DETAILED ACTION
In application filed on 03/29/2023, Claims 36, 38-42, 44-49 and 51-55 are pending. The claim set submitted on 07/28/2026 is considered because this is the most recent claim set with some preliminary amendments. Claims 42 and 44-48 are considered in the current office 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 .
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 04/04/2024 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Claim Objections
Claim 42 objected to because of the following informalities:
Claim 42 recites “a plasma NfL level” in lines 6 and 10 of the claim.
It appears that the “a plasma NfL level” in line 10 same as “a plasma neurofilament light chain (NfL) level in line 6 of the claim.
For the purpose of expedited prosecution, the limitation "when the subject has a plasma NfL level of more than about 44 pg/mL" is interpreted by the Examiner as "when the plasma NfL level of the subject is more than about 44 pg/mL ".
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
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.
Claim 42 is rejected under 35 U.S.C. 103 as being unpatentable over by Hrusovsky et al. (WO2019199871A1, submitted in IDS on 04/04/2024) in view of Jensen et al. (US20190112379A1, submitted in IDS on 04/04/2024) and further in view of Lewczuk et al. ("Plasma neurofilament light as a potential biomarker of neurodegeneration in Alzheimer’s disease." Alzheimer's research & therapy 10.1 (2018): 71.”).
Regarding Claim 42, Hrusovsky teaches a method comprising:
providing a biological sample (referred to as sample of physiological fluid [Para 0021]) from the subject (See Para 0012…the sample of physiological fluid may be obtained from a subject within 24 hours after a medical procedure is performed on a subject; See Para 0030… the test may comprise providing a sample of venous blood plasma or serum from a subject); and wherein the biological sample (referred to as sample of physiological fluid [Para 0021]) comprises plasma (See Para 0021…the physiological fluid may be a plasma);
measuring a plasma neurofilament light chain (NfL) level in the biological sample (See Para 0022…the single-assay test may comprise obtaining, via an immunoassay, a concentration of NF-L in the at least one liquid sample; See Para 0021… the physiological fluid may be a plasma;); and
Hrusovsky does not explicitly teach a method of treating immunotherapy-associated neurotoxicity in a subject in need thereof;
wherein the subject has an immunotherapy-associated neurotoxicity; and
administering a treatment for the immunotherapy-associated neurotoxicity before, after, and/or during an immunotherapy when the subject has an NfL level of more than about 44 pg/mL.
In the analogous art of methods for preventing or ameliorating toxicity caused by or due to a therapy, such as an immunotherapy or a cell therapy, by pre-emptive or early administration of a toxicity-targeting agent(s), Jensen teaches:
a method of treating immunotherapy-associated neurotoxicity (See Abstract… methods for preventing or ameliorating toxicity caused by or due to a therapy, such as an immunotherapy or a cell therapy, by pre-emptive or early administration toxicity-targeting agent(s).) in a subject in need thereof (See Claim 1… the subject has been previously administered a therapy, which therapy comprises an immunotherapy and/or a cell therapy);
wherein the subject has an immunotherapy-associated neurotoxicity (See Para 0020…the steroid is administered at a time in which the subject exhibits grade 2 neurotoxicity or within 24 hours after the subject exhibits a first sign or symptom of grade 2 neurotoxicity following administration of the therapy); and
administering a treatment for the immunotherapy-associated neurotoxicity before, after, and/or during an immunotherapy (See Para 0020…the steroid is administered at a time in which the subject exhibits grade 2 neurotoxicity or within 24 hours after the subject exhibits a first sign or symptom of grade 2 neurotoxicity following administration of the therapy; See Para 0019…the agent or other treatment is or comprises tocilizumab. In some such embodiments, the tocilizumab is administered, thereby teaching “an immunotherapy”).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method of Hrusovsky to incorporate “a method of treating immunotherapy-associated neurotoxicity in a subject in need thereof; wherein the subject has an immunotherapy-associated neurotoxicity; and administering a treatment for the immunotherapy-associated neurotoxicity before, after, and/or during an immunotherapy” as taught by Jensen for the benefit of treating, preventing, delaying, or attenuating the development of a toxicity when the subject has been previously administered a therapy, such as a therapy including an immunotherapy and/or a cell therapy (Jensen, Para 0005-0006), which allows for the provision of a method including the timing of the administration of the agents or treatments for toxicity, that provide various advantages, such as lower toxicity while maintaining persistence and efficacy of the administered cells (Jensen, Para 0003).
