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 present application, filed March 13, 2023, is a national stage application of PCT/JP2021/034305, filed September 17, 2021, which claims priority to foreign priority application JP2020-156460, filed September 17, 2020.
Status of the Application
Applicant’s preliminary amendment, received April 24, 2023, is acknowledged. Claims 1-13 are pending and examined on the merits herein.
Claim Interpretation
Claim 8 recites: “The autophagy activator according to claim 1, which is used for prevention or treatment of Alzheimer's disease.” The limitation “which is used for prevention or treatment of Alzheimer's disease” is interpreted as an intended use of the autophagy activator according to claim 1.
MPEP 2111.02 (at II) states: “During examination, statements in the preamble reciting the purpose or intended use of the claimed invention must be evaluated to determine whether or not the recited purpose or intended use results in a structural difference (or, in the case of process claims, manipulative difference) between the claimed invention and the prior art. If so, the recitation serves to limit the claim. …To satisfy an intended use limitation which is limiting, a prior art structure which is capable of performing the intended use as recited in the preamble meets the claim.” In this instance, claim 8 is satisfied by an autophagy activator that satisfies the limitation of claim 1, even if the autophagy activator is not used for prevention or treatment of Alzheimer's disease.”
In addition, claims 9-13 recite “a composition for activating autophagy.” The limitation “for activating autophagy” is interpreted as an intended use of this composition, and accordingly, claims 9-13 are satisfied by a composition that satisfies the requirements of claims 9-13, even if that composition is not used for activating autophagy.
Claim Rejections - 35 USC § 112
As described in the above claim interpretation section, the limitation “which is used for prevention or treatment of Alzheimer's disease” is interpreted as an intended use of the product of claim 8. However, if claim 8 were drawn to a method for preventing or treating Alzheimer's disease, then claim 8 would lack enablement for preventing Alzheimer’s disease.
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.
Claim 8 is 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 treatment of Alzheimer's disease, does not reasonably provide enablement for prevention of Alzheimer’s disease. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the invention commensurate in scope with these claims.
The Applicant’s attention is drawn to In re Wands, 8 USPQ2d 1400 (CAFC1988) at 1404 where the court set forth eight factors to consider when assessing if a disclosure would have required undue experimentation. Citing Ex parte Forman, 230 USPQ 546 (BdApls 1986) at 547 the court recited eight factors:
(1) The nature of the invention; (2) the state of the prior art; (3) the relative skill of those in the art; (4) the predictability or unpredictability of the art; (5) the breadth of the claims; (6) the amount of direction or guidance presented; (7) the presence or absence of working examples; and (8) the quantity of experimentation necessary.
Nature of the invention: The claimed invention is drawn to the autophagy activator according to claim 1, which is used for prevention or treatment of Alzheimer's disease.
In the absence of a definition of prevention provided in the specification, the term is given is customary meaning in the art. The Oxford English Dictionary defines the verb “to prevent” as “to preclude the occurrence of (an anticipated event, state, etc.); to render (an intended, possible, or likely action or event) impractical or impossible by anticipatory action; to put a stop to” (p. 8, definition II.9.a of “prevent”; cited in PTO-892). “Preventing” as recited in the instant claims, is interpreted to mean the complete and total blocking of all symptoms of a disease for an indefinite period of time. Merely making the disease less likely would not render the disease impossible, and thus would not qualify as preventing.
The state of the prior art: With respect to the prevention of different neurodegenerative diseases, the U.S. Department of Health and Human Services’ Agency for Healthcare Research and Quality published a review by the Minnesota Evidence-based Practice Center related to interventions for cognitive decline (Minnesota Evidence-based Practice Center, "Interventions to Prevent Age-Related Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer’s-Type Dementia" March 2017; cited in PTO-892; hereafter Minnesota). This report evaluated the effectiveness of 263 eligible studies addressing 13 classes of interventions for cognitive decline, cognitive impairment, and Clinical Alzheimer’s-Type Dementia (page vii, Results section, lines 1-4). The report states “We found no high-strength evidence for the effectiveness of any intervention to delay or prevent age-related cognitive decline, MCI, and/or CATD” (wherein MCI is mild cognitive impairment and CATD is clinical Alzheimer’s-type dementia) (page vii, Results section, lines 4-6).
