DETAILED ACTION
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Applicant's amendment and remarks, filed 6/12/26, are acknowledged.
Claims 1, 3, 8-12, 20-21, 24-25, 33-34, 37-38, 46, and 50 have been amended.
Claims 1, 3, 8-12, 20-21, 24-25, 33-34, 37-38, 46, 50, and 58-59 are pending.
Claims 58-59 are withdrawn from further consideration by the examiner, 37 CFR 1.142(b), as being drawn to a non-elected invention.
Claims 1, 3, 8-12, 20-21, 24-25, 33-34, 37-38, 46, and 50 are being acted upon.
The prior art rejections are withdrawn in view of Applicant’s claim amendments.
The rejections under 112b and 112a have been modified to the extend necessary to address Applicant’s claim amendments. Applicant’s arguments will be addressed below.
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 is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 1, 3, 8-12, 20-21, 24-25, 33-34, 37-38, 46, and 50 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 1, as amended, recites a method comprising administering to the subject a therapeutically effective amount of recipient antigen-specific regulatory T cells and “expanding said regulatory T cells in vitro” and “contacting said plurality of regulatory T cells with a plurality of recipient antigen presenting cells”. As an initial matter, it is not at all clear if the expanding and contacting steps are meant to define how the administered cells have been prepared. Or do the claim mean to require administering regulatory T cells, and then expanding the administered regulatory cells in vitro thereafter? The amended claim is further unclear in that it also recites a separate wherein clause reciting that “said recipient antigen specific regulatory T cells” are (i) obtained by a method comprising steps (i) and (ii). Does the wherein clause further limit the prior expanding/contacting steps? Is it meant to refer to the fact that the administered recipient antigen specific regulatory T cells are obtained by a particular method? The amended wherein limitations are further unclear in that the claim recites in part (i) that said regulatory T cells are from “said donor”. There is a lack of antecedent basis for this term in the claim. Although part (ii) subsequently recites “a donor of a tissue transplant”, this does not provide clear antecedent basis for a term that is recited in a preceding limitation.
For the purposes of applying prior art, the expanding and contacting steps are being interpreted as process steps that come before the administering step, wherein they define how the administered regulatory T cells have been made.
Furthermore, the scope of the claimed “recipient antigen-specific T cells” and “recipient antigen presenting cells” is still unclear. Normally, these would be understood as antigen presenting cells of recipient origin, whereby the method would be understood to generate donor Tregs that are specific for recipient antigens. However, the specification on page 22 discloses that “recipient antigen” refers to an antigen derived from the recipient of a tissue transplant, and that it can be derived from the allogenic transplant that is produced by the recipient. In other words, the “recipient antigen” of the claims would appear to actually encompass allogeneic donor antigen from the transplant.
The same is true for “recipient antigen presenting cells”. The specification discloses recipient antigen presenting cells refers to immune cells taken from the recipient of an allogenic transplant, and that in embodiments the recipient antigen presenting cells are derived from the transplanted tissue. In other words, the “recipient antigen presenting cells” appear to also encompass APCs of donor origin that originate form the allogeneic transplant. Given that a recipient antigen in the claims could be donor antigen and a recipient antigen presenting cells could be donor antigen presenting cells, the scope of the claimed method is rendered unclear and indefinite. For example, would the claims require administration or formation of regulatory T cells that can actually recognize recipient antigen that originates in the recipient or not. Could the regulatory T cells actually be donor specific, if the donor antigen is one that resides on the transplant in the recipient?
Claims 33 and 46 are indefinite in the recitation of recipient antigen presenting cells and recipient antigen for the same reason set forth above.
Claim 8 is unclear since it recites the method of claim 1, “contacting said plurality of regulatory T cells”, i.e. there is a missing word. Is it meant to recite the method of claim 1, “wherein”, the method of claim 1, “further comprising”. Additionally, it is unclear if the claim is reciting a further step or whether it is defining one of the steps from the claim from which it depends.
Claims 10 and 20 are indefinite for similar reasons. The claims repeat certain steps already in the independent claim, and it is not clear if they are required to be performed again, or are meant to further limit the step already recited in the independent claim. For example, claim 20, recites wherein said recipient antigen-specific regulatory T cells are formed by a method comprises: step (a) –(c). At least step (a), expanding, is identical to the expanding step already recited in claim 1. Does claim 20 require repeating the expanding step? Or is a single expanding step encompassed? Is claim 20 intending to merely limit the contacting step of claim 1, i.e. the method of claim 1, wherein the contacting of said plurality of regulatory T cells with said plurality of recipient antigen presenting cells induces activation of the recipient antigen presenting cells? The scope of the claims is unclear and indefinite.
Applicant’s arguments filed 6/12/26 have been fully considered, but they are not persuasive
Applicant argues that the amendment overcomes the rejection. In particular, Applicant argues that dependent claims now expressly require that the recipient antigen presenting cells comprise B cells and dendritic cells isolated from the peripheral blood of the subject. Applicant cites Figs. 4 and 5 and in paragraphs 320-332 which Applicant argues show that said APC populations are host-origin immune cells that are not cells originating from transplanted tissue.
None of the independent claims have been amended to clarity the issue. The limitations regarding B cells and dendritic cells are in dependent claims. However, they would still appear to encompass donor type B cells, for example, from the transplanted tissue, as broadly encompassed by the definition of the specification for “recipient antigen presenting cells”. Furthermore, claim 24 specifically recites that the recipient antigen presenting cells are taken from said subject when the subject has GVHD. A subject who has GVHD after bone marrow transplantation would have PBMC (including B cells and dendritic cells) that originate from the donor. In other words, said PBMC would not be “host origin immune cells” as argued by Applicant. They would be donor origin. Therefore, the scope of the claimed recipient antigen presenting cells is not at all clear. Is it limited to host origin, i.e. APC originating from the recipient, as argued by Applicant? Or is meant to encompass donor origin APC that are found in the blood of a subject that has GVHD after bone marrow transplantation.
Regarding claims 33 and 46, Applicant argues that the amendment to the claims resolves the issue, and that with respect to the antigen presenting cells, the claim would encompass cells derived form the subject at an relevant time point. It is also noted that the instant specification on page 25 discloses that “derived from” indicates from the stated source at some point in time. Therefore, the limitation that the plurality of recipient antigen presenting cells “is from a subject who has received said tissue transplant” is being interpreted as encompassing antigen presenting cells that are derived from the recipient at any point in time, i.e. the APC could be derived from the recipient prior to a tissue transplant or after tissue transplant. However, the scope of “recipient antigen presenting cells” in claims 33 and 46 is still indefinite for the reasons set forth above, i.e. do the claims actually encompass donor type antigen presenting cells from the transplant, or do the claims require host(recipient) type APC as argued by Applicant.
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, 3, 8-12, 20-21, 24-25, 33-34, 37-38, 46, and 50 are rejected under 35 U.S.C. 112, 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.
The specification disclosure is insufficient to enable one skilled in the art to practice the invention as claimed without an undue amount of experimentation. Undue experimentation must be considered in light of factors including: the breadth of the claims, the nature of the invention, the state of the prior art, the level of one of ordinary skill in the art, the level of predictability of the art, the amount of direction provided by the inventor, the existence of working examples, and the quantity of experimentation needed to make or use the invention, see In re Wands, 858 F.2d at 737, 8 USPQ2d at 1404 (Fed. Cir. 1988).
In re Fisher, 427 F.2d 833, 839, 166 USPQ 18, 24 (CCPA 1970) states, “The amount of guidance or direction needed to enable the invention is inversely related to the amount of knowledge in the state of the art as well as the predictability in the art.” “The “amount of guidance or direction” refers to that information in the application, as originally filed, that teaches exactly how to make or use the invention. The more that is known in the prior art about the nature of the invention, how to make, and how to use the invention, and the more predictable the art is, the less information needs to be explicitly stated in the specification. In contrast, if little is known in the prior art about the nature of the invention and the art is unpredictable, the specification would need more detail as to how to make and use the invention in order to be enabling” (MPEP 2164.03). The MPEP further states that physiological activity can be considered inherently unpredictable. With these teachings in mind, an enabling disclosure, commensurate in scope with the breadth of the claimed invention, is required.
The present claims are directed to methods of treating GVHD in a subject by administering recipient antigen specific regulatory T cells or methods of forming recipient antigen specific regulatory T cells by expanding regulatory T cells from a tissue transplant donor with a plurality of recipient antigens presenting cells. The state of the art is such that GVHD is initiated after allogeneic bone marrow transplantation, wherein donor T cells originating from the donor bone marrow recognize and attack the host (recipient). Regulatory T cells from the transplant donor can suppress GVHD when they are activated in response to recipient (host) APC cells (see the 20030147865, of record, and the prior art cited below). In this situation, the donor regulatory T cells are activated to expand in response to allogeneic recipient antigens, and the Tregs upon administration to the recipient, will suppress the aberrant immune response against the same recipient antigens that are the cause of GVHD.
However, the present claims are much broader than this. For example, the instant specification on page 22 discloses that “recipient antigen” refers to an antigen derived from the recipient of a tissue transplant, and that it can be derived from the allogenic transplant that is produced by the recipient. In other words, the “recipient antigen” of the claims would also encompass allogeneic donor antigen from the transplant. The same is true for “recipient antigen presenting cells”. The specification discloses recipient antigen presenting cells refers to immune cells taken from the recipient of an allogenic transplant, and that in embodiments the recipient antigen presenting cells are derived from the transplanted tissue of an allogenic transplant. In other words, the “recipient antigen presenting cells” would also encompass donor type APCs that originate from the allogeneic transplant.
For example, in the claimed methods, if the “recipient antigen presenting cells” are of donor type originating from the donor tissue transplant, it would be highly unpredictable as to how “recipient antigen specific regulatory T cells” could even be formed. If there is no foreign/alloantigen, what would induce said T cells to form into antigen specific T cells? Additionally, if the “recipient antigen” can be a donor antigen, obtaining donor Tregs that would form ‘recipient antigen specific T regs” would also be highly unpredictable.
Regarding claims 33 and 46, they would encompass taking the antigen presenting cells directly from the subject who has received the tissue transplant. The preferred embodiment disclosed by the instant specification is a bone marrow transplant. A patient who has received a bone marrow transplant would comprise donor type APCs, and using said donor type APCs, to expand “recipient antigen” specific T cells would be highly unpredictable. Dependent claims also recite that the recipient antigen presenting cells are taken from said subject when the subject has GVHD. In other words, the recipient antigen presenting cells are taken after bone marrow transplant, when the recipients immune cells (including APCs) in the blood have been replaced by those originating from the donor bone marrow used for transplant. See Chakraverty, 2007, after bone marrow transplantation and GVHD onset, the APC environment undergoes dramatic distortion. The types phenotype and function of APCs after bone marrow transplantation is highly variable and dependent on the time following transplantation, the mode of conditioning, the site, and the stage of GVHD (See page 10 and 13, in particular). Furthermore, the state of the art is that it is host (recipient) APC that expand alloantigen donor T regs (see Chakraverty page 14, in particular). See also Young, 2012, which teaches that donor B cells in particular augment CD4 T cell expansion an a way that is pathogenic and exacerbates GVHD. Thus, producing recipient Treg cells and treating GVHD with said Treg cells, wherein the Tregs are produced using recipient APCs that are taken from the subject that has graft versus host disease, would be highly unpredictable.
Based on the unpredictably of the art and the breadth of the claim limitations, the instant specification must provide a sufficient and enabling disclosure commensurate in scope with the instant claims. The specification does not provide any examples of treating GVHD or any guidance on providing recipient antigen or recipient antigen presenting cells, including from the subject after GVHD onset, or originating from the donor as broadly encompassed by the instant claims. In Figure 1 and the examples, it appears that the experiments are performed PBMC from the patient are frozen (i.e. they obtained prior to transplant) and mixed with Tregs from a donor to induce Tregs. This is similar to the prior art process taught below, which although is within the scope of some of the claims, is not commensurate in scope with the breadth of the present claims. No other guidance is provided. Thus, based on the unpredictability of the art, the breadth of the claims, and the lack of guidance provided by the instant specification, it would require undue experimentation to practice the full scope of the claimed methods.
Applicant’s arguments filed 6/12/26 have been fully considered, they are not persuasive.
Applicant argues that the enablement rejection is predicated on the claim construction that recipient antigen presenting cells encompass donor type APC, which Applicant acknowledges is one possible reading of the specifications definition of recipient antigen. Applicant argues however, that as amended, the claims expressly define the APCs by peripheral blood phenotype, wherein the APCs are obtained prior to transplant.
The independent claims all encompass any “recipient antigen presenting cell”. Claim 11 recites that the APCs are take from said subject, but does not limit to those taken prior to transplant. Claims 24 and 27 explicitly recite that the APCs are taken when the subject has GVHD, i.e. after transplant. None of the claims limit the plurality of APCs used in the contacting step of claims 1, 33, or 46 to those obtained prior to transplant, as argued by Applicant. As conceded by Applicant the scope of the recipient antigen presenting cells, as defined in the specification, would encompass donor type APCs and donor type antigen.
As noted above, the phenotype and function of APCs after transplantation is highly variable and dependent on the time following transplantation, the mode of conditioning, the site, and the stage of GVHD (See page 10 and 13, in particular). Furthermore, the state of the art is that it is host (recipient) APC that expand alloantigen donor T regs (see Chakraverty page 14, in particular). See also Young, 2012, which teaches that donor B cells in particular augment CD4 T cell expansion an a way that is pathogenic and exacerbates GVHD. Given the lack of guidance provided by the instant specification, the breadth of the claims, and the unpredictably of the art, it would require undue experimentation to practice the full scope of the claimed methods.
The following are new grounds of rejection necessitated by Applicant’s amendment.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claims 1, 3, 8-12, 20-21, 25, 33-34, 38, 46, 50 is/are rejected under 35 U.S.C. 103 as being unpatentable over Davies, 2009 (Davies I) and Davies, 2012 (Davies II), in view of US 2008/0131445.
Davies I teaches a method of expanding alloantigen specific CD4+CD25+CD127-/low regulatory T cells comprising culturing said regulatory T cells with allogeneic PBMC (i.e. APC) in the presence of a CD28 blocking agent, wherein the culturing expands said CD4+CD25+CD127-/low regulatory T cells (see page 5 and Fig. 3, in particular). Davies I also teach a further step of re-stimulating said regulatory T cells in the presence of a second population of said allogeneic APC, which further expands said CD4+CD25+CD127low-regulatory T cells Treg cells (See page 6 and Fig. 4, in particular). Davies teach obtaining the cells from the blood. Davies teaches that the alloanergization process in the presence of the costimulatory molecule blockage expands pre-existing Treg cells in vitro (See page 6 and supplemental figures , in particular). Davies I teach that after expansion, said Tregs can be sorted to isolate CD4+CD25+CD127lo/- Tregs, which are highly potent (see pages 6 and Fig. 5, in particular). Davies teaches that the high degree of antigen specificity provided by the in vitro method suggests that this approach can be used as a cell therapy for the prophylaxis or treatment of GVHD (see page 9, in particular). Davies I teaches that in the context of GVHD, donor T cells recognize recipient antigens as alloantigen, and thus causing GVHD and the reference teaches using recipient PBMC (i.e. APC) as the alloantigen to stimulate Treg cells from a bone marrow donor (i.e. the alloantigen specific regulatory T cells taught by Davies for use in GVHD are “recipient antigen” specific, see page 2, supplemental Figure S1, in particular). The method of Davies I, wherein donor regulatory T cells are culture with allogeneic, recipient PBMC (i.e. APC) in the presence of a CD28 blocking agent, which expands CD4+CD25+CD127-/low regulatory T cells would be within the scope of the expanding and contacting step of claim 1 (or within steps a) and (b) as recited in claims 32 and 46). For example, in the culture with alloantigenic (recipient) APC and CD28 blockade in Davies, the regulatory T cells expand to form a plurality of Tregs, and said plurality of Tregs is in also in contact with said APCs and CD28 inhibitory compound.
Although Davies I teaches sorting CD4+CD25+CD127low/- regulatory T cells after expansion, the reference does not explicitly teach selecting said CD4+CD25+CD127low/- regulatory T cells from the donor prior to expansion. Davies I also does not explicitly teach belatacept.
The ‘445 publication teaches a method of isolating and expanding Treg cells comprising isolating a population of CD4+CD25+CD127lo/- from a biological sample and expanding the Treg cells in vitro (see pages 2-3, in particular). The ‘445 publication teaches that the Tregs can be expanded by culturing the isolated cells with alloantigen (See page 2, in particular). The ‘445 publication teaches that the Treg cells are FoxP3+ (see page 2, in particular). The ‘445 publication teaches that the Treg can be used for treating GVHD, in which case the Tregs are derived from donor tissue and used in a recipient subject (See paragraph 146-149, in particular). The ‘445 publication also teaches Tregs can be obtained from peripheral blood. The ‘445 publication that the process of enriching said CD4+CD25+CD127lo/- regulatory T cells can be achieved prior to the expanding step, or after the expanding step (see page 11, in particular).
Davies II teach the same method of expanding alloantigen specific CD4+CD25+CD127-/low regulatory T cells comprising culturing said regulatory T cells with allogeneic PBMC (i.e. APC) in the presence a CD28 blocking agent, wherein the culturing expands said CD4+CD25+CD127-/low regulatory T cells. Davies II also teach a further step of re-stimulating said regulatory T cells in the presence of a second population of said allogeneic APC, which further expands said CD4+CD25+CD127low-regulatory T cells Treg cells (See Fig. 4, in particular). Davies II teaches that the ex vivo cellular manipulation is simple and easily adopted, and provides a platform to generate immunoregulatory cell products (See page 2059, in particular). Davies II teach using belatacept as the CD28 blocking agent, and that is more efficacious in producing said regulatory T cells (see page 2055, in particular).
Therefore, it would have been prima facie obvious to one of ordinary skill in the art at the time the invention was made to isolate CD4+CD25+CD127-/low regulatory T cells prior to expansion, as taught by the ‘445 publication, in the method of Davies I. Doing so would involve choosing among a finite number of predictable options which could be pursued with a reasonable expectation of success. A person of ordinary skill has good reason to pursue the known options within his or her technical grasp. If this leads to the anticipated success, it is likely the product not of innovation but of ordinary skill and common sense (see KSR International Co. V. Telefex Inc 82 USPQ2d 1385). The ordinary artisan would have a reasonable expectation of success, since the ‘445 publication teaches that enriched, expanded alloantigen specific CD4+CD25+CD127-/low regulatory T cells can be used to treat GVHD, and that the isolation procedure can be performed either before or after expansion.
The cited references teach obtaining the recipient PBMC prior to transplantation (See Figure S1 of Davies I), and these would be withing the scope of from the recipient who has received a transplant at some point in time (i.e. before the transplant), and therefor are within the scope of APCs “from a recipient subject who has received a tissue transplant” as recited in claims.
Regarding claims 9 and 50, Davies I and II teach using alloantigen (recipient) PBMC as the alloantigen and said PBMC would inherently comprise both B cells and CD303+, CD1c+ and/or CD141+ dendritic cells.
Regarding claims 25 and 38, the references teach that sorting on the basis of CD4+CD25+CD127-/low enriches for FoxP3+ Treg cells,. For example, see Fig. 3 of the ‘445 publication, wherein CD127 low T cells are 94% positive for FoxP3. Having unmethylated TSDR flows naturally from expression of FoxP3. In other words, a cell population having at least 70% FOxP3+T regs, as made obvious by the cited prior art, would inherently also have unmethylated TSDR.
Regarding claim 12, 25 and 50, obtaining the recipient PBMC (APC) prior to transplantation would be prior to administration of GVHD treatment.
Regarding claim 20, this would be a latent property of the method made obvious above, i.e. the allogeneic (recipient) APC would inherently become activated in the culture).
Regarding claim 21, Davies I teaches that PBMC can be cryopreserved (see page 3), and the ordinary artisan would find it obvious to use cryopreserved PBMC as a matter of convenience.
Claims 25 and 38 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 claim(s) 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. This is a new matter rejection.
The specification and the claims as originally filed do not provide support for the invention as now claimed, specifically:
A) A method wherein said recipient antigen specific regulatory T cells have “at least 70%” unmethylated FoxP3 TSDR.
It is noted that applicant has not cited any support for the new limitation in the specification. A review of the specification fails to reveal support for the new limitations.
Regarding, A), in Fig. 12, the specification discloses a specific example of particular percent of unmethylated FOXP3 TSDR. However, this specific example (where the amount is not disclosed, but from the bar graph appears to correspond to a value of 80%) does not provide support for the range recited in the instant claims, which encompass 70% or 99%, for example.
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 extension fee 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 date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to AMY E JUEDES whose telephone number is (571)272-4471. The examiner can normally be reached on M-F from 7am to 3pm.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Misook Yu can be reached on 571-272-0839. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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Amy E. Juedes
Patent Examiner
Technology Center 1600
/AMY E JUEDES/Primary Examiner, Art Unit 1644
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