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 .
DETAILED ACTION
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
Election/Restrictions
Applicant’s election with traverse of Group I, claims 1, 2 and 21-24, in the reply filed on Dec. 11, 2025 is acknowledged. Claims 4-7 and 25-41 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected invention.
The traversal is based on the argument that the group of inventions are linked to form a single general inventive concept and the Office did not specify what the recognized technical feature is and only asserted that invariant NKT cells and precursors and a iNKT cell agonist is taught by Das (Remarks pg. 1 last para. to pg. 2 para. 2). Applicant argues that required elections are improper, since the application relates to methods of reducing the number of senescent cells in a subject by administering an iNKT cell activator which is not taught by Das (Remarks pg. 2 para. 3).
The traversal is on the grounds that the groups of inventions share the special technical feature. This is not found persuasive because as indicated by the rejections below, the groups do not share the special technical feature which contributes over the prior art at the time the invention was made.
It is noted that the special technical feature was accidentally left out of the sentence spanning pg. 2 and 3 of the Office Action mailed on Jul. 11, 2025. It is clear from the second sentence of the same paragraph that the special technical feature is an invariant natural killer (iNKT) or a iNKT precursor cell.
The requirement is still deemed proper and is therefore made FINAL.
Claims 1, 2 and 21-24 are presented for examination on the merits.
Status of the Claims
Claims 1-7 and 21-41 are currently pending.
Claims 3-7 and 25-41 have been withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected Invention, there being no allowable generic or linking claim.
Claims 8-20 are cancelled.
Claims 1, 2 and 21-24 have been considered on the merits.
Specification
The disclosure is objected to because of the following informalities: the use of trademarks.
The use of the terms: Vi-Cell® XR cell viability analyzer in 0108; FlowJo® in 0111; Tween®-20 in 0113; Attune® acoustic flow cytometer in 0114; SYBR® reagent in 0120; FACS Aria™ II cell sorter in 0121, which are a trade names or a marks used in commerce, have been noted in this application. The terms should be accompanied by the generic terminology; furthermore the terms should be capitalized wherever they appear or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the terms.
Although the use of trade names and marks used in commerce (i.e., trademarks, service marks, certification marks, and collective marks) are permissible in patent applications, the proprietary nature of the marks should be respected and every effort made to prevent their use in any manner which might adversely affect their validity as commercial marks.
Appropriate correction is required.
Claim Objections
The disclosure is objected to because of the following informalities: minor grammatical error in claims.
Claims 1 and 23 are objected to because of the following informalities: the first time an acronym is utilized in a claim-set, said acronym should be spelled out in its entirety followed by said acronym in parenthesis (e.g. invariant natural killer T (iNKT) cell; T-cell receptor (TCR)).
Appropriate corrections are appreciated.
Claim Rejections - 35 USC § 112
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.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
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 of carrying out his invention.
Claims 1 and 2 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claims contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention.
The instant claims are drawn to a method of reducing the number of senescent cells in a selected target tissue, organ, or compartment of a subject by administering a therapeutically effective amount of an agent that contains an iNKT cell activator which has a wide array of activities and/or effects. Thus, the claims are broadly drawn to any compound, molecule, or cell which activates iNKT cells. Therefore, these claims are considered genus claims that encompass a wide array of compounds. The claims encompass any activator of iNKT cells which are not described by their function, structure or relation thereto. The genus is highly variant, inclusive to numerous structural variants because a significant number of structural differences between genus members is permitted.