The combination of Hrusovsky and Jensen does not teach “when the subject has a plasma NfL level of more than about 44 pg/mL”.
In the analogous art of the use of plasma neurofilament light as a potential biomarker of neurodegeneration in Alzheimer’s disease, Lewczuk teaches that “when the subject has a plasma NfL level of more than about 44 pg/mL” (See Page 1… The findings revealed baseline mean NfL levels were higher in patients with … Alzheimer's dementia (45.9 ng/L) than in cognitively unimpaired controls (32.1 ng/L)..
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method of Hrusovsky and Jensen to incorporate the step of “when the subject has a plasma NfL level of more than about 44 pg/mL” as taught by Lewczuk for the benefit of disclosing that the plasma NfL concentrations measured in subjects at the stage of early dementia (Lewczuk , Abstract, Background) allowing for consideration of the plasma concentration of the neurofilament light chain as a plasma biomarker for the screening of neurodegeneration in Alzheimer’s disease (AD) (Lewczuk , Abstract, Background).
Claim 44 is rejected under 35 U.S.C. 103 as being unpatentable over Hrusovsky et al. (WO2019199871A1, submitted in IDS on 04/04/2024) in view of Jensen et al. (US20190112379A1, submitted in IDS on 04/04/2024) and further in view of Lewczuk et al. ("Plasma neurofilament light as a potential biomarker of neurodegeneration in Alzheimer’s disease." Alzheimer's research & therapy 10.1 (2018): 71.”) as applied to claim 42 above, and further in view of Farwell et al. (WO2019147960A1) and further in view of Liles et al. (US20190361026A1).
Regarding Claim 44, the method of claim 42 is obvious over Hrusovsky, Jensen and Gisslén.
The combination of Hrusovsky, Jensen and Lewczuk does not teach that measuring the plasma NfL level in the biological sample is performed up to 30 days before the subject is expected to receive the immunotherapy.
In the analogous art of the diagnosis and prognosis of spinal muscular atrophy (SMA) as well as identification of responders to treatment of SMA. Also provided are methods of treating subjects with SMA, Farwell teaches that the measuring the plasma NfL level (See Claims 45…wherein the neurofilament is a neurofilament light chain; See Page 8; Claim 46… the biological sample is blood, serum, plasma, or cerebrospinal fluid) in the biological sample (See Claim 2…measuring a neurofilament level in a biological sample) is performed before the subject is expected to receive the immunotherapy (See Claims 2, 4, 22 and 26…measuring a neurofilament level in a biological sample obtained from the human subject before initiation of an SMA therapy; and administering a therapeutically effective amount of the SMA therapy to the human subject; See Page 8; Claim 46… the biological sample is blood, serum, plasma, or cerebrospinal fluid).
