ordinary skills in the art would have a reasonable expectation of success given the disclosures of the prior art teachings as applied to claim 34 and as recited supra. This is analogous to some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the invention as claimed in claim 34. See KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 415-421, 82 USPQ2d 1385, 1395-97 (2007) (see MPEP § 2143, example of rationales, A-G).
14. Claims 76, 78, and 80 are rejected under 35 U.S.C. 103 as being unpatentable over combined teachings of Ma et al 2021 (JHEP Reports 2021 (3) p. 1-11), Hoa et al 2009 (Antimicrob Agents Chemother. 2009 Dec;53(12):5134-40), Chen 2021 (Clinical Trial NCT04749368 first posted 02/11/2021, see PDF printout, BRII Biosciences Limited, Vir Biotechnology, Inc, and VBI Vaccines Inc), Sepp-Lorenzino et al 2018 (WO2018195165A1 published 10/15/2018), Hui et al 2022 (Clin Mol Hepatol. 2022 Feb 17;28(3):408–424), and as evidenced by Ji et al 2025 (Gastroenterology 2025;169:136–149) as applied to claims 27 and 34 above, and further in view of Vasconcelos et al 2022 (Case Reports in Infectious Diseases, vol 2022, Article ID 3890309), Wang et al 2016 (Scientific Reports volume 6, Article number: 29605), and Anderson et al 2020 (WO2020254878A1, 03/11/2021).
Claims: 76, 78 and 80 (dependent on claim 27): The combined teachings of Ma et al 2021, Hoa et al 2009, Chen 2021, Sepp-Lorenzino et al 2018, Hui et al 2022, and as evidenced by Ji et al 2025 teaches claim 27 as recited supra. The combined teachings do not recite pegylated interferon alfa (IFNα).
Claim 76: Both Ma et al 2021, and Chen et al 2021 (Cohort B treatment) teaches added limitation of instant claim 76 (dependent on claim 27), wherein the HBV therapy further comprises an interferon alfa (IFNα) by disclosing a recently initiated clinical study (NCT04749368) is evaluating the combination of HBV-specific small-interfering RNA and BRII-179, with the aim of reducing immunosuppressive viral antigen levels via gene silencing before stimulating HBV-specific immunity with multidoses of BRII-179 (See, p.10, col 2, last para); a randomized phase Ib/IIa study in CHB subjects, NA plus BRII-179 with co-adjuvant IFN-α (See, Ma et al 2021 abstract, p.7 Table 3; p.10, col 2, last para, Chen et al 2021 Cohort B treatment).
Sepp-Lorenzino et al 2018 is in the art and is directed to a method for the treatment of a subject having a Hepatitis B virus (HBV) infection, e.g., a chronic HBV infection, using a combination of an RNAi agent that targets HBV and an HBV vaccine (combinatorial approach of treatment). The methods further comprise administration of an immune stimulator to the subject. In certain embodiments, the immune stimulator is selected from the group pegylated interferon alfa 2a (PEG-IFN-alpha-2a), Interferon alfa-2b, PEG-IFN-alpha-2b (See, claim 69).
Vasconcelos et al 2022 is in the art and teaches a case of PEG-INFα-treated CHB patients that attained sustained off-treatment virological response with only 16 weeks of treatment, with loss of both HBeAg and HBsAg (this latter the optimal treatment endpoint) (See, abstract, entire article). We report a singular CHB case with a surprising response to PEG-IFNα; with only 16 weeks of treatment, our patient attained loss of HBsAg and sustained off-treatment virological response (See, pages 1-3, discussion and conclusion sections).
Wang et al 2016 is in the art and teaches predictors of response to pegylated interferon in chronic hepatitis B: a real-world hospital-based analysis. Pre-treatment HBsAg level is an important predictor of virological response in CHB patients undergoing PEG-IFN alpha treatment (See, abstract, entire article).
Anderson et al 2020 (WO2020254878A1) is in the art and discloses methods useful for inducing an immune response and overcoming immune tolerance in a subject suffering from chronic Hepatitis B virus infection. The compositions of the disclosure comprise HBsAg having S, Pre-S1 and Pre- S2 proteins, an aluminum phosphate adjuvant and interferon-α. The addition of a low dose of interferon- mg (3 MIU) to a prophylactic Hepatitis B vaccine improved antibody titers in immunocompromised or non-responder populations but not in healthy subjects (See, para [0038], abstract, and entire prior art WO2020254878A1).