The specification defines “iNKT agents” as “an agent which promotes the clearance of senescent cells in a target organ, tissue or compartment of the body by the direct and/or indirect action of iNKT cells (0028). The specification generally describes that the agent can achieve an increase in the clearance of senescent cells by any number of mechanisms which can include activating resident iNKT cells, increasing the number of iNKT cells and/or recruiting iNKT cells to the target (0028). Additionally, the
specification states iNKT activators can include glycolipids, a composition of matter that increases the recruitment of iNKT1 cells to the target organ, tissue or compartment, a iNKT1 cell or a iNKT1 cell precursor (0029-0030). The specification describes alpha-Galactosylceramide (α-GalCer) or KRN7000 as a well-known iNKT activator and variants of α-GalCer which share structure similarity to α-GalCer (0033-0038). The specification describes synthetic aminocyclitolic ceramides, such as HS44, as an iNKT activator (0039) and lists specific glycolipids as activators (0040-0042). The specification states that the iNKT activator contemplates antibodies that binds to the TCR of iNKT cells and small molecule activators (0043-0044). Although the specification lists some and contemplates species, specification does not disclose the diverse genus. The specification does not place any structure, chemical or functional limitations on the embraced by genus “iNKT activator”. The recitation of “iNKT activator” does not convey a common structure or function and is not so defined in the specification. In sum, specification and the claim do not provide any guidance on the structure of the ““iNKT activator”.
The MPEP states that written description for a genus can be achieved by a representative number of species within a broad generic. It is unquestionable that the claims are broad generics, with respect to all of the potential species of antagonists that may exhibit one, all, of or any of the claimed activity. The possible variations of compounds and compositions of matter including cells are limitless with potentially thousands of compounds that may exhibit the claimed activities or potential compositions of matter. The purpose of the written description requirement is to ensure that the invention had possession, as of the filing date of the application, of the specific subject matter later claimed by him or her. A patent specification must describe an invention and do so in sufficient detail that one skilled in the art can clearly conclude that the inventor invented the claimed invention. Thus, an applicant complies with the written description requirement "by describing the invention, with all its claimed limitations," and by using "such descriptive means as words, structures, figures, diagrams, formulas, etc., that set forth the claimed invention."
Further, it is not sufficient to define it solely by its principal biological property, because an alleged conception having no more specificity than that is simply a wish to know the identity of any material with that biological property. Per the Enzocourt’s example, (Enzo Biochem, Inc. v. Gen-Probe Inc., 63 USPQ2d 1609 (CA FC 2002) at 1616) of a description of an anti-inflammatory steroid, i.e., a steroid (a generic structural term) couched “in terms of its function of lessening inflammation of tissues” which, the court stated, “fails to distinguish any steroid from others having the same activity or function” and the expression “an antibiotic penicillin” fails to distinguish a particular penicillin molecule from others possessing the same activity and which therefore, fails to satisfy the written description requirement. Similarly, the function of the iNKT cell activator does not distinguish a particular compound, molecule or a composition of matter from others having the same activity or function and as such, fails to satisfy the written-description requirement. Applicant has disclosed limited relevant, identifying characteristics, such as structure or other physical and/or chemical properties for a few compounds, which is not sufficient to show possession of the claimed genus. Mere idea or function is insufficient for written description; isolation and characterization at a minimum are required. A description of what a material does, rather than what it is, usually does not suffice. Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406.
Absent of such teachings and guidance as to the structure and function of these compounds, molecules or compositions of matter, the specification does not describe the claimed iNKT cell activator in such full, clear, concise and exact terms so as to indicate that Applicant had possession of all iNKT cell activators at the time of filing of the present application. Thus, the written description requirement has not been satisfied.
Claims 1, 2, and 21-24 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for reducing the number of senescent cells in a mammal subject, mice, by administering the iNKT cell activator, α-GalCer or α-GalCer activated iNKT cells, does not reasonably provide enablement for administering a therapeutically effective amount of any iNKT cell activator, non-activated iNKT cells or iNKT precursor cells, or any antibody that binds to the TCR of iNKT cells by all modes of delivery, or in any type of subject or animal. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
The factors to be considered in determining whether a disclosure meets the enablement requirements of 35 U.S.C. 112, first paragraph, have been described in In re Wands, 858 F.2d 731, 8 USPQ2d 1400 (Fed. Cir., 1988). The court in Wands states, “Enablement is not precluded by the necessity for some experimentation, such as routine screening. However, experimentation needed to practice the invention must not be undue experimentation. The key word is ‘undue’, not ‘experimentation’” (Wands, 8 USPQ2sd 1404). Clearly, the enablement of a claimed invention cannot be predicated on the basis of quantity of experimentation required to make or use the invention. “Whether undue experimentation is needed is not a single, simple factual determination, but rather is a conclusion reached by weighing many factual considerations” (Wands, 8 USPQ2d 1404). Among these factors are: (1) the nature of the invention; (2) the breadth of the claims; (3) the state of the prior art; (4) the predictability or unpredictability of the art; (5) the relative skill of those in the art; (6) the amount of direction or guidance presented; (7) the presence or absence of working examples; and (8) the quantity of experimentation necessary.