In addition, The Mayo Clinic (Mayo Clinic website, website updated July 28, 2018, accessed via Wayback Machine December 9, 2025; cited in PTO-892; hereafter Mayo Clinic) teaches there are no proven Alzheimer’s prevention strategies, although certain strategies may be effective in reducing the risk of Alzheimer’s disease and other types of dementia (p. 1, Title and paragraph 1, lines 1-6).
Therefore, on the effective filing date of the instant invention, the prior art taught that there are no known strategies to prevent Alzheimer’s disease.
The relative skill of those in the art: The relative skill of those in the art is high.
The predictability or unpredictability of the art: The lack of prior art disclosing a prevention for Alzheimer’s disease means that one skilled in the art cannot predict the usefulness of a method to make these conditions possible. As recited above, Mayo Clinic teaches there is no known strategy to prevent Alzheimer’s disease, and Minnesota teaches they found no high-strength evidence for the effectiveness of any intervention to delay or prevent age-related clinical Alzheimer’s type dementia. Accordingly, one of ordinary skill in the art would have found a therapy that may render Alzheimer’s disease impossible by anticipatory action to be unpredictable.
Prevention of a disease is not the same as treatment of said disease. In order to prevent a disease, as opposed to merely delaying or reducing symptoms, a method must either render the subject completely resistant to said disease after a limited number of treatments, or, when continued indefinitely, continue to suppress the occurrence of that disease. Many therapies that are suitable for short-term relief of symptoms are not suitable for lifelong prevention of disease.
Therefore the claimed invention is unpredictable.
The breadth of the claims: The scope of the claims specifically includes product, the autophagy activity of claim 1, for prevention of Alzheimer’s disease. Preventing is interpreted as described above under “Nature of the invention”.
The amount of direction or guidance presented: The specification provides that in neurodegenerative diseases such as Alzheimer's disease, decreased autophagy activity is believed to be observed, and thus activation of autophagy is known to contribute to the treatment and prevention of neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, and Parkinson's disease (p. 2, lines 3-5).
The presence or absence of working examples: The specification discloses working examples wherein an inositol derivative A produced by the method described in International
Publication No. 2019/045113 was used to test the effect of gene expression in senescent fibroblasts (see results on p. 58, Table 4), the suppression of mTOR gene expression in senescent fibroblasts (see results on pp. 61-62, Table 5), the relative expression LC3, ATG5, and Beclin 1 in human neuroblastoma cells with amyloid β added (see results on p. 65, Table 6), and the apoptosis suppressing action caused by amyloid β in human neuroblastoma cells (see results on p. 69, Table 7).
The specification does not provide working examples that show preventing Alzheimer’s disease in vitro or in vivo.
Note that lack of working examples is a critical factor to be considered, especially in a case involving an unpredictable and undeveloped art such as the prevention of Alzheimer’s diseases. See MPEP 2164.
The quantity of experimentation required: In order to practice the invention of preventing Alzheimer’s disease, one of ordinary skill in the art would be required to undertake a novel and extensive research program to show that administration of the presently claimed autophagy activator rendered Alzheimer’s disease in a patient impossible. Because this research would need to be exhaustive, because it would involve a wide scope of different patients with Alzheimer’s disease, and because one may need to develop a new statistical method or conduct a large-scale clinical trial to show that Alzheimer’s disease has been rendered impossible by administration of the claimed autophagy activator, it would constitute an undue and unpredictable search burden.
Genentech, 108 F.3d at 1366, sates that, “a patent is not a hunting license. It is not a reward for search, but compensation for its successful conclusion.” And “patent protection is granted in return for an enabling disclosure of an invention, not for vague intimations of general ideas that may or may not be workable.”
Therefore, in view of the Wands factors, as discussed above, particularly the breadth of the claims and the nature of the invention, Applicants fail to provide information sufficient to practice the claimed invention of prevention of Alzheimer’s disease using the claimed autophagy activator of claim 1.
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 4-7 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.