Claim 78: Ma et al 2021 teaches added limitation of instant claim 78 (dependent on claim 27), wherein the HBV antibody concentration is a serum anti-HBs concentration by disclosing antibody response to HBs, Pre-S1 and Pre-S2 antigens (See, abstract; p.2, col 2, para 3).
Claim 80. Ma et al 2021 teaches added limitation of instant claim 80 (dependent on claim 27), wherein the subject is identified as a responder subject if the post-baseline HBV antibody concentration is 5 times greater than the baseline HBV antibody concentration by disclosing antibody response to HBs, post-baseline anti-HBs ≥ 5 times the baseline anti-HBs if baseline anti-HBs was ≥2 IU/L (See, p.2, col 2, para 3; p.6 Fig 3 A-B and legends).
It would have been obvious to an artisan of ordinary skill in the art before the effective filing date of the claimed invention to modify the combined prior teachings of Ma et al 2021, Chen et al 2021, Sepp-Lorenzino et al 2018 and Hui et al 2022 as applied to render obvious claims 27 and 34 with additional teachings of Vasconcelos et al 2022, Wang et al 2016, and Anderson et al 2020 to arrive at the invention of claims 76, 78 and 80 as recited supra. Based on the combined prior art teachings as recited supra, it is obvious that CHB subjects/patients are immunologically exhausted and requires restimulation or awakening of the immune system to HBV antigens. Having identified the immune responders to HBs Ag it would be obvious to not repeatedly stimulate the subjects only with HBs Ag (VLP), however additionally comprise the anti-viral anti-HBV interferon alfa (IFNα) or pegylated interferon alfa (IFNα) to target the HBV replication, to lower the HBV production, and also as an immune stimulator. Combination therapies known in the art would be obvious to practice e.g. anti-HBV siRNA and interferon alfa (IFNα) or pegylated interferon alfa (IFNα). The motivation based on the applied prior art teachings for the combination therapy would be to comprise an additional anti-HBV therapy to reduce replication/production of HBV to mitigate exhaustion of the subject’s or patients’ immune system to overcome HBV replication engaging immune system and better allow engagement of already exhausted (CHB patients) immune system to better respond to the administered HBs Ag (VLP) vaccination or immunization for better outcome of treatment in CHB patients and for commercial success. The motivation to select subjects with post-baseline HBV Ab concentration >5 times than baseline would be the CHB subjects would be good responders and would help for superior HBV therapy outcome (instant claims 78, and 80). One of the ordinary skills in the art would have a reasonable expectation of success to arrive at the inventions of claims 76, 78 and 80 given the disclosures of the prior art teachings as applied to claims as recited supra. This is analogous to some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the invention as claimed in claims 76, 78 and 80. See KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 415-421, 82 USPQ2d 1385, 1395-97 (2007), MPEP § 2143, example of rationales, A-G).
15. Claims 72-73, 75 and 81, 83-84 are rejected under 35 U.S.C. 103 as being unpatentable over combined teachings of Ma et al 2021 (JHEP Reports 2021 (3) p. 1-11), Hoa et al 2009 (Antimicrob Agents Chemother. 2009 Dec;53(12):5134-40), Chen 2021 (Clinical Trial NCT04749368 first posted 02/11/2021, see PDF printout, BRII Biosciences Limited, Vir Biotechnology, Inc, and VBI Vaccines Inc), Sepp-Lorenzino et al 2018 (WO2018195165A1 published 10/15/2018), Hui et al 2022 (Clin Mol Hepatol. 2022 Feb 17;28(3):408–424), and as evidenced by Ji et al 2025 (Gastroenterology 2025;169:136–149) as applied to claims 27 and 34 above, and further in view of Gupta et al 2021 (Clinical Trial NCT03672188 by Vir Biotechnology, Inc conducted during 09/14/2018 to 12/13/2021 and related publication in Drugs in R&D (2021) 21:455–465), Ma et al 2019 (Front Immunol. 2019 Sep 24;10: 2308), Vasconcelos et al 2022 (Case Reports in Infectious Diseases, vol 2022, Article ID 3890309), Wang et al 2016 (Scientific Reports volume 6, Article number: 29605) and Anderson et al 2020 (WO2020254878A1, 03/11/2021).