While all of these factors are considered, a sufficient amount for a prima facie case is discussed below.
(1) The nature of the invention and (2) the breadth of the claims:
The claims are drawn to a method of reducing the number of senescent cells in a selected target tissue, organ, or compartment of a subject by administering a therapeutically effective amount of an iNKT cell activator, iNKT cell or iNKT cell precursor to the subject. Claims 21 and 22 recite that the iNKT cell activator can be a CD1d-expressing cell functionalized with or loaded with glycolipid iNKT activators. Claim 22 recites that the CD1d-expressing cell is a dendritic cell. Claim 23 recites that iNKT cell activator is an antibody that selectively binds to and activates the TCR of iNKT cells. Thus, the claims taken together with the specification imply that any kind of iNKT cell activator, any iNKT cell or iNKT cell precursor, or any CD1d-expressing cell functionalized or dendritic cell with or loaded with any glycolipid iNKT activator can reduce the number of senescent cells in any animal subject by any delivery means.
(3) The state of the prior art and (4) the predictability or unpredictability of the art:
The prior art in general teaches iNKT response depends on the type of activation, there is potential in using iNKT cells in cell therapy for cancers and infectious diseases, there are differences in iNKT cells among mammal species. Additionally, activated iNKT cells are known to induce a response, but not iNKT cells which have not been activated.
For instance, Tognarelli et al. (Cancers, 2023) reports that exposure to different signals exerts pressure over the plasticity of iNKT cells causing them to adapt their transcriptional proteomic profiles to modulate the downstream immune responses (pg. 4 para. 2). In addition, Tognarelli reports that α-GalCer variants with different modifications can produce a Th1-type polarized response or a Th2 response in iNKT cells, and some activator molecules produce stronger responses than others (pg. 6 para. 2). This indicates that the type of iNKT activator is important in determining whether the iNKT cells would reduce the number of senescent cells in a subject and not all iNKT activators would be predicted to do so. Tognarelli further reports that administering α-GalCer to treat infectious diseases can cause concomitant secretion of multiple cytokines that have opposing functions limiting the effectiveness of α-GalCer as an immunomodulator and potentially causing other diseases. As an example, Tognarelli reports a single injection of α-GalCer has been shown to lead to long-term anergy in iNKT cells, liver injury in mice and liver toxicity in humans (pg. 8 para. 2). In further support of the unpredictability nature of the type of iNKT activation, Pinco et al. (Cells, 2025) teaches intratumoral microbiota significantly impacts the development, function, and activation of unconventional (UC) T cells, which includes iNKT cells (abstract). Pinco reports that iNKT activated with Fusobacterium nucleatum (Fn) were able to increase the survival rate of neutrophils and induce their recruitment, but iNKT activated with α-GalCer were not (pg. 6 last para).
With respect to the difference in the species of the subject, Wang et al. (Current Research in Translational Medicine, 2025) reports that there are significant differences between the iNKT cells of mice and humans which influences their function and therapeutic potential and these include being highly abundant in mice but less frequent in humans, producing predominantly Th1 cytokines in mice but a broader cytokine profile in humans, and differences in development and activity (pg. 1-2 bridging para.). Similarly, Tognarelli reports differences among human, mice guinea-pig and rabbit iNKT cells (pg. 4 para. 2).
Finally with respect to the mode of delivery, Tognarelli reports work is being done to develop vehicles for the delivery of glycolipid ligands for therapy including α-GalCer-pulsed DC (dendritic cells) and liposomal formulations (pg. 18 para. 2-3).
Thus, as the state of the art stands, the method would be unpredictable depending on factors including the subject, the type of iNKT cell activator, the type of iNKT cell administered, and the mode of administration or delivery.
(5) The relative skill of those in the art:
The relative skill of those in the art is high.