Claims 4-7 depend from claim 1 and require promotion or suppression of expression of a specific gene. However, claim 1 is drawn to an autophagy activator comprising, as an active ingredient, an inositol derivative in which a saccharide is bound to inositol. Claim 1 does not require administering the autophagy activator to a subject, and thus it is unclear under what conditions the expression of genes recited in claims 4-7 are promoted or suppressed. Accordingly, claims 4-7 are indefinite.
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.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], 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 8 is rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, 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.
Claim 8 depends from claim 1 and requires the autophagy activator is used for prevention or treatment of Alzheimer's disease. As described above, the limitation requiring the autophagy activator is used for prevention or treatment of Alzheimer's disease is interpreted as an intended use of the product of claim 1 and is satisfied by an autophagy activator that satisfies claim 1. Therefore, claim 8 fails to further limit the subject matter of the claim upon which it depends.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 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 1-10 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Fujita (Publication No. WO 2019045113 A1; cited in PTO-892).
Fujita is published in a language other than English. Both the original document and an English language machine translation of Fujita are provided with this office action and cited in the PTO-892. citations below refer to the English language machine translation.
Fujita was published July 3, 2019, which is more than one year before the filing date of the foreign priority application associated with the present application, JP2020-156460. Therefore, Fujita is eligible as prior art under 35 U.S.C. 102(a)(1).
Fujita teaches and claims a mixture of inositol derivatives in which sugars are bound to inositol. In one example, the mixture contains 5% by mass or more of inositol derivative (A7) in which the total number of sugars bound to one inositol molecule is 7 or more in terms of monosaccharide units, relative to the total amount (100% by mass) of the inositol derivatives (English translation, document p. 72, claim 8).
Fujita further teaches and claims this mixture, wherein the inositol derivative (A7) is at least one inositol derivative selected from the group consisting of the following (a) and (b): (a) an inositol derivative in which one or more glucose and one or more oligosaccharides containing glucose as a structural unit are bound to inositol; and (b) an inositol derivative in which one or more oligosaccharides containing glucose as a structural unit are bound to inositol (English translation, document p. 72, claim 9).
Fujita further teaches and claims wherein the inositol is myo-inositol (English translation, document p. 73, claim 11).
In addition, Fujita teaches that other components may be added as appropriate to the mixture of inositol derivatives, providing pharmaceutically acceptable carriers as one example of another component (p. 31, lines 1-4). Fujita teaches the inositol derivative mixture in the pharmaceutical composition can be 0.01 to 50% by mass, and specifically cites 0.6 to 1.5% by mass as one example (English translation, p. 37, lines 1-8).
Fujita does not teach these inositol derivatives as activators of autophagy. To the extent the limitation of these inositol derivatives act as autophagy activators limits the claim, the product of Fujita activates autophagy, as evidenced by the instant specification.
The instant specification provides that an inositol derivative A was produced by the method described in International Publication No. 2019/045113 (p. 54, [0173], lines 2-3), which is the publication of Fujita. The specification provides that this inositol derivative promotes expression of the LC3, ATG5, and Beclin1 genes in cell culture (p. 58, Table 4), and suppresses expression of mTOR in cell culture (pp. 61-62, Table 5). The specification provides that expression of the LC3 gene is an autophagy marker, and that the ATG5 and Beclin 1 genes are contained in autophagosomes and can activate autophagy (p. 6, [0013], lines 6-8). Accordingly, as evidenced by the present specification, the inositol derivative of Fujita is reasonably considered as an autophagy activator, absent evidence to the contrary.
The MPEP 2112.01 (especially at I) citing In re Best, 562 F.2d 1252, 195 USPQ 430 (C.C.P.A. 1977) and In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990) discusses the support of rejections wherein the prior art discloses subject matter which there is reason to believe inherently includes functions or characteristics that are newly recited or is identical to a product instantly claimed. In such a situation the burden is shifted to the applicants to show the products of the applicant and the prior art are not the same or that the prior art products do not necessarily possess the characteristics of the claimed product.
Accordingly, the product of Fujita described above satisfies the structural limitations of claims 1-10, and acts as an activator of autophagy, as evidenced by the present specification.
Thus Fujita anticipates claims 1-10.
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 factual inquiries for establishing a background for determining obviousness under 35
U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1 and 9-10 are rejected under 35 U.S.C. 103 as being unpatentable over Fujita (Publication No. WO 2019045113 A1; cited in PTO-892).