Claims 72-73, 75 and 81, 83-84: The combined teachings of Ma et al 2021, Hoa et al 2009, Chen 2021, Sepp-Lorenzino et al 2018, Hui et al 2022, and as evidenced by Ji et al 2025 teaches claims 27 and 34 as recited supra and the teachings are incorporated here in its entirety.
Ma et al 2021 provides additional teaching: a recently initiated clinical study (NCT04749368) is evaluating the combination of HBV-specific small-interfering RNA and BRII-179, with the aim of reducing immunosuppressive viral antigen levels via gene silencing before stimulating HBV-specific immunity with multi-doses (See, Ma et al 2021, p. 10, col 2 last para conclusion).
Ma et al 2021 does not teach the added limitations of steps of the methods of claims
72-73, 75, 81, and 83-84.
Vir Biotechnology, Inc 2021 (Clinical Trial NCT03672188) teaches by disclosing doses of siRNA VIR-2218 that are applicable to the instant claims 72-75, 81, and 83-84 reciting limitations for HBV therapy, or elected species anti-HBV siRNA therapy. A phase 1/2, randomized, placebo-controlled study to evaluate the safety, tolerability, pharmacokinetics, and antiviral activity of VIR-2218 in subjects with chronic HBV. VIR-2218, also known as Elebsiran, is an investigational small interfering RNA (siRNA) that targets hepatitis B virus (HBV) transcripts administering to chronic HBV (CHB) patents different doses ranging from Chronic HBV (CHB), Chronic HBV, HBeAg negative, subjects received 2 SC doses of 20 mg VIR-2218 administered 4 weeks apart, HBeAg negative, subjects received 2 SC doses of 100 mg VIR-2218 administered 4 weeks apart to Chronic HBV, HBeAg positive, subjects received 2 SC doses of 200 mg VIR-2218 administered 4 weeks apart (See, Clinical Trial NCT03672188, study design).
Chen 2021 (Clinical Trial Number NCT04749368) as evidenced by Ji et al 2025 teaches the added limitations of steps of the methods of claims 72-73, 75, 81, and 83-84 by disclosing: a phase 2a open-label study was conducted from March 11, 2021, to July 4, 2023, at 25 investigational sites in 7 countries/ regions across the Asia and Pacific Region. Eligible participants were randomly assigned to an elebsiran monotherapy cohort or 2 elebsiran + BRII-179 combination therapy cohorts. All cohorts received nine 4-weekly doses of 100 mgelebsiran via subcutaneous injection from day 1 through week 32 (cohorts A, B, and C). Two combination therapy cohorts received additional nine 4-weekly doses of admixture of 40 mg BRII-179 and 3 million IU IFN-a coadministration (cohort B) or 40 mg BRII-179 (cohort C) via intramuscular injection from week 8 through week 40, respectively (See, Chen 2021 (Clinical Trial Number NCT04749368; Ji et al 2025 p.3 col 1 para 2 Study design).
Accordingly, the “Vir Biotechnology, Inc 2021” and “Chen” references, taken separately or in combination, suggest that the timing of the “initial dose of the HBV therapy” (e.g. “at least 4 doses of the HBsAg: claims 72, 75, 81); the HBsAg amount and weekly protocol (claim 73: 20ug-100ug/dose every 2-4 weeks). All three references (“Ma”; “Vir Biotechnology”; and “Chen”) teach “serum” concentrations of anti-HBV as in instant claim 84. Additionally, it is noted that the HBV therapy as being anti-HBV siRNA or interferon α (instant claim 83 limitation) is taught/suggested by Ma et al 2021, interferon α taught by Anderson et al 2020, pegylated interferon α (instant claim 83 limitation) is taught/suggested by Sepp-Lorenzino et al 2018, Vasconcelos et al 2022, Wang et al 2016 as recited supra.
Further, it is noted that the above dependent claim method parameters (e.g. bioactive amounts/timing) are art-recognized result effective-variables, which a medical practitioner or researcher, would alter and optimize. See MPEP 2144; 2144.05 and In re Aller, 220 F.2d 454,456 (CCPA 1955).