While combination of Hrusovsky, Jensen, Lewczuk and Farwell does not explicitly teach the measuring the plasma NfL level in the biological sample being performed up to 30 days before, Farwell teaches that the measuring the plasma NfL level in the biological sample being performed up to 30 days before by using an overlapping range disclosure (See Claims 2, 4, 22 and 26…measuring a neurofilament level in a biological sample obtained from the human subject before initiation of an SMA therapy; Under BRI, Examiner submits the measuring a neurofilament level in a biological sample obtained from the human subject before initiation of an SMA therapy is done as least zero days before SMA therapy; See Page 8; Claim 46… the biological sample is blood, serum, plasma, or cerebrospinal fluid ) and since the claimed ranges overlap ranges disclosed by the prior art, a prima facie case of obviousness exists. Please see MPEP 2144.05 (I) and In re Wertheim, 541 F.2d 257, 191USPQ 90 (CCPA 1976) for further details.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method of Hrusovsky, Jensen and Lewczuk to incorporate that measuring the plasma NfL level in the biological sample is performed up to 30 days before the subject is expected to receive the immunotherapy for the benefit of finding the neurofilament levels that serve as effective biomarkers for spinal muscular atrophy (SMA) wherein the human subject has been previously determined to have, in a biological sample obtained from the human subject, a neurofilament level prior to initiation of the SMA therapy that is higher than a control (Farwell, Claim 1, Page 68; Page1, lines 24-32-Page 2, lines 1-4), allowing for the timely and proper treatment of subjects with SMA, thus, requiring a need for biomarkers of SMA (Farwell, Page 1, Lines 13-21).
The combination of Hrusovsky, Jensen, Lewczuk and Farwell does not teach measuring biomarker concentrations in the biological sample is performed up to 30 days before the subject is expected to receive the immunotherapy.
In the analogous art of methods for diagnosing or detecting the risk of an adverse event associated with immunotherapy, such as cytokine release syndrome (CRS), neurotoxicity or both, Liles teaches measuring biomarker concentrations (See Para 0128…evaluation of biomarker concentrations) in the biological sample is performed up to 30 days (See Para 0129…day 0 before CAR-T cell) before the subject is expected to receive the immunotherapy (See Para 0128-0129…evaluation of Clinical Laboratory Parameters, CAR-T Cell Counts, and Biomarker Concentrations; See Para 0129…Blood was collected before lymphodepletion, on day 0 before CAR-T cell infusion…).
Further, Liles teaches that adverse event biomarkers may be measured in a subject before pre-conditioning chemotherapy, before immunotherapy (e.g., adoptive immunotherapy infusion comprising a chimeric antigen receptor (CAR) modified T cell), or shortly after pre-conditioning chemotherapy and/or immunotherapy (See Abstract).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method of Hrusovsky, Jensen, Gisslén and Lewczuk to incorporate that measuring biomarker concentrations in the biological sample is performed up to 30 days before the subject is expected to receive the immunotherapy in the biological sample is performed up to 30 days before the subject is expected to receive the immunotherapy, as taught by Liles for the benefit of measuring adverse event biomarkers in identifying subjects at risk of adverse events after immunotherapy (Liles, Abstract, Para 0070), allowing for the treatment of subjects identified as at risk of developing cytokine release syndrome (CRS), neurotoxicity, or both to minimize such potential adverse events (Liles, Abstract).
Claims 45-48 are rejected under 35 U.S.C. 103 as being unpatentable over Hrusovsky et al. (WO2019199871A1, submitted in IDS on 04/04/2024) in view of Jensen et al. (US20190112379A1, submitted in IDS on 04/04/2024) and further in view of Lewczuk et al. ("Plasma neurofilament light as a potential biomarker of neurodegeneration in Alzheimer’s disease." Alzheimer's research & therapy 10.1 (2018): 71.”) as applied to claim 42 above, and further in view of Mcmahon et al. (WO2019200251).
Regarding Claim 45, the method of claim 42 is obvious over Hrusovsky, Jensen and Lewczuk.
The combination of Hrusovsky, Jensen and Lewczuk does not teach that the immunotherapy- associated neurotoxicity is immune effector cell-associated neurotoxicity syndrome (ICANS).