The examiner believes claim 10 is anticipated by Fujita, as described in the above rejection under 35 U.S.C. 102. However, for the sake of argument, if Fujita does not anticipate claim 10 because, for example, Fujita does not teach a specific composition that includes a total content of inositol derivative of 0.1 to 2% by mass, then claim 10 would have been obvious over Fujita.
Fujita teaches as described in the above rejection under 35 U.S.C. 102. In addition, Fujita teaches that the pharmaceutical composition of this embodiment can be used, for example, to promote cell activation of skin cells with reduced cell proliferation activity, such as at sites where cells have been damaged by, for example, wounds, burns, frostbite, inflammation, or the like, and that the pharmaceutical composition of this embodiment is particularly effective in activating human fibroblasts or human epidermal keratinocytes (English translation, document p. 39, [0072], lines 1-6) (emphasis added).
Fujita does not teach a specific composition that includes total content of inositol derivative of 0.1 to 2% by mass.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the present application to prepare a composition comprising the inositol derivative taught by Fujita that includes a total content of inositol derivative of 0.1 to 2% by mass. One of ordinary skill in the art would have been motivated to prepare a composition comprising the inositol derivative taught by Fujita that includes a total content of inositol derivative of 0.1 to 2% by mass because Fujita suggests compositions comprising, for example, 0.6 to 1.5% by mass (English translation, p. 37, lines 1-8), and because such a composition may provide an effective dose for promoting cell activation of skin cells with reduced cell proliferation activity, such as at sites where cells have been damaged, or for activating human fibroblasts or human epidermal keratinocytes, as taught by Fujita.
Therefore the invention taken as a whole is prima facie obvious.
Claims 1, 9, and 11-12 are rejected under 35 U.S.C. 103 as being unpatentable over Fujita (Publication No. WO 2019045113 A1; cited in PTO-892) in view of Duarte (Duarte, T. L.; et al. Free Radical Biology and Medicine 2008, vol. 46, pp. 78-87; cited in PTO-892).
Fujita teaches as described in the above rejections under 35 U.S.C. 102 and 35 U.S.C. 103.
Fujita does not teach a composition for activating autophagy according to claim 9, further comprising at least one vitamin derivative or a salt thereof selected from a group consisting of vitamin C derivatives, vitamin E derivatives, and vitamin P derivatives, as required by claim 11, wherein the vitamin derivative or a salt thereof is at least one vitamin derivative or a salt thereof is selected from a group consisting of ascorbyl phosphate or a salt thereof, fatty acid esters of ascorbyl phosphate or a salt thereof, tocopherol phosphate or a salt thereof, and methyl hesperidin or a salt thereof as recited in claim 12.
Duarte teaches the effect of ascorbic acid 2-phosphate (abbreviated as AA2P by Duarte), a stable vitamin C derivative, on fibroblast cells (p. 78, Abstract, lines 3-7). Duarte teaches that quiescent fibroblast cells exposed to AA2P increased the expression of genes associated with DNA replication and repair and with the G2/M phase of the cell cycle, and consistent with these, gene expression changes, AA2P increased the mitogenic stimulation of quiescent fibroblasts by serum factors and cell motility in the context of wound healing. Duarte teaches that AA2P-treated fibroblasts showed faster repair of oxidatively damaged DNA bases (p. 78, Abstract, lines 5-11). Duarte proposes that vitamin C may protect the skin by promoting fibroblast proliferation, migration, and replication-associated base excision repair of potentially mutagenic DNA lesions (p. 78, Abstract lines 11-12).
It would have been prima facie obvious before the effective filing date of the present application to prepare a composition comprising the inositol derivative (A7) of Fujita and ascorbic acid 2-phosphate. One of ordinary skill in the art would have been motivated to prepare a composition comprising the inositol derivative (A7) of Fujita and ascorbic acid 2-phosphate because Fujita teaches their inositol derivatives as activators of skin cells, including fibroblasts, with reduced cell proliferation activity, and because Duarte teaches ascorbic acid 2-phosphate stimulated quiescent fibroblasts, showed faster repair of oxidate damage to DNA, and may protect the skin by promoting fibroblast proliferation, migration, and replication.