Still further, Ma et al 2019 reviews approaches toward a functional cure for Hepatitis B: The Rationale and Challenges for Therapeutic Targeting of the B Cell Immune Response teaches: Long-term antiviral treatment by nucleoside analogs, by targeting viral translation by siRNA, by inhibiting HBsAg release via nucleic acid polymers, or by neutralizing HBsAg via specific antibodies could potentially reduce the HBsAg load in CHB patients. A combined strategy including a reduction of the HBsAg load via the above treatments and the therapeutic targeting of B cells by vaccination may induce the appearance of anti-HBs antibodies and lead to a functional cure of CHB.
It would have been obvious to one of the ordinary skill in the art before the effective filing date of the claimed invention to modify the prior arts teachings of Ma et al 2021 as applied to claims 27, and 34, as recited supra, by incorporating the teachings of Chen 2021 on clinical trial number NCT04749368, Gupta et al 2021 teachings on Clinical Trial NCT03672188 and related publication in Drugs in R&D (2021) 21:455–465) and Ma et al 2019 as evidenced by Ji et al 2025 (Gastroenterology. 2025 Mar 3: S0016-5085(25)00466-4) to arrive at the invention of claims 72-73, 75, 81, and 83-84. One of the ordinary skills would have been motivated to modify the prior arts teachings as applied to claims 27 and 34 with the additional prior art teachings as recited supra to arrive at the methods of combination therapy against Chronic Hepatitis B virus infection in subjects with CHB as claimed in claims 72-73, 75, 81, and 83-84 for developing an effective anti-HBV treatment for the CHB responder subjects and would have a motivation for commercial success. There would have been a reasonable expectation of success given the combined prior art teachings in the same field of subjects with CHB and combination therapy approach as applied to claims 72-73, 75, 81, and 83-84. It is similar to some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skills to modify the primary prior art reference to combine secondary prior art references teachings to arrive at the claimed inventions of claims 72-73, 75, 81, and 83-84. This is analogous to some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the invention as claimed in claims 72-73, 75, 81, and 83-84. See KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 415-421, 82 USPQ2d 1385, 1395-97 (2007), MPEP § 2143, example of rationales, A-G).
Response to Applicant’s Arguments
16. Applicant's arguments filed 07/22/2026 have been fully considered but they are not persuasive. Additional inherence or obviousness analysis is applied commensurate with the teachings of prior art in this office action to the extent necessary to address the amended claims and arguments relying on the amended language.
Applicants Arguments regarding Claim Rejections - 35 USC § 102:
Claims 27 and 34 are rejected under 35 U.S.C. 102 as allegedly anticipated by Chen 2021. To reach this conclusion, the Office reads the claims to encompass the clinical protocol in Chen 2021 which allegedly entails "determining a bassline HBV antibody concentration in a subject prior to administering the VLP (HBs Ag), identification of responders following administration of the VLP based on increase in antibody titers to HBs Ag and subsequent administration of anti-HBV siRNA are inherent to the study protocol."
As Chen 2021 does not disclose the administration of an anti-HBV siRNA after
identification of responders, presumably this rejection is on the ground that the Office interprets the rejected claims to recite the steps in no particular order and to define the HBV therapy to further include the HBsAg. Without acquiescing to rejection, Applicant has amended both independent claims for clarity.
As currently amended, the HBV therapy "does not comprise the HBsAg." Further, at least based on the antecedent basis, the steps of the claims are in a particular order. More specifically, in claim 27, step (a) must be before step (b), since step (a) clearly recites that the determining is "prior to" administering the HBsAg of step (b). Likewise, step (b) must be before step (c) since the determining of step (c) is "after" the HBsAg administration. Moreover, step (d) is after step (c) because step (d) recites the "responder subject" which is determined in step (c).
At least because the clarification of the claim language, the Section 102 is necessarily moot and should be withdrawn.
In Response:
Chen 2021 (Clinical Trial NCT04749368) has anticipated claim 27 and 34 with evidence from Ma et al 2021 and Ji et al 2025 on administration of BRII-835 (an anti-HBV siRNA). The steps in sequence as claimed by the applicant are inherent to the study protocol in view of identification of responders to HBs antigen administration and an anti-HBV siRNA being critical component of the claims as recited in the office action.
The anticipation rejection is maintained.