In the analogous art of a method of preventing, lessening the effects, or treating cytokine release syndrome (CRS) or related disorders, and/or neurotoxicity associated with immunotherapy comprising administering defibrotide, Mcmahon teaches that the immunotherapy- associated neurotoxicity is immune effector cell-associated neurotoxicity syndrome (ICANS) (See Para 0017… methods of preventing, lessening the effects, or treating CAR-related encephalopathy syndrome (CRES) (i.e. CAR-T associated neurotoxicity/ICANS) in a patient comprising administering a therapeutically effective amount of defibrotide; Also See Para 0019).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method of Hrusovsky, Jensen and Lewczuk to incorporate that the immunotherapy- associated neurotoxicity is immune effector cell-associated neurotoxicity syndrome (ICANS) as taught by Mcmahon for the benefit of preventing, lessening the effects, or treating CAR-related encephalopathy syndrome (CRES) (i.e. CAR-T associated neurotoxicity/ICANS) in a patient comprising administering a therapeutically effective amount of defibrotide (Mcmahon, Para 0017), allowing for the provision of methods of administering defibrotide to prevent and/or treat cytokine release syndrome (CRS), especially CRS associated with CAR-T therapy (Mcmahon, Para 0005).
Regarding Claim 46, the method of claim 42 is obvious over Hrusovsky, Jensen and Lewczuk.
While Jensen teaches that when the plurality of receptors are ligated, such as upon encounter of a cell expressing the first and second antigens, a desired response is achieved, such as full immune activation or stimulation, e.g., as indicated by secretion of one or more cytokine, proliferation, persistence, and/or carrying out an immune effector function such as cytotoxic killing of a target cell (Para 0167),
The combination of Hrusovsky, Jensen and Lewczuk does not explicitly teach that the immunotherapy comprises an immune effector cell therapy.
In the analogous art of a method of preventing, lessening the effects, or treating cytokine release syndrome (CRS) or related disorders, and/or neurotoxicity associated with immunotherapy (See Page 0016…immunotherapy; See Para 0023…(i.e. CAR-T associated neurotoxicity/ICANS) after administration of immunotherapy) comprising administering defibrotide, Mcmahon teaches that the immunotherapy comprises an immune effector cell therapy (See Claim 2… treating CAR-related encephalopathy syndrome (CRES) or chimeric antigen receptor (CAR)-T associated neurotoxicity or immune effector cell (IEC) therapy associated neurotoxicity syndromes (ICANS)…; See Para 0023…ICANS).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method of Hrusovsky, Jensen and Lewczuk to incorporate that the immunotherapy comprises an immune effector cell therapy as taught by Mcmahon for the benefit of preventing and/or lessening the effects of and/or treating CAR-related encephalopathy syndrome (CRES) or chimeric antigen receptor (CAR)-T associated neurotoxicity or immune effector cell (IEC) therapy associated neurotoxicity syndromes (ICANS) in a patient comprising administering a therapeutically effective amount of defibrotide (Mcmahon, Claim 2; Para 0023), allowing for the provision of methods of administering defibrotide to prevent and/or treat cytokine release syndrome (CRS), especially CRS associated with CAR-T therapy (Mcmahon, Para 0005).
Regarding Claim 47, the method of claim 46 is obvious over Hrusovsky, Jensen and Lewczuk.
The combination of Hrusovsky, Lewczuk and Mcmahon does not teach that the immune effector cell therapy is a CAR T cell therapy selected from engineered CAR T, universal allogeneic CAR T, CD19-specific CAR T, anti-CD19 CAR T, anti-BCMA CAR T, anti-CD22, anti- CAIX, anti-PSMA, anti-MUC1, anti-FRa, anti-meso-RNA, anti-CEA, anti-IL13Ra2, or anti- HER2.-T.
In the analogous art of a method of preventing, lessening the effects, or treating cytokine release syndrome (CRS) or related disorders, and/or neurotoxicity associated with immunotherapy comprising administering defibrotide, Mcmahon teaches that the immune effector cell therapy (See Para 0066… CAR-T cell therapy; See Para 0067…immunotherapy ( e.g.CAR-T cell therapy or monoclonal antibody) administration…; See Para 00126-00127…patients undergoing CAR-T therapy may have undergone or be undergoing allogenic or autologous CAR-T therapy) is a CAR T cell therapy (See Para 0066… CAR-T cell therapy; See Para 0067…immunotherapy ( e.g.CAR-T cell therapy or monoclonal antibody) administration…; See Para 00126-00127…patients undergoing CAR-T therapy may have undergone or be undergoing allogenic or autologous CAR-T therapy) selected from engineered CAR T, universal allogeneic CAR T, CD19-specific CAR T, anti-CD19 CAR T, anti-BCMA CAR T, anti-CD22, anti- CAIX, anti-PSMA, anti-MUC1, anti-FRa, anti-meso-RNA, anti-CEA, anti-IL13Ra2, or anti- HER2.-T (See Para 00126-00127…patients undergoing CAR-T therapy may have undergone or be undergoing allogenic or autologous CAR-T therapy…the present disclosure has undergone allogenic CAR-T therapy, wherein Universal CAR-T Therapy is also known as Allogeneic CAR-T Therapy).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method of Hrusovsky, Jensen and Lewczuk to incorporate that the immune effector cell therapy is a CAR T cell therapy selected from engineered CAR T, universal allogeneic CAR T, CD19-specific CAR T, anti-CD19 CAR T, anti-BCMA CAR T, anti-CD22, anti- CAIX, anti-PSMA, anti-MUC1, anti-FRa, anti-meso-RNA, anti-CEA, anti-IL13Ra2, or anti- HER2.-T, as taught by Mcmahon for the benefit of having a patient undergo a type of CAR-T therapy (Mcmahon, Para 00126-00127) in treating a variety of underlying primary diseases ((Mcmahon, Para 00125), allowing for the provision of methods of administering defibrotide to prevent and/or treat cytokine release syndrome (CRS), especially CRS associated with CAR-T therapy (Mcmahon, Para 0005).
Regarding Claim 48, the method of claim 42 is obvious over Hrusovsky, Jensen and Lewczuk.
While Hrusovsky teaches detection assays involving the use of multispecific Hrusovsky, Lewczuk and Mcmahon does not teach that the immunotherapy comprises a bispecific antibody therapy.
In the analogous art of a method of preventing, lessening the effects, or treating cytokine release syndrome (CRS) or related disorders, and/or neurotoxicity associated with immunotherapy comprising administering defibrotide, Mcmahon teaches that the immunotherapy (See Page 0016…immunotherapy; See Para 0023…(i.e. CAR-T associated neurotoxicity/ICANS) after administration of immunotherapy) comprises a bispecific antibody therapy (See Para 0016…the immunotherapy is a bispecific antibody).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method of Hrusovsky, Jensen and Lewczuk to incorporate that the immunotherapy comprises a bispecific antibody therapy, for the benefit demonstrating that bispecific antibody is a form of immunotherapy used in preventing, lessening the effects, or treating Cytokine Release Syndrome (CRS) in a patient (Mcmahon, Para 0016) allowing for the provision of methods of administering defibrotide to prevent and/or treat cytokine release syndrome (CRS), especially CRS associated with CAR-T therapy (Mcmahon, Para 0005).
Response to Arguments
Applicant's arguments filed on 07/28/2026, with respect to the objections to the drawings filed 03/29/2023 have been fully considered and are persuasive.
Applicant notes that the drawings are objected to for low legibility and resolution. Replacement Drawing Sheets 1/4 through 4/4 (corresponding to FIG. 1 (A-D)) are submitted herewith.The Replacement Drawings add no new matter and are the best version available. Accordingly, Applicant respectfully requests entry of the Replacement Drawings into the record and withdrawal of the objection to the drawings.
Examiner respectfully agrees and the objections to the drawings filed 03/29/2023 are withdrawn.
Applicant’s arguments, see Page 6, filed 07/28/2026, with respect to the rejection(s) of claim(s) 42 under 35 U.S.C. §103 (e been fully considered and are persuasive. Therefore, the rejection has been withdrawn. However, upon further consideration, a new ground(s) of rejection is made for amended Claim 42 by Hrusovsky et al. (WO2019199871A1, submitted in IDS on 04/04/2024) in view of Jensen et al. (US20190112379A1, submitted in IDS on 04/04/2024) and further in view of Lewczuk et al. ("Plasma neurofilament light as a potential biomarker of neurodegeneration in Alzheimer’s disease." Alzheimer's research & therapy 10.1 (2018): 71.”).