(6) The amount of direction or guidance presented and (7) the presence or absence of working examples:
The instant specification provides working examples and guidance for the use of the instantly claimed method for reducing the number of senescent cells in a mammal subject, mice, by administering the iNKT cell activator, α-GalCer or α-GalCer activated iNKT cells. For instance, the specification presents data showing that α-GalCer when presented on CD1d increases iNKT cell numbers in eWAT (epididymal white adipose tissue), both in vitro and in vivo in mice and that the α-GalCer activation of iNKT cells in the mice reduces the number of senescent cells (0098-0099). In addition, the specification presents data showing that when 150,000-300,000 iNKT cells, isolated from the eWAT of α-GalCer-treated HFD mice using a CD1d-loaded tetramer, are administrated by injection to HFD (high fat diet) mice there is a reduction in senescent preadipocytes in HFD mice (0099-0100, 0117). The specification presents data showing that activation of iNKT cells by systemic treatment with α-GalCer in an idiopathic lung fibrosis (IPF) mouse model decreased the number of senescent cells and reduced fibrosis. The specification presents data showing that activated iNKT cells are preferentially cytotoxic to human senescent cells in vitro (0103) and that iNKT cells can be activated in culture by co-culturing α-GalCer loaded dendritic cells for in vitro cytotoxicity assays (0118).
However, the specification does not provide any guidance for the use of the instantly claimed method for administering a therapeutically effective amount of any iNKT cell activator, non-activated iNKT cells or iNKT precursor cells, or any antibody that binds to the TCR of iNKT cells by all modes of delivery, or in any type of subject or animal. The applicants have provided no additional data demonstrating the claimed method with other iNKT cell activators, non-activated iNKT cells, or antibodies in other animal subjects using other modes of delivery. Therefore, there is no conclusive evidence in the instant disclosure to indicate that the instantly claimed method can be used to reduce the number of senescent cells in a selected target tissue, organ or compartment of any animal subject, with any iNKT activator, any iNKT cell or iNKT precursor cell, or any antibody that binds to the TCR of iNKT by any mode of delivery. Additionally, the efficacy of cell therapy faces numerable obstacles in vivo. For example, the mode of delivery of the cells and the delivery of cells in amounts needed to be efficacious, but not lethal to the subject requires testing in order to adequately determine the proper usage for the subject. Also, activated iNKT cells were known to induce a response, it cannot be inferred that any iNKT cell or iNKT precursor cell which has not been activated would have the same effect.
(8) The quantity of experimentation necessary:
The test of enablement is not whether any experimentation is necessary, but whether, it any experimentation is necessary, it is undue. Due to the large quantity of experimentation necessary to establish whether additional iNKT agents are effective in reducing the number of senescent cells in any animal would require undue experimentation for one skilled in the art at the time of the invention to practice over the full scope of the invention claimed. Considering the state of the art as discussed above and the high unpredictability and the lack of guidance provided in the specification, one of ordinary skill in the art would be burdened with undue experimentation to use the claimed invention within the broad scope as instantly claimed.
Therefore, claims 1, 2, and 21-24 are rejected under 35 U.S.C. 112, first paragraph, for scope of enablement.
Claim Rejections - 35 USC § 102
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.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1, 2, and 24 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Mossanen et al. (Gastroenterology, 2019) (ref. of record).
With respect to claim 1, Mossanen teaches a method of reducing the number of senescent cells in the liver (a selected target organ) of a mouse by administering a therapeutically effective amount of α-galactosylceramide (α-GalCer) to activate invariant natural killer T (iNKT) cells (abstract and pg. 1878 Col. 2 para. 3 and pg. 1884 Col. 2 para. 2-3, and Fig. 6). With respect to claim 2, Mossanen teaches a method of reducing the number of senescent cells in the liver (a selected target organ) (abstract). With respect to claim 24, Mossanen teaches administering iNKT cells into DEN-treated (induces liver cancer) Cxcr6-/- (lacks NKT cells) mice and that the administration of the iNKT cells reduced the numbers of senescent cells to level seen in DEN-treated WT mice (liver tumor model) (pg. 1881 para. 2 and Fig. 3).
Therefore, the reference anticipates the claimed subject matter.
Claims 1, 2, 21 and 22 are rejected under 35 U.S.C. 102(a)(1) and (a)(2) as being anticipated by Teyton et al. (WO 2006/083671 A2) (ref. of record).
With respect to claims 1, 21 and 22, Teyton teaches activation of NKT cells (iNKT) by antigen present cells such as dendritic cells in the presence of a bacterial glycolipid activator or putative activator (pg. 5 lines 6-10). Teyton teaches the method where the antigen presenting cells are dendritic cells, which are CD1d expressing cells, and teaches the cells are functionalized with a bacterial glycolipid activator or putative activator so that there is complexing of the bacterial glycolipids with the CD1d molecules expressed by the antigen presenting cell (pg. 9 line 5-22 and claims 1 and 15-17). Further with respect to claim 1, Teyton teaches the method where the antigen presenting cells are administered to a subject to provide a suitable immune response (therapeutically effective amount) (pg. 9 line 5-22). With respect to claim 2, Teyton teaches method where the target tissue is lung, liver and spleens (pg. 3 lines 33-36, pg. 13 lines 18-25 and pg. 14 lines 1-6).
It is noted that Teyton does not teach that their method can be used in the manner instantly claimed for reducing the number of senescent cells in a selected target tissue, organ or compartment of a subject as recited in claim 1. However, the teachings of Teyton teach the claimed method of administering CD1-expressing dendritic cells functionalized with glycolipid iNKT activators. Once administered to the subject the cells would treat whatever conditions are present. Thus, the claimed result of reducing the number of senescent cells in a selected target tissue, organ or compartment of a subject must be inherent to the method as taught by the references and a necessary effect of practicing the method.
Therefore, the reference anticipates the claimed subject matter.
Claims 1 and 23 are rejected under 35 U.S.C. 102(a)(1) and (a)(2) as being anticipated by Truneh et al. (WO 2013/063395 A1) (ref. of record).
With respect to claims 1 and 23, Truneh teaches a method of activating iNKT cells in a subject by contacting the cells with an effective amount of an activating antibody (pg. 8-9 bridging para., pg. 11 para. 2). Truneh teaches the antibody binds to the T-cell receptor (TCR) of iNKT cells (pg. 6 last para., pg. 7 para. 2).
It is noted that Truneh does not teach that their method can be used in the manner instantly claimed for reducing the number of senescent cells in a selected target tissue, organ or compartment of a subject as recited in claim 1. However, the teachings of Truneh teach the claimed method of administering an antibody that selectively binds to and activates the TCR of iNKT cells. Once administered to the subject the antibody would treat whatever conditions are present. Thus, the claimed result of reducing the number of senescent cells in a selected target tissue, organ or compartment of a subject must be inherent to the method as taught by the references and a necessary effect of practicing the method.
Therefore, the reference anticipates the claimed subject matter.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
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.
Claims 1, 2, 21, 22 and 24 are rejected under 35 U.S.C. 103 as being unpatentable over Mossanen et al. (Gastroenterology, 2019) (ref. of record) in view of Teyton et al. (WO 2006/083671 A2) (ref. of record).
With respect to claim 1, Mossanen teaches a method of reducing the number of senescent cells in the liver (a selected target organ) of a mouse by administering a therapeutically effective amount of α-galactosylceramide (α-GalCer) to activate invariant natural killer T (iNKT) cells (abstract and pg. 1878 Col. 2 para. 3 and pg. 1884 Col. 2 para. 2-3, and Fig. 6). With respect to claim 2, Mossanen teaches a method of reducing the number of senescent cells in the liver (a selected target organ) (abstract). With respect to claim 24, Mossanen teaches administering iNKT cells into DEN-treated (induces liver cancer) Cxcr6-/- (lacks NKT cells) mice and that the administration of the iNKT cells reduced the numbers of senescent cells to level seen in DEN-treated WT mice (liver tumor model) (pg. 1881 para. 2 and Fig. 3).
Mossanen does not teach the method where the agent is a CD1d-expressing cell functionalized or loaded with glycolipid iNKT activators as recited in claim 21. Similarly, Mossanen does not teach the method where the CD1d-expressing cell is a dendritic cell as recited in claim 22.
Teyton teaches activation of NKT cells (iNKT) by antigen present cells such as dendritic cells in the presence of a bacterial glycolipid activator or putative activator (pg. 5 lines 6-10). Teyton teaches the method where the antigen presenting cells are dendritic cells, which are CD1d expressing cells, and teaches the cells are functionalized with a bacterial glycolipid activator or putative activator so that there is complexing of the bacterial glycolipids with the CD1d molecules expressed by the antigen presenting cell (pg. 9 line 5-22 and claims 1 and 15-17). Further with respect to claim 1, Teyton teaches the method where the antigen presenting cells are administered to a subject to provide a suitable immune response (therapeutically effective amount) (pg. 9 line 5-22).
Accordingly, at the effective time of filing of the claimed invention, one of ordinary skill in the art would have been motivated to modify the method of Mossanen so that the iNKT activating agent is a CD1-expressing dendritic cells functionalized with glycolipid iNKT activators for the benefit of activating iNKT in a subject as taught by Teyton. Furthermore, it would have been obvious to one skilled in the art to have further modified Mossanen such that the iNKT activating agent is a CD1-expressing dendritic cells functionalized with glycolipid iNKT activators, since methods of administering such cells to subjects were known for activating iNKT cells in vivo as taught by Teyton. Such a modification involves the substitution of one known type of iNKT activator for another for activating iNKT cells in vivo. For these reasons one of ordinary skill in the art would have a reasonable expectation of success in making such a modification to Mossanen.
Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective time of filing of the invention, especially in the absence of evidence to the contrary.
Claims 1, 2, 23 and 24 are rejected under 35 U.S.C. 103 as being unpatentable over Mossanen et al. (Gastroenterology, 2019) (ref. of record) in view of Truneh et al. (WO 2013/063395 A1) (ref. of record).
With respect to claim 1, Mossanen teaches a method of reducing the number of senescent cells in the liver (a selected target organ) of a mouse by administering a therapeutically effective amount of α-galactosylceramide (α-GalCer) to activate invariant natural killer T (iNKT) cells (abstract and pg. 1878 Col. 2 para. 3 and pg. 1884 Col. 2 para. 2-3, and Fig. 6). With respect to claim 2, Mossanen teaches a method of reducing the number of senescent cells in the liver (a selected target organ) (abstract). With respect to claim 24, Mossanen teaches administering iNKT cells into DEN-treated (induces liver cancer) Cxcr6-/- (lacks NKT cells) mice and that the administration of the iNKT cells reduced the numbers of senescent cells to level seen in DEN-treated WT mice (liver tumor model) (pg. 1881 para. 2 and Fig. 3).
Mossanen does not teach the method where the agent is an antibody that selectively binds to and activates the TCR of iNKT cells as recited in claim 23.
However, Truneh teaches a method of activating iNKT cells in a subject by contacting the cells with an effective amount of an activating antibody (pg. 8-9 bridging para., pg. 11 para. 2). Truneh teaches the antibody binds to the T-cell receptor (TCR) of iNKT cells (pg. 6 last para., pg. 7 para. 2).
Accordingly, at the effective time of filing of the claimed invention, one of ordinary skill in the art would have been motivated to modify the method of Mossanen so that the iNKT activating agent is an antibody which selectively binds to and activates the TCR of iNKT cells for the benefit of activating iNKT in a subject as taught by Truneh. Furthermore, it would have been obvious to one skilled in the art to have further modified Mossanen such that the iNKT activating agent is an antibody which selectively binds to and activates the TCR of iNKT cells, since methods of administering such antibodies to subjects were known for activating iNKT cells in vivo as taught by Truneh. Such a modification involves the substitution of one known type of iNKT activator for another for activating iNKT cells in vivo. For these reasons one of ordinary skill in the art would have a reasonable expectation of success in making such a modification to Mossanen.
Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective time of filing of the invention, especially in the absence of evidence to the contrary.
Conclusion
No claims are allowed.
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/EMILY A CORDAS/Primary Examiner, Art Unit 1632