Applicants Arguments regarding Claim Rejections - 35 USC § 103:
Claims 27, 34, 76, 78, and 80 are rejected under 35 U.S.C. 103 as allegedly being unpatentable over Ma 2021 (JHEP Reports 2021), and further in view of Sepp-Lorenzino (WO2018195165A1), Anderson (WO2020254878A1), Hui (Clin Mal Hepatol. 2022), Vasconcelos (Case Reports in Infectious Diseases, 2022), and Wang (Scientific Reports 2016). Claims 72-75 and 81-84 are rejected under 35 U.S.C. 103 as allegedly being unpatentable over combined teachings of Ma, Sepp-Lorenzino, Anderson, Hui, Vasconcelos, and Wang and further in view of Chen (Clinical Trial Number NCT04749368 2021), Gupta (Clinical Trial NCT03672188, 2021), Ma 2019 (Front lmmunol. 2019) as evidenced by Ji (Gastroenterology 2025). Applicant respectfully submits that these Section 103 rejections should be withdrawn at least in view of the claim amendments, for the reasons that follow.
(A) The Amended Claims
Both independent claims, claims 27 and 34, as currently amended, recite the administration of an HBV therapy to treat hepatitis B viral (HBV) infection in a subject with chronic hepatitis B (CHB) that has been identified as a responder to an HBsAg. Moreover, the HBV therapy comprises an anti-HBV siRNA and does not include the HBsAg. It is important to note that, at least in view of the amendments and contrary to the Office's allegations, there are two important features of the instant claims (see explanation in response to Section 102 rejection above):
1. Sequential steps: the HBV therapy is administered after determination of responder subjects to HBsAg; and
2. Proviso: the HBsAg is not administered with the siRNA.
(B) The Cited Art Fails to Support a Prima Facie Case of Obviousness
With respect to step (d) of claim 27, the Office alleges that "Ma et al 2021 teaches administering anti-HBV therapy IFN-a to the responder subject by disclosing study design treatment group and responders BRll-179 20 ug+ IFN-a +NA. Ma et al 2021 further shows express motivation by disclosing that a recently initiated clinical study (NCT04749368) is evaluating the combination of HBV-specific small-interfering RNA and BRII-179, with the aim of reducing immunosuppressive viral antigen levels via gene silencing before stimulating HBV-specific immunity with multi-doses of BRII-179." Office Action at page 14, 2nd paragraph (emphasis in original and added).
At least in view of the current amendments, however, such an allegation by the Office includes two critical errors.
i. Ma 2021 Does Not Suggest Targeting HBsAg Responders for Further Treatment
First, Ma 2021 does not teach administering a therapy targeting patients determined as
responders, which is required by the claims. The Office points to the "Study Design" section and Table 3 as allegedly disclosing this. However, this is incorrect. Both locations of Ma 2021 only disclose administering the HBsAg to patients, some of whom later turned out to be responders. Such an interpretation of Ma 2021 is also consistent with the Office's acknowledgement that Ma 2021 proposed to run a clinical study (as reported in Chen 2021, NCT04749368) of a combination of siRNA and BRII-179 before the patients are treated with BRII-179.
Moreover, a knowledgeable reader of Ma 2021 would have recognized that the experimental data presented there would not have motivated one to further treat the responders upon their determination. In this context, it is important to note that the term "response" as used in Ma 2021 concerns specifically "immune response" (see, e.g., Abstract) instead of a general response to therapies. Indeed, Ma 2021 explicitly concluded that its responder patients actually failed to respond to the therapeutic activity of BRII-179:
Although BRII-179 displayed promising immunogenicity in patients with CHB in our study, we did not observe a notable association between detected HBV-specific immune responses and reductions of circulating HBsAg levels. There was also no significant change in circulating HBV RNA and HBcrAg levels across all treatment groups
throughout the study (data not shown).
Id. at page 9, last paragraph.
Based on this observation, Ma 2021 then hypothesized that "the lack of significant antiviral efficacy may be related to high baseline HBsAg levels and insufficient BRII-179 doses in this study." Id. at page 10, last paragraph (emphasis added). In order to achieve efficacy, therefore, Ma 2021 proposed a combination therapy to decrease HBsAg levels at the baseline (i.e., before the BRII-179 administration).