MPEP 2144.06 states: “It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art.” In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ.1069, 1072 (CCPA 1980).”
In this instance, both Fujita and Duarte are concerned with promoting proliferation of fibroblasts. Accordingly, one of ordinary skill in the art would have been motivated to combine the inositol derivative taught by Fujita and the ascorbyl-2-phosphate taught by Duarte, because each is taught as promoting fibroblast proliferation, and because the combination of the two components may be more effective in promoting fibroblast proliferation than the inositol derivative alone.
Therefore, the invention taken as a whole is prima facie obvious.
Claim 13 is rejected under 35 U.S.C. 103 as being unpatentable over Fujita (Publication No. WO 2019045113 A1; cited in PTO-892) in view of Duarte (Duarte, T. L.; et al. Free Radical Biology and Medicine 2008, vol. 46, pp. 78-87; cited in PTO-892) as applied to claims 1, 9, and 11-12 above, and further in view of Hata (Hata, R; et al. European Journal of Biochemistry 1988, vol. 173, pp. 261-267; cited in PTO-892).
Fujita and Duarte teach as described in the above rejections under 35 U.S.C. 102 and 35 U.S.C. 103.
Fujita and Duarte do not teach wherein the total content of the vitamin derivative or a salt thereof is 0.01 to 15% by mass relative to a total amount of the composition for activating autophagy, as recited in claim 13.
Hata teaches the effect of ascorbic acid on collagen metabolism and cell growth in cultured human skin fibroblasts (p. 261, Title). Hata teaches that L-ascorbate (vitamin C) stimulated growth and collagen synthesis, as well as synthesis of non-collagenous proteins, in cultured skin fibroblasts (p. 261, Abstract, lines 6-7). Hata teaches that they added increasing amounts of sodium ascorbate to the culture medium, and observed that collagen and non-collagenous protein synthesis was stimulated by the presence of 0.05 -0.1 mM ascorbate, with stimulative effects being slightly less pronounced with 0.2 mM or higher concentrations of ascorbate (p. 264, left column, second full paragraph, lines 1-8). Hata teaches that reason for lesser effects of ascorbate at 0.2 mM or higher concentrations on collagen and non-collagenous protein synthesis is not clear, but the phenomenon is probably due to the cellular toxicity of hydrogen peroxide produced by the autooxidation of ascorbate under culture conditions (p. 264, left column, second full paragraph, lines 14-18). Moreover, Hata teaches that cell culture with 0.1 mM and 1 mM ascorbate also stimulated fibroblast growth, but that the magnitude of growth stimulation was lower with 1 mM than with 0.1 mM (p. 264, left column, third full paragraph, lines 2-4; p. 264, right column, lines 8-12; data shown on p. 264, Figure 5).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the present application to prepare a composition comprising the inositol derivative A and ascorbic acid-2-phosphate, wherein the total content of the ascorbic acid-2-phsophate is 0.01 to 15% by mass relative to a total amount of the composition. One of ordinary skill in the art would have been motivated to prepare a composition comprising the inositol derivative A and ascorbic acid-2-phosphate, wherein the total content of the ascorbic acid-2-phsophate is 0.01 to 15% by mass relative to a total amount of the composition because Fujita and Duarte render obvious a composition comprising the inositol derivative of Fujita and ascorbic acid-2-phosphate, and because Hata demonstrates the concentration-dependent effect of ascorbate in promoting collagen synthesis and stimulating fibroblast growth. Therefore, one of ordinary skill in the art would have considered compositions with a range of ascorbic acid-2-phosphate concentrations to identify the optimal concentration for stimulating fibroblast in the composition obvious over Fujita in view of Duarte, because the effect of ascorbic acid on collagen synthesis and cellular growth in fibroblasts is concentration dependent, and thus one of ordinary skill in the art would reasonably expect the effect of the stable ascorbic acid analog AA2P to also be concentration dependent.
MPEP 2144.05 II at A states: “Generally, differences in concentration or temperature will not support the patentability of subject matter encompassed by the prior art unless there is evidence indicating such concentration or temperature is critical. "[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation." In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955).” Therefore, in view of Duarte teaching a concentration-dependent effect on ascorbic acid, and because ascorbic acid-2-phosphate is a stable ascorbic acid derivative, one of ordinary skill in the art would have also identified the optimal concentration of ascorbic acid-2-phosphate using routine experimentation.
