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 .
Claim Status
Applicant’s amendment filed March 5, 2026 has been received and entered.
Claims 1-4 have been amended.
Claims 10, 13-15, 17-22, 26, 28, and 31-33 have been canceled.
Claims 5-7, 9, 11-12, 16, 23-25, 27, 29-30, and 34 were previously canceled.
Claims 1-4 and 8 are pending and under consideration.
Priority
The previous objection over the benefit of priority for claims 10, 13-15, 18, and 28 has been withdrawn as these claims have been canceled with the reply received March 5, 2026.
This application is a 371 of PCT/US22/20459 filed March 15, 2022, which is a continuation of U.S. Application 17/209,160 filed March 22, 2021, which is a continuation-in-part of PCT/US19/59275 filed October 31, 2019, which claims the benefit of U.S. Provisional Application 62/753,485 filed October 31, 2018.
Information Disclosure Statement
The information disclosure statement (IDS) submitted March 5, 2026 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Claim Objections
Claims 1-4 are objected to because of the following informalities:
Claim 1 (line 4) recites CAR-T cells, which should be written in expanded form the first time it is used. The claim should read chimeric antigen receptor (CAR) T cells.
Claim 2 recites “wherein nucleic acid encoding said GM-CSF polypeptide…”, which is grammatically incorrect and is missing (a or the) between “wherein” and “nucleic acid”.
Claim 3 recites “wherein nucleic acid encoding said IL-6 polypeptide…”, which is grammatically incorrect and is missing (a or the) between “wherein” and “nucleic acid”.
Claim 4 (lines 1-2) should read “wherein the cancer is a lymphoma”.
Appropriate correction is required.
Claim Rejections - 35 USC § 112(b) - Withdrawn
In view of Applicant’s cancelation of rejected claims 10, 13-15, 18-20, 28, and 31-33, the previous grounds of rejection under 35 U.S.C. 112(b) have been withdrawn.
Claim Rejections - 35 USC § 112(b) - New
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following are new grounds of rejection necessitated by Applicant’s claim amendments.
Claims 1-4 and 8 are rejected under 35 U.S.C. 112(b) as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor regards as the invention.
Claim 1 recites “A method for administering CAR-T cell therapy to treat cancer without neurotoxicity…”, which suggests the method is for treating types of cancers that do not cause any type of neurotoxicity, such as tumors in the central nervous system that cause neurophysiological alterations. However, the instant specification is drawn to methods for treating cancer without inducing neurotoxic effects associated with CAR-T therapy, such as CRS, making the scope of the claim unclear. Applicant may amend the claim to read “A method for administering CAR-T cell therapy to treat cancer without causing neurotoxicity…”, or similar language.
Claims 2-4 and 8 are included in the rejection because they depend from and otherwise require all the limitation of the rejected claim.
Claim 1 recites the term “undetectable expression”, which is a relative term that renders the claim indefinite. The term “undetectable expression” is not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention. Furthermore, it is unclear how GM-CSF expression is undetectable, when Figure 10A shows CD19 GM-CSF knockout CAR-T cells have ~10% expression, which is far from “undetectable”.
Claims 2-4 and 8 are included in the rejection because they depend from and otherwise require all the limitation of the rejected claim.
Claim 2 recites “The method of claim 1, wherein nucleic acid encoding said GM-CSF polypeptide of said CAR-T cells is knocked out”. However, there is no antecedent basis for a nucleic acid in claim 1.
Claim 2 recites “The method of claim 1, wherein nucleic acid encoding said GM-CSF polypeptide of said CAR-T cells is knocked out”. The claim is unclear as currently written, and suggests that the nucleic acid encoding GM-CSF is knocked out, which does not make sense.
The claims are interpreted in light of the specification, which discloses a method for making a chimeric antigen receptor T cell having a reduced level of GM-CSF polypeptides, said method comprising: introducing a nucleic acid construct into an ex vivo T cell, wherein said nucleic acid construct comprises: a) a nucleic acid encoding a guide RNA, wherein said guide RNA is complementary to a GM-CSF messenger RNA; b) a nucleic acid encoding a Cas nuclease, and c) a nucleic acid encoding said chimeric antigen receptor [011].
Therefore, it is interpreted that the CAR-T cells comprise (in part) a CAR encoded by a nucleic acid and a nucleic acid encoding a guide RNA complementary to GM-CSF mRNA that carries out the function of knocking out GM-CSF in said CAR-T cell along with Cas9 nuclease.
Claim 3 recites “The method of claim 1, wherein nucleic acid encoding said IL-6 polypeptide of said CAR-T cells is knocked out”. However, there is no antecedent basis for a nucleic acid in claim 1.