Applicant submits the independent claims (Claim 42) are amended herein to clarify that the threshold for administering a treatment for the immunotherapy-associated neurotoxicity before, after, and/or during an immunotherapy is defined as a plasma concentration threshold, i.e., when the subject has a plasma NfL level of more than about 44 pg/mL. The Office states that the combination of Hrusovsky+Jensen fails to teach Applicant's claimed threshold (see Office Action, p. 7). Applicant agrees.
However, the Office alleges Gisslen to cure the deficiencies of Hrusovsky+Jensen. Applicant respectfully disagrees. The Office merely cites to Gisslen's assay for measuring plasma NFL and its limit of detection (see Gisslen at Section 2.5, p. 137). Attention is further drawn to Gisslen's statements: "[L]aboratory cutoffs for blood NFL have not yet been defined" (see Gisslen at Section 2.5, p. 137, left column) and "[U]nlike CSF, age- related reference values have not yet been established for plasma NFL" (see Gisslen at Section 3, p. 138, left column). Moreover, Gisslen is altogether silent regarding immunotherapy and immunotherapy-associated neurotoxicity. In fact, Gisslen fails to disclose, teach, or suggest a plasma NfL concentration threshold for determining a treatment in any context. Therefore, Gisslen provides no suggestion to one of ordinary skill to combine with Hrusovsky+Jensen for disclosing, teaching, or suggesting a plasma NfL concentration threshold for determining that a immunotherapy-associated neurotoxicity is to be administered before, after, and/or during an immunotherapy for a subject in need thereof.
Consequently, the subject matter of the pending independent claims, and the claims dependent thereon, is neither taught nor suggested by any of the cited reference combinations. That is, the combinations of Hrusovsky+Jensen+Gisslen, Hrusovsky+Jensen+Gisslen+Farwell+Liles, and Hrusovsky+Jensen+Gisslen+McMahon each fail to disclose, teach, or suggest the subject matter of the currently pending claims. Applicant submits that the cited reference combinations fail to render obvious the subject matter of the pending claims and that the pending claims are patentable over the cited reference combinations. Accordingly, Applicant respectfully requests that the § 103 rejections of the claims be withdrawn.
Applicant’s arguments with respect to amended claim 42 has been considered and Examiner respectfully disagrees.
Examiner submits that the limitations of amended Claim 42 is taught as disclosed in the rejection of amended Claim 42 (Supra) by Hrusovsky et al. (WO2019199871A1, submitted in IDS on 04/04/2024) in view of Jensen et al. (US20190112379A1, submitted in IDS on 04/04/2024) and further in view of Lewczuk et al. ("Plasma neurofilament light as a potential biomarker of neurodegeneration in Alzheimer’s disease." Alzheimer's research & therapy 10.1 (2018): 71.”).
Accordingly, the combination of Hrusovsky, Jensen and Lewczuk discloses the limitation of a plasma NfL concentration threshold for determining that a immunotherapy-associated neurotoxicity is to be administered before, after, and/or during an immunotherapy for a subject in need thereof provided in Amended Claim 42.
Further, Examiner submits that the combinations of Hrusovsky,Jensen, Lewczuk ,Farwell and Liles discloses Claim 44 limitations in view of amended Claim 42; and Hrusovsky, Jensen, Lewczuk and McMahon discloses Claim 45-48 limitations in view of amended Claim 42.
Accordingly, Examiner respectfully submits that the § 103 rejections of claims 44-48 are maintained.
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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to OYELEYE ALEXANDER ALABI whose telephone number is (571)272-1678. The examiner can normally be reached on M-F 7:30am-5:30pm.
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/OYELEYE ALEXANDER ALABI/ Examiner, Art Unit 1797
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