Therefore the invention taken as a whole is prima facie obvious.
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 1-2, 4-9, and 11-13 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 11, 12, and 15-16 of copending U.S. patent application 18/026,057 (reference application, hereafter ‘057).
The present application and ‘057 are each assigned to Resonac Corporation and include Yuko Nakagami as an inventor.
Claim 1 of ‘057 claims an autophagy activator comprising methyl hesperidin as an active
ingredient.
Claim 11 claims a composition for activating autophagy, comprising the autophagy activator according to claim 1 and a pharmaceutically acceptable carrier, and claim 12 claims a total amount of methyl hesperidin is 0.01 to 2% by mass relative to a total amount of the composition for activating autophagy.
Claim 15 claims the composition for activating autophagy according to claim 11, further comprising an inositol derivative in which a saccharide is bound to inositol, and claim 16 claims the saccharide is glucose or an oligosaccharide containing glucose as a constituent unit.
Therefore, the claims of ‘057 claim a composition that comprises inositol derivative in which a saccharide is bound to inositol, methyl hesperidin in a concentration of 0.01-2% by mass, and a pharmaceutically acceptable carrier. The composition claimed by ‘057 thus satisfies all limitations of present claims 1-2, 4-9, and 11-13.
Regarding the inositol derivative as the active ingredient in the autophagy activator of claim 1, as evidenced by the present specification described above, the inositol derivative in which a saccharide is bound to inositol, wherein the saccharide is glucose or an oligosaccharide containing glucose as a constituent unit, is believed to be an inherent activator of autophagy, absent evidence to the contrary.
This is a provisional nonstatutory double patenting rejection because the patentably distinct claims have not been patented.
Claims 1 and 3 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 11, 12, and 15-16 of copending U.S. patent application 18/026,057 (reference application, hereafter ‘057) in view of Fujita (Publication No. WO 2019045113 A1; cited in PTO-892).
Claims 1, 11, 12, and 15-16 of ‘057 claim as described in the above nonstatutory double patenting rejection.
The claims of ‘057 do not claim wherein the inositol is myo-inositol as recited in claim 3.
Fujita teaches as described in the above rejection under 35 U.S.C. 102 and 35 U.S.C. 103.
It would have been prima facie obvious to one of ordinary skill in the art to formulate the composition claims 15 and 16 of ‘057 with the inositol derivative taught by Fujita. Because the claims of ‘057 requiring an inositol derivative in which a saccharide is bound to inositol, one of ordinary skill in the art would have contemplated the full scope of inositol derivatives bound to saccharides known in the prior art, including those taught by Fujita, which include myo-inositol.
Regarding the inositol derivative as the active ingredient in the autophagy activator of claim 1, as evidenced by the present specification described above, the inositol derivative in which a saccharide is bound to inositol, wherein the saccharide is glucose or an oligosaccharide containing glucose as a constituent unit, is believed to be an inherent activator of autophagy, absent evidence to the contrary.
This is a provisional nonstatutory double patenting rejection because the patentably distinct claims have not been patented.
Claims 1-9 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3 of U.S. patent 10,918,585 (reference patent, hereafter ‘585). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of ‘585 anticipate the claimed invention.
The present application and ‘585 are each assigned to Resonac Corporation and include Yuko Nakagami as an inventor.
Claim 1 of ‘585 recites an anti-aging composition for skin comprising one or more inositol derivatives in which glucose or an oligosaccharide comprising glucose as a constituent unit is bonded to inositol, and a total amount of the glucose or the oligosaccharide bonded to one inositol molecule is 1 or greater in terms of monosaccharide unit,
wherein the one or more inositol derivatives comprises, as an active component, at least one inositol derivative in which glucose or an oligosaccharide comprising glucose as a constituent unit is bonded to inositol, and a total amount of the glucose or the oligosaccharide bonded to one inositol molecule is 2 or greater in terms of monosaccharide unit,
a proportion of the active component among all of said one or more inositol derivatives contained in the anti-aging composition being 79% