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 .
Priority
The instant application, filed on 14 December, 2023, is a 371 of PCT/US2022/034062 filed 17 June, 2022 and which claims domestic benefit to US provisional application no. 63/211,989, filed on 17 June, 2021.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 28 April, 2025 has been considered by the examiner.
The information disclosure statement (IDS) submitted on 14 December, 2023 has been considered by the examiner.
Status of Application, Amendments, and/or Claims
The response filed on 25 November, 2024 has been entered in full. These are the amended claims of the original claim set received on 14 December, 2023. In the amendment, claims 3, 5, 7-9, 11, 12, 15, 16, 19, 22, 37, 31-33, 35-37, and 41-44 are amended and claims 4, 6, 10, 13, 14, 17, 18, 20, 21, 23-26, 28-30, and 34 are cancelled. Therefore, claims 1-3, 5, 7-9, 11, 12, 15, 16, 19, 22, 27, 31-33, and 35-44 are pending and are the subject of this Office Action.
Specification
The use of the term Poros, Sepharose, Sephadex, etc., which are trade names or marks used in commerce, has been noted in this application. The terms should be accompanied by the generic terminology; furthermore, the terms should be capitalized wherever it appears 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.
Claim Objections
Claim 9 is objected to because of the following informalities: between some of the cytokine/ chemokines of the list recited in claim 9, there are periods (.) instead of commas (,). Appropriate correction is required.
Claim 32 is objected to because of the following informalities: the word isotonic in the last line of the claim is misspelled. Appropriate correction is required.
Claim Rejections - 35 USC § 112(b)
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.
Claim 9 is 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 9 recites “wherein said fibroblasts are selected for expression of CD73, CD70, CD105, CD16, CD55, CD37, interleukin-10 receptor, interferon or wherein said fibroblasts…” the lack of an “and,” “or,” or “and/or” between the last two molecules makes it unclear if the list is inclusive (all must be met) or exclusive (only one or more must be met). For the purpose of further examination and in light if the specification which states ” In certain embodiments, the fibroblasts are selected for expression of CD73, CD70. CD105, CD16. CD55. CD37, interleukin-10 receptor, and/or interferon gamma receptor” (pg.3, lines 29-30), the claim will be interpreted to only need one or more of the listed molecules to meet the limitation of the claim.
Claim 16 is 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 16 recites “wherein said dendritic cell maturation is associated with: … (b) enhances ability to; and/or proliferation of allogeneic T cell; (c) enhanced ability to induce production of interferon gamma from allogeneic T cells.” The language in (b) is unclear due to the misplacement of and/or in the middle of the statement. Further the lack of an “and” or ”or” between (b) and (c) makes it unclear if (a) – (c) are options in which one needs to fulfilled to meet the claim limitation or if all must be fulfilled to meet the claim limitation. For the purpose of further examination and in light of the specification which recites “In specific cases, the dendritic cell maturation is associated with upregulation of expression of one or more markers selected from the group consisting of: a) HLA-II; b) CD40; c) CD80; d) CD86; and e) a combination thereof. The dendritic cell maturation may be associated with enhanced ability to activate proliferation of allogeneic T cells. The dendritic cell maturation may be associated with enhanced ability to induce production of interferon gamma from allogeneic T cells (pg.4, lines 7-12)” the claim will be interpreted such that (a) – (c) are options in which only one needs to be met to meet the claim limitation.
Claim 19 is 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 19 recites “wherein said T regulatory cells are activated by: … (b) exposure to interleukin-10; (c) administration of immature dendritic cells.” The lack of an “and” or ”or” between (b) and (c) makes it unclear if (a) – (c) are options in which one needs to fulfilled to meet the claim limitation or if all must be fulfilled to meet the claim limitation. For the purpose of further examination and in light of the specification which recites “In specific embodiments, the T regulatory cells are activated by exposure to CD3, CD28. interleukin-10 and/or by administration of immature dendritic cells, which may express PD-1L. (pg.4, lines 12-14)” the claim will be interpreted such that (a) – (c) are options in which only one needs to be met to meet the claim limitation.