Claim 3 recites “The method of claim 1, wherein nucleic acid encoding said IL-6 polypeptide of said CAR-T cells is knocked out”. The claim is unclear as currently written, and suggests that the nucleic acid encoding IL-6 is knocked out, which does not make sense.
The claims are interpreted in light of the specification, which discloses a method for making a chimeric antigen receptor T cell having a reduced level of cytokine polypeptides. The methods can include, or consist essentially of, introducing a complex into an ex vivo T cell, where the complex includes: a) a gRNA complementary to a cytokine mRNA; and b) a Cas nuclease; and introducing a nucleic acid encoding the CAR into the ex vivo T cell. The cytokine polypeptides can include GM-CSF polypeptides and/or IL-6 polypeptides [021].
Therefore, it is interpreted that the CAR-T cells comprise (in part) a CAR encoded by a nucleic acid and a nucleic acid encoding a guide RNA complementary to IL-6 mRNA that carries out the function of knocking out GM-CSF in said CAR-T cell along with Cas9 nuclease.
Claim Rejections - 35 USC § 112(a)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
ENABLEMENT
Claims 1-4 and 8 are rejected under 35 U.S.C. 112(a), first paragraph, as failing to comply with the enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
As a general rule, enablement must be commensurate with the scope of claim language. MPEP § 2164.08 states, “The Federal Circuit has repeatedly held that “the specification must teach those skilled in the art how to make and use the full scope of the claimed invention without undue experimentation.” In re Wright, 999 F.2d 1557, 1561, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993)” (emphasis added). The “make and use the full scope of the invention without undue experimentation” language was repeated in 2005 in Warner-Lambert Co. v. Teva Pharmaceuticals USA Inc., 75 USPQ2d 1865, and Scripps Research Institute v. Nemerson, 78 USPQ2d 1019 asserts: “A lack of enablement for the full scope of a claim, however, is a legitimate rejection.” The principle was explicitly affirmed in Auto. Tech. Int’l, Inc. v. BMW of N. Am., Inc., 501 F.3d 1274, 84 USPQ2d 1108 (Fed. Cir. 2007), Monsanto Co. v. Syngenta Seeds, Inc., 503 F.3d 1352, 84 U.S.P.Q.2d 1705 (Fed. Cir. 2007), and Sitrick v. Dreamworks, LLC, 516 F.3d 993, 85 USPQ2d 1826 (Fed. Cir. 2008). See also In re Cortright, 49 USPQ2d 1464, 1466 and Bristol-Myers Squibb Co. v. Rhone-Poulenc Rorer Inc., 49 USPQ2d 1370.
The factors to be considered in determining whether a disclosure meets the enablement requirement of 35 U.S.C. 112, first paragraph, have been described in In re Wands, 8 USPQ2d 1400 (Fed. Cir. 1988). Among these factors are: (1) the nature or the invention; (2) the state of the prior art; (3) the relative skill of those in the art; (4) the predictability or unpredictability of the art; (5) the breadth of the claims; (6) the amount of direction or guidance presented; (7) the presence or absence of working examples; and (8) the quantity of experimentation necessary. When the above factors are weighed, it is the examiner’s position that one skilled in the art could not practice the invention without undue experimentation. Some experimentation is not fatal; the issue is whether the amount of experimentation is “undue”; see In re Vaeck, 20 USPQ2d 1438, 1444.
(1) The nature of the invention and (5) The breadth of the claims:
Claim 1 is drawn to a method for administering CAR-T cell therapy to treat cancer without causing neurotoxicity, comprising administering CAR-T cells having undetectable levels of GM-CSF polypeptide expression and undetectable levels of IL-6 polypeptide expression.
(2) The state of the prior art and (4) The predictability or unpredictability of the art:
Norelli et al. (Nat Med, 2018; 24(6):739-748) teaches chimeric antigen receptor T (CAR T) cell therapy is frequently associated with life-threatening cytokine release syndrome (CRS) and neurotoxicity. However, the cellular and molecular players involved in life-threatening toxicities induced by CAR-T cells remain poorly understood [Abstract]. However, it is emerging that neurotoxicity by CAR-T cells may be more diversified than initially assumed [pg. 747, col. 2, par. 1].
Neurotoxicity by CD19 CAR-T cells is more frequent in acute lymphoblastic leukemia (ALL) and appears to occur independently from leukemic CNS localization. Signs of neurological dysfunction often develop during CRS but usually subside after its resolution. However, a delayed and potentially lethal form of neurotoxicity has been reported days to weeks after disappearance of CRS signs. Currently available preclinical xenograft mouse models are poorly predictive of the clinical behavior of CAR-T cells and to the almost invariant development of xenogeneic graft-versus-host disease. Most importantly, these models fail at reproducing severe CRS and lethal neurotoxicity [pg. 739].
Additionally, Norelli et al. teaches humanized mice with high leukemia burden administered CAR-T cell therapy triggered high fever and elevated IL-6 levels, which are hallmarks of CRS [Abstract]. Norelli et al. found that human circulating monocytes, not CAR-T cells, are primarily responsible for the systemic release of IL-6, which ultimately causes CRS [Discussion, pg. 747, col. 1, par. 2]. In humans, the anti-IL-6 antibody tocilizumab is often used, either alone or in combination with steroids, to manage CAR T-cell toxicities, ameliorating fever and hypotension typical of severe CRS, but fails to revert severe neurotoxicity [pg. 744, col. 2]. Additionally, some CD19 CAR-T cell trials have been halted due to neurotoxicity [Discussion, pg. 747, col. 1, par. 4].
Santomasso et al. (Cancer Discov, 2018; 8(8):958-971) teaches comprehensive clinical descriptions and analyses of neurotoxicity biomarkers are scarce, and there is no consensus on which therapeutic interventions are most effective for preventing or reducing the severity or duration of neurologic symptoms [Introduction, par. 2]. Although, there have been some reports of an association between neurotoxicity and elevated cerebrospinal fluid (CSF) cytokines IL6, IL2, GM-CSF, and VEGF Using a nonhuman primate model of CAR T-cell neurotoxicity. Despite these observations, the precise pathobiology of the neurotoxicity remains obscure [Introduction, par. 2].
Given the lack of predictability in the mechanisms regulating neurotoxicity function, one of ordinary skill in the art would have to engage in undue experimentation to identify subjects in which the method applies.
6) the amount of direction or guidance provided by the inventor; 7) the existence of working examples;
The instant specification discloses methods for making a CAR T cell having a reduced level of cytokine polypeptide consisting of introducing a gRNA complementary to a cytokine mRNA, a Cas nuclease, and a nucleic acid encoding the CAR into an ex vivo T cell. The cytokine polypeptides can include GM-CSF polypeptides and/or IL-6 polypeptides [021].
Norelli et al. teaches that upon tumor recognition in vitro, CAR-T cells produce negligible levels of IL-6 [Discussion, pg. 747, col. 1, par. 4].
However, the instant specification does not provide any examples of a GM-CSF/IL-6 double knockout CAR-T cell.
Furthermore, the specification does not provide any examples of administering GM-CSF knockout CD19 CAR-T cells to a mammal with cancer without causing neurotoxicity observed with wild type CD19 CAR-T cells, or how inhibiting IL-6 further contributes to preventing neurotoxicity.
In the context of ameliorating neurotoxicity with knockout CAR-T cells, the specification discloses GM-CSF knockout CAR-T cells can be incorporated into adoptive T cell therapies (e.g., CAR-T cell therapies) to treat, for example, mammals having cancer without resulting in CRS and/or neurotoxicity [017]. The specification further discloses that a high level of CD14+ myeloid cells in the central nervous system (CNS) of the subject is indicative of neurotoxicity [067]. However, Examples 2 and 4 of the specification shows CD19 CAR-T induced neurotoxicity can be ameliorated by administrating a neutralizing anti-GM-CSF antibody (lenzilumab) which causes a reduction in CNS infiltration by CD14+ cells and by CD11b+ cells in a primary ALL mouse xenograft model. Figure 14C contains a graph showing that human CD3 T cells were present in the brains of mice after treatment with CD19 CAR-T cell therapy. GM-CSF neutralization resulted in a trend toward decreased CD3 infiltration in the brain as assayed by flow cytometry in brain hemispheres [042]. The specification further discloses that CD14+ cells are a greater proportion of the CNS cell population in human patients with grade 3 or above neurotoxicity and that lenzilumab caused a reduction in CNS infiltration by CD14+ cells and by CD11b+ cells in the primary ALL mouse model used for the NT experiments [044].
Therefore, the instant application is not enabled for a method of administrating CAR-T cell therapy without inducing neurotoxicity by administering a population of CAR-T cells without detectable GM-CSF and IL-6 expression. One of skill in the art would be required to engage in extensive, difficult experimentation to carry out the recited method, as no examples are provided. This required experimentation is undue.
In conclusion, the claimed invention does not provide enablement for administering CAR-T cells without detectable GM-CSF and IL-6 expression to a subject with cancer without resulting in neurotoxicity. Thus for the reasons outlined above, the specification is not considered to be enabling for one skilled in the art to make and use the claimed invention as the amount of experimentation required is undue, due to the broad scope of the claims, the lack of guidance and working examples provided in the specification. Therefore, the specification is not representative of the instant claims and the specification is not fully enabled for the instant claims. In view of the above, one of skill in the art would be forced into undue experimentation to practice the claimed invention.
Claim Rejections - 35 USC § 102
The previous rejection of claim 1 under 35 U.S.C. 102(a)(1) and 35 U.S.C. 102(a)(2) as being anticipated by Sentman et al. (WO 2015/066262; cited IDS 8/18/2025) has been withdrawn in view of Applicant’s claim amendments.
Specifically, the instant claims have been amended to recite a method for administering CAR-T cells having undetectable levels of GM-CSF polypeptide expression, and undetectable levels of IL-6 polypeptide expression for the treatment of cancer without causing neurotoxicity. Sentman teaches methods of preventing cytokine storm release, but does not teach methods for preventing neurotoxicity as recited in the instant claims.
Claim Rejections - 35 USC § 103 - Updated
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.
The following rejection has been updated to reflect Applicant’s claim amendments. All other rejections have been withdrawn as those claims have since been canceled, thus making the rejections moot.
Claims 1-4 and 8 are rejected under 35 U.S.C. 103 as being unpatentable over Sentman et al. (WO 2015/066262; cited IDS 8/18/2025) (“Sentman”), in view of Santomasso et al. (Cancer Discov, 2018; 8(8):958-971) (“Santomasso”), and in further view of Norelli et al. (Nat Med, 2018; 24(6):739-748) (“Norelli”).
The instant claims are drawn to a method for treating administering CAR-T cell therapy to treat cancer without inducing neurotoxicity, comprising administering CAR-T cells having undetectable levels of GM-CSF polypeptide expression and undetectable levels of IL-6 polypeptide expression, wherein the GM-CSF and IL-6 are knocked out. The cancers that can be treated with said method is a lymphoma, or a leukemia or multiple myeloma, wherein the lymphoma is a diffuse large B cell lymphoma (DLBCL), mantle cell lymphoma, or follicular lymphoma, and wherein the leukemia is acute lymphoblastic leukemia (ALL), wherein the CAR- T cells target tumor antigen CD19 on lymphoma or leukemia cancer cells.
Sentman discloses methods for preventing toxicity of CAR-T cell therapy by administering to a subject with cancer, GM-CSF deficient CAR-T cells comprising a GM-CSF gene deletion or GM-CSF gene disruption (instant claims 1 (partial)-2). Sentman teaches toxicity includes a cytokine storm or cytotoxicity toward healthy cells, and blockade of GM-CSF prevents toxicity of adoptive cell therapy [0005]. The result of the GM-CSF gene deletion or GM-CSF gene disruption results in a CAR-T cell that does not express GM-CSF [0014] (instant claim 1 (partial)). The expression of endogenous GM-CSF is blocked/deleted by genetically modifying the immune cell using an engineered nuclease such as a zinc finger nuclease (ZFP), TALE-nuclease (TALEN), or CRISPR/Cas nuclease [0019].
Specifically, Sentman teaches that when infusing a high dose of GM-CSF-deficient CAR-T cells, serum cytokine levels produced in response to adoptive cell therapy are reduced up to 90%, including IL-6, and cytokine storm is prevented [(Fig. 1-2, 4), [0011-0012]] (instant claim 1 (partial).
CAR-T cells can be engineered to target antigens on tumor cells, such as CD19 in B cell lymphoma [0003] (instant claim 8). Sentman teaches the subsequent GM-CSF deficient CAR-T cells can be used in adoptive cell therapies for the treatment of a variety of cancers, including leukemia, acute lymphocytic leukemia, acute lymphoblastic leukemia, B-cell lymphoma, T cell lymphoma, and follicular lymphoma [0072] (instant claim 4). The CAR-T cells can be formulated into a pharmaceutical composition and delivered via various routes and sites in a mammalian, particularly human, body [0067] (instant claim 1 (partial)).
Sentman teaches methods for preventing cytokine storm associated with CAR-T cell therapy, but does not teach methods for administering CAR-T cell therapy without causing neurotoxicity, or that the CAR-T cells have undetectable levels of IL-6 polypeptide expression, or that IL-6 is knocked out in the CAR-T cells.
Santomasso teaches anti-IL6R monoclonal antibody tocilizumab, with or without corticosteroid, is often used to mitigate CRS and neurotoxicity. However, analysis shows that neurotoxicity did not respond to tocilizumab administration in most patients, confirming previous findings that neurotoxicity is less responsive than CRS to these treatment interventions. Serum cytokines, most notably IL-6, but also IL-8, IFNg, GM-CSF, and IL-10, peaked after tocilizumab administration [pg. OF4].
Santomasso further teaches there was a significant correlation of neurotoxicity with the presence and severity of CRS, wherein all 33 patients who developed neurotoxicity had at least grade 1 CRS with fever preceding the onset of neurologic symptoms. The onset of neurologic symptoms in relation to CRS was variable, however, neurotoxicity typically occurs after the start of CRS, and severe neurotoxicity can occur simultaneously with or without severe CRS, although it is always preceded by at least fever [pg. OF3, col. 2, last 2 paragraphs]. Lastly, Santomasso teaches serum cytokines can potentially have greater access to the CNS during situations of increased blood- cerebrospinal fluid barrier permeability, and several cytokines including GM-CSF and IL-6 were found to be significantly elevated in the cerebrospinal fluid of patients with severe neurotoxicity. Furthermore, blood- cerebrospinal fluid barrier disruption was significantly correlated with cerebrospinal fluid levels of cytokines including, GM-CSF [pg. OF8, col. 2] (instant claim 1 (partial)).
Santomasso does not teach CAR-T cells with IL-6 knocked out.
Norelli teaches that human circulating monocytes, not CAR-T cells, are primarily responsible for the systemic release of IL-6, which ultimately causes CRS [Discussion, pg. 747, col. 1, par. 2], wherein CAR-T cells produce negligible levels of IL-6 upon tumor recognition in vitro, [Discussion, pg. 747, col. 1, par. 4] (instant claim 1 (partial)). Therefore, Norelli teaches CAR-T cells do not have detectable levels of IL-6.
Sentman teaches administering GM-CSF knockout CAR-T cells can prevent toxicity associated CAR-T cell therapy, however, does not explicitly teach that it is for treatment of neurotoxicity. Given that Santomasso teaches CRS is correlated with neurotoxicity and is associated with elevated levels of GM-CSF and IL-6, one of ordinary skill in the art would have a reasonable expectation of success modifying the CAR-T cells taught by Sentman to further comprise one or more additional deletions of other cytokines implicated in neurotoxicity, such as IL-6 as taught by Santomasso. One would have a reasonable expectation of success in carrying out the second knockout using the methods taught by Sentman (e.g., Cas nuclease) which were known to those of ordinary skill in the art before the effective filing date of the instant invention.
KSR International Co. v. Teleflex Inc., 127 S. Ct. 1727, 1741 (2007), discloses that if a technique has been used to improve one method, and a person of ordinary skill would recognize that it would be used in similar methods in the same way, using the technique is obvious unless its application is beyond that person’s skill. It would be obvious to apply a known technique to a known product to be used in a known method that is ready for improvement to yield predictable results. Therefore, the instant invention was prima facie obvious to a person having ordinary skill in the art before the effective filing date of the claimed invention in view of the combined references.
One would be motivated to knock out IL-6 in addition to GM-CSF in the CAR-T cells because Sentman teaches the deletion of GM-CSF reduced serum IL-6 levels up to 90%, but not completely. Therefore, deleting both GM-CSF and IL-6 from the CAR-T cells would eliminate any residual IL-6 release from the CAR-T cells or from bystander monocytes. One would be further motivated to make such a construct because both GM-CSF and IL-6 were significantly elevated in the serum and cerebrospinal fluid of patients with CAR-T induced neurotoxicity as evidenced by Santomasso, therefore making them promising targets for reducing or eliminating CAR-T-associated neurotoxicity. Therefore, the instant invention was prima facie obvious to a person having ordinary skill in the art before the effective filing date of the claimed invention in view of the combined references.
Double Patenting - Withdrawn
The terminal disclaimers filed March 5, 2026 to obviate the provisional nonstatutory double patenting rejections over U.S. Application Nos. 17/209,160 and 17/290,185 are in compliance with 37 CFR 1.321(c) or 1.321(d). Accordingly, the previous nonstatutory double patenting rejections are withdrawn.
Conclusion
No claim is allowed.
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 MAUREEN DRISCOLL whose telephone number is (571) 270-0730. The examiner can normally be reached Monday through Friday.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Samira Jean-Louis can be reached on (571) 270-3503. The fax phone number for the organization where this application or proceeding is assigned is (571) 273-8300.
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/MAUREEN VARINA DRISCOLL/ Examiner, Art Unit 1642
/SAMIRA J JEAN-LOUIS/Supervisory Patent Examiner, Art Unit 1642
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