In summary, even though Ma 2021 showed that certain patients exhibited immune response to BRII-179, those that so responded did not exhibit therapeutic response. Consistent with this, Ma 2021 does not suggest to target such immune responders for further treatment; instead, Ma 2021 suggested to pre-treat patients with the alleged combination therapy so that the patients could respond therapeutically to BRII-179. Such a pre-treatment, however, is totally distinguishable from the instant claims which recite a siRNA therapy to a responder after it has been determined from BRII-179 administration.
ii. The Combination Therapy of Chen 2021 is Opposite to What the Claims Recite
Second, the Office considers the combination therapy of Chen 2021, which includes a
siRNA and BRII-179, to be within the scope of the instant claims. It actually is not. To clarify this, Applicant has further amended the claims to recite that "the responder subject is not administered the HBsAg after the subject is identified as a responder subject" and "the HBV therapy does not comprise the HBsAg."
From the foregoing, it is apparent that not only do the references fail to teach or suggest any treatment step after a patient is determined as to respond to a HBsAg, they also fail to teach or suggest a therapy with a siRNA without the HBsAg that could be used in conjunction with the HBsAg treatment. At least for these reasons, the cited references fail to support a prima facie case of obviousness. Accordingly, the Section 103 rejections should be withdrawn.
In Response:
The combined prior art teachings and obviousness analysis as applied for rejection of claims 27, 34, 76, 78, and 80 under 35 U.S.C. 103 as recited in the office action above renders obvious the claims.
In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
In response to applicant’s argument that there is no teaching, suggestion, or motivation to combine the references, the examiner recognizes that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007).
ARGUMENT DOES NOT REPLACE EVIDENCE WHERE EVIDENCE IS NECESSARY:
An argument by the applicant is not evidence unless it is an admission, in which case, an
examiner may use the admission in making a rejection. See MPEP § 2129 and § 2144.03 for a discussion of admissions as prior art. Arguments presented by applicant cannot take the place of evidence in the record. See In re De Blauwe, 736 F.2d 699, 705, 222 USPQ 191, 196 (Fed. Cir. 1984); In re Schulze, 346 F.2d 600, 602, 145 USPQ 716, 718 (CCPA 1965); In re Geisler, 116 F.3d 1465, 43 USPQ2d 1362 (Fed. Cir. 1997) ("An assertion of what seems to follow from common experience is just attorney argument and not the kind of factual evidence that is required to rebut a prima facie case of obviousness."). See MPEP § 716.01(c) for examples of applicant statements which are not evidence and which must be supported by an appropriate affidavit or declaration. See, MPEP 2145.
No secondary considerations or unexpected or surprising findings:
The Applicant has not filed any secondary considerations showing unexpected results or
surprising findings or results obtained from the claimed invention prior to the effective filing date of the claimed invention or application. See, MPEP 2145.
The rejections are maintained in this office action as recited supra.
17. The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
(i) Bertoletti A, Ferrari C. Adaptive immunity in HBV infection. J Hepatol. 2016 Apr;64(1 Suppl): S71-S83.
(ii) Yuen et al 2022. Efficacy and Safety of Bepirovirsen in Chronic Hepatitis B Infection. N Engl J Med. 2022 Nov 24;387(21):1957-1968. Yuen et al 2022 teaches New therapies are being developed for the treatment of chronic HBV infection, including small interfering RNAs (siRNAs).
(iii) Gane E, Lim YS, Cloutier D, et al. Safety and antiviral activity of VIR-2218, an X-targeting RNAi therapeutic, in participants with chronic hepatitis B infection: week 48 follow-up results. J Hepatol 2021;75: Suppl 2: S287-S288.
(iv) Luangsay et al 2023 (WO2023083906A2) discloses pharmaceutical combinations for treating hepatitis B virus (HBV) infection comprising administering at least two, preferably two or three, different HBV therapeutics. In particular, the present invention relates to pharmaceutical combinations comprising an RNAi oligonucleotide targeting HBV and an anti-PDL1 antisense oligonucleotide.
(v) Fisicaro et al 2020. Pathogenetic Mechanisms of T Cell Dysfunction in Chronic HBV Infection and Related Therapeutic Approaches. Front Immunol. 2020 May 12; 11:849.
Conclusion
18. No claim is allowed.
19. THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
20. 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SAMADHAN J JADHAO whose telephone number is (703)756-1223. The examiner can normally be reached M-F 8:00-5:00.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Thomas J Visone can be reached at 571-270-0684. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/SAMADHAN JAISING JADHAO/Examiner, Art Unit 1672
/BENNETT M CELSA/Primary Examiner, Art Unit 1600