Claim 32 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 32 recites, “wherein said small molecule blocker of NF-kappa B activity is selected from a group comprising of,” comprising of render the claim unclear because the claim is a Markush claim (a claim reciting a list of alternatives) requiring selection from a closed group and thus should use the transitional language of “consisting of” (See MPEP 2117(I)).
Claim Rejections - 35 USC § 112(d)
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claim 3 is rejected under 35 U.S.C. 112(d), as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends. The statement "wherein the fibroblasts are allogeneic, autologous, or xenogeneic" does not further limit the scope of claim 1 from which it depends because the three options listed are the only three classes of cellular therapeutic source types. Applicant may cancel the claim, amend the claim to place the claim in proper dependent form, rewrite the claim in independent form, or present a sufficient showing that the dependent claim complies with the statutory requirements.
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.
Claims 1, 3, 5, 7-9, 11, and 44 are rejected under 35 U.S.C. 103 as being unpatentable over Ichim et al. (2020) Fibroblasts as an Alternative to Mesenchymal Stem Cells with Successful Treatment and Immune Modulation in EAE Model of Multiple Sclerosis bioRxiv 2020.06.04.133249 (hereafter Ichim) in view of Forostyak and Sykova (2017) Neuroprotective Potential of Cell-Based Therapies in ALS: From Bench to Bedside Front. Neurosci. 11:591 (hereafter Forostyak and Sykova), and Saresella et al. (2013) T helper-17 activation dominates the immunological milieu of both amyotrophic lateral sclerosis and progressive multiple sclerosis Clinical Immunology 148, 79-88 (hereafter Saresella).
In regards to claim 1 Ichim teaches the treatment of a rat model of multiple sclerosis called experimental autoimmune encephalomyelitis by the administration of fibroblast (pg.4, lines 15-16/pg.5, lines 33-36), and further teaches the fibroblasts are more effective and less expensive than commonly used mesenchymal stem cells (MSCs) making them an attractive alternative (pg.11, lines 16-18).
In regards to claim 3 Ichim teaches the use of rat dermal cells obtained from ATCC thus the fibroblasts are allogeneic to the rat mouse models (pg.5, line 5).
In regards to claim 5 Ichim teaches the rat dermal fibroblast and human fibroblast were propagating (mitotically active) (pg. 5, lines 1-3).
In regards to claim 9 Ichim teaches that fibroblasts like MSCs are fundamental cell type in wound healing and both express markers CD73 and CD105 (pg.4, lines 3-5).
In regards to claims 11 Ichim teaches the fibroblast can elicit generation of Treg cells (Treg), as evidenced by the increase in the number of FoxP3+ cells (pg.6, lines 26-27).
It is also noted that Ichim teaches the mechanism by which fibroblasts improve treatment is by promoting Treg generation and blocking the IL-17 inflammatory pathway which promotes Th17 cells (pg.6 line 37 – pg.7 line 6).
Ichim fails to teach the method of treating , preventing, or reducing the risk of Amyotrophic Lateral Sclerosis (ALS) of claim 1, the ALS associated from with an elevation of inflammatory cytokines of claims 7 and 8, and the administration of riluzole of claim 44.
Forostyak and Sykova, however, in regards to claim 1, teach that MSCs have shown promising results for the treatment of ALS in pre-clinical rodent models and clinical trials (pg.4, col 1, lines 33-39 / Table 1). ALS immune response is dominated by Th-17 cells similar to the multiple sclerosis model of Ichim, as evidenced by Saresella which recites that Th17 and Th1 lymphocytes dominate the immune response in both ALS and primary progressive multiple sclerosis indicating the presence of a complex and shared inflammatory milieu (pg.84, col 2, lines 3-6). Further Saresella teaches the reduction in Tregs seen in both further favors neuroinflammation, and suggest that the two diseases share a number of pathogenic mechanism (pg.86, col 2, lines 52-55 / pg.87, col 1, lines 1-7). Therefore, Forostyak and Sykova teach ALS is an IL-17 mediated sclerosis has shown pre-clinical success with MSCs much like multiple sclerosis.
In regards to claim 44, Forostyak and Sykova teaches Riluzole is a standard therapy for ALS which works by reducing the presynaptic release of glutamate and the disease progression and extends the patients lifespan by 2-3 months (pg.2, col 1, line 50 – pg.2, col 2, line 1).
Forostyak and Sykova fails to teach the ALS associated from with an elevation of inflammatory cytokines of claims 7 and 8.
Saresella however, teaches ALS patient when age matched to healthy controls (pg.80, col 1, lines 43-57) expressed higher levels of IL-17, IL-21, IL-22, IFN-γ, and IL-6 (pg.81, sections 3.1 and 3.2).
Thus, Ichim discloses a method of treating multiple sclerosis by the administration of allogeneic fibroblast which elicit generation of Treg cells which are FoxP3+, and Forostyak and Sykova teach that ALS models have shown pre-clinical response to MSCs similar to IL-17 mediated multiple sclerosis, as evidenced by Saresella, and the administration of riluzole is a standard care to prolong patient life expectancy, and Saresella, teaches ALS is associated with augmented inflammatory cytokines, and further both MS and ALS are implicated in the IL-17 inflammatory pathway and further facilitate neuroinflammation through reduction of Treg cells. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to try combine the teachings of the method of treatment of Ichim with the substitution of the disease model from MS to ALS, informed by the teachings of Saresella and, Forostyak and Sykova and further administering riluzole to extend a patient’s life expectancy and slow disease progression with a reasonable expectation of success because the two diseases are implicated in the IL-17 pathway and the fibroblast has shown success in inhibiting the pathway, and are a more efficient and less expensive alternative to MSCs.
Claims 12, 15, 16, 19, 22, 27, 31-33, and 35 are rejected under 35 U.S.C. 103 as being unpatentable over Ichim in view of Forostyak and Sykova, and Saresella as applied to claim 1 above, and further in view of Pletinckx et al. (2011) Role of dendritic cell maturity/costimulation for generation, homeostasis, and suppressive activity of regulatory T cells Front. Immun. 2:39 (hereafter Pletinckx) and Iruretagoyena et al. (2006) Inhibition of Nuclear Factor-κB Enhances the Capacity of Immature Dendritic Cells to Induce Antigen-Specific Tolerance in Experimental Autoimmune Encephalomyelitis The Journal of Pharmacology and Experimental Therapeutics, 318 (1), 59-67 (hereafter Iruretagoyena).
Ichim in view of Forostyak and Sykova, and Saresella fails to teach the T regulatory cells having (a) and/or (d) of claim 12, the T regulatory cells suppressing the ability of immature dendritic cells to mature wherein the maturation is associated with options (a) – (c) of claims 15 and 16, and the T regulatory cells are activated by options (a)-(c) of claim 19.
Pletinckx, however, in regards to claims 12, 15, and 16 teaches that Treg cells prevent DC maturation by precluding the upregulation of costimulatory molecules including CD80, CD86, and CD40 as well as the reduction of production of inflammatory cytokines such as IL-12, IL-1β, IL-6, and IL-8 (pg.10, col 1, lines 9--14) and further teaches prevention of DC maturation make them incapable of eliciting strong productive immune responses and leads to induction of tolerance could be a significant regulatory mechanism to avoid unwanted immunity (pg.10, col 2, lines 12-18).
In regards to claim 19 Pletinckx teaches immature DCs have a crucial role in Treg homeostasis and proliferation (pg.9, col 2, lines 26-30).
In regards to claims 33 and 35 Pletinckx teaches stimulation of Tregs with IL-2 is essential for growth, survival, and expansion in the periphery (pg.9, col 1, lines 23-25).
Pletinckx fails to teach the dendritic cells having at least one of (a)-(e) of claim 22, the inhibition of NFκB by means of (a)-(e) of claim 27, and the NFκB inhibition by a small molecule blocker of claim 31, and selected from the list of inhibitors of claim 32.
Iruretagoyena however, in regards to claims 22, 27, and 31 teaches that immature DCs would induce antigen-specific tolerance and mature DCs would promote immunity by priming naïve T cells (pg.60, col 1, lines 3-7) and further that an immature and tolerogenic phenotype can be promoted in DCs by pharmacologically blocking NF-κB function and this approach could be useful to enhance DCs capacity to promote tolerance to self-antigens (pg.60, col 2, lines 2-6).
In regards to claim 32 Iruretagoyena uses the NF-κB inhibitors Andrographolide which is a diterpene (pg.61, col 2, lines 53-57).
Thus, Ichim in view of Forostyak and Sykova, and Saresella discloses a method of treating ALS by delivering fibroblast and stimulating Treg development, Pletinckx teaches that DCs can be kept in an immature state and further the DCs and IL-2 are important activators of Tregs to support survival and expansion, and Iruretagoyena teaches NF-κB inhibition with a diterpene keep DCs in an immature state and help promote a tolerogenic immune response. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to combine the teachings of Ichim, Forostyak and Sykova, and Saresella and further the teachings of Pletinckx and Iruretagoyena with a reasonable expectation of success to develop a method of treating ALS with fibroblasts which can stimulate the generation of Treg cells and further wherein DC cells are maintained as immature to activate Treg cells to improve treatment efficacy and further to support a tolerogenic immune response in subjects.
Claim 36 is rejected under 35 U.S.C. 103 as being unpatentable over Ichim in view of Forostyak and Sykova, and Saresella as applied to claim 1 above, and further in view of Zorn et al. (2006) IL-2 regulates FOXP3 expression in human CD4+CD25+ regulatory T cells through a STAT-dependent mechanism and induces the expansion of these cells in vivo Blood 108(5), 1571-1579 (hereafter Zorn).
Ichim in view of Forostyak and Sykova, and Saresella fails to teach the administration of IL-2 daily at a dose of 0.3x106 to 3.0x106 IU/per square meter of body surface area for 1 – 16 week.
Zorn, however, teaches administering various concentrations of IL-2 which fall within the range of the claim and over various time period between 1-16 weeks (Table 1) to adults and find that IL-2 treatment resulted in a 1.9 median fold increase in the frequency of CD4+CD25+ cells in peripheral blood as well as a 9.7 median fold increase in FOXP3 expression in CD3+ T cells (abstract).
Thus, Ichim in view of Forostyak and Sykova, and Saresella discloses a method of treating ALS by delivering fibroblast and stimulating Treg development, and Zorn teaches an IL-2 treatment daily for an extended amount of time induces the generation of FOXP3+ regulatory T cells. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to combine the teachings of Ichim, Forostyak and Sykova, and Saresella and further the teachings or Zorn with a reasonable expectation of success to develop a method of treating ALS wherein IL-2 is administered instead of fibroblasts to generate Treg cells in vivo as a cell free alternative.
Claims 2 and 37-40 are rejected under 35 U.S.C. 103 as being unpatentable over Ichim in view of Forostyak and Sykova, and Saresella as applied to claim 1 above, and further in view of Ablamunits et al. (2010) Acquisition of regulatory function by human CD8+ T cells treated with anti-CD3 antibody requires TNF Eur. J. Immunol. 40: 2891–2901 (hereafter Ablamuntis).
Ichim in view of Forostyak and Sykova, and Saresella fail to administering another rapamycin, N-acetylcysteine, anti-CD3 antibodies, or a combination thereof of claim 2, administering one or more immune modulatory compounds of claim 37, the compound being oxytocin, prolactin, IL-10,IL-35, CD3 inhibitor, or a combination thereof of claim 38, and further wherein the CD3 inhibitor is an anti-CD3 antibody (claim 39) and said anti-CD3 antibody is Teplizumab (claim 40).
Ablamuntis however, in regards to claims 2 and 37-40 teaches that the addition of the anti-CD3 antibody, Teplizumab induces CD8+ T cells with regulatory function and inhibit responses of autologous and allogeneic T cells. They inhibit CD4+ T-cell proliferation by mechanisms involving TNF and CCL4, and by blocking target cell entry into G2/M phase of cell cycle but neither kill them, nor compete for IL-2 (abstract).
Thus, Ichim in view of Forostyak and Sykova, and Saresella discloses a method of treating ALS by delivering fibroblast and stimulating Treg development, and Ablamuntis teaches an anti-CD3 antibody Teplizumab induces regulatory T cells and inhibits CD4+ T cell proliferation without compete for IL-2. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to combine the teachings of Ichim, Forostyak and Sykova, and Saresella and further the teachings Ablamuntis with a reasonable expectation of success to develop a method of treating ALS with fibroblasts which can stimulate the generation of Treg cells and further wherein an anti-CD3 antibody is also administered to improve Treg expansion treatment efficacy and inhibit unwanted T cell proliferation to improve treatment efficiency.
Claims 41-43 are rejected under 35 U.S.C. 103 as being unpatentable over Ichim in view of Forostyak and Sykova, and Saresella as applied to claim 1 above, and further in view of A van Es et al. (2017) Amyotrophic lateral sclerosis Lancet 390: 2084-2098 (hereafter van Es).
Ichim in view of Forostyak and Sykova, and Saresella fails to teach the ALS being familial of claim 41, idiopathic of claim 42, and having one or more mutations in the C9orF72 gene of claim 43.
Van Es, however, in regards to claims 41 and 42 teaches that ALS has traditionally been classified as either the sporadic (idiopathic) or familial form (pg.2084, col 1, 23-24), and the familial form has been linked to 30 different genes (pg.2084, col 1, 23-24).
In regards to claim 43 Van Es teaches that hexanucleotide repeat expansions (a mutation) in the C9orf72 gene is the major genetic cause of ALS (pg.2084, col 1, lines 16-22).
Thus, Ichim in view of Forostyak and Sykova, and Saresella discloses a method of treating ALS by delivering fibroblast and stimulating Treg development, and Van Es teaches idiopathic and familial ALS are the traditional classification for the forms of the disease and further that mutations in the C9orf72 gene is the major genetic cause of ALS. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to combine the teachings of Ichim, Forostyak and Sykova, and Saresella and further the teachings Van Es with a reasonable expectation of success to develop a method of treating ALS with fibroblasts which can stimulate the generation of Treg cells and further wherein the treatment is used to treat the most common and prevalent forms of ALS.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1, 3, 9, and 38 rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 17-25 of U.S. Patent No. 11,878,037 in view of Forostyak and Sykova as evidenced by Saresella.
Claim 1 of the U.S. patent recites claim to a method of correcting or ameliorating one or more abnormalities associated with multiple sclerosis by administering an effective amount of fibroblast. This significantly overlaps with instant application claim 1.
Claim 17 of the U.S. patent recites claim to the fibroblast being selected for marker expression of a list that includes CD73 and CD105. This significantly overlap with instant application claim 9.
Claims 18 and 19 of the U.S. patent recite the fibroblast are autologous or allogeneic, respectively. This significantly overlaps with the instant application claim 3.
Claims 20-25 of the U.S. patent recite claim to the fibroblast being treated with oxytocin under various conditions. These significantly overlaps with instant application claim 38.
The U.S. patent fails to teach the method of treating, preventing, or reducing the risk of having ALS. Saresella, however, teaches that Th17 and Th1 lymphocytes dominate the immune response in both ALS and primary progressive multiple sclerosis indicating the presence of a complex and shared inflammatory milieu as outlined above.
Thus, the U.S. patent discloses a treatment for multiple sclerosis complications associated with elevated IL-17, and Saresella teaches ALS is also implicated in the Th17/IL-17 pathway. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to try the teachings of the U.S. patent with the simple substitution of the disease model informed by the teachings of Saresella with a reasonable expectation of success.
Claims 1, 9, and 38 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 32, and 33 of copending Application No. 17/757,383 (claim set 03/31/2026) (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other.
Claims 1 and 32 of the reference application recite claim to a method of treating inflammation by providing and effective amount of fibroblast that have been exposed to oxytocin, to reduce the production of IL-17 from IL-17 producing cells (a key driver of ALS as explained above). This encompasses instant application claims 1 and 38.
Claims 2 and 33 of the reference application recite claim to the fibroblast expressing CD73. This encompasses instant application claim 9.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
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/D.A.A/Examiner, Art Unit 1647
/JOANNE HAMA/Supervisory Patent Examiner, Art Unit 1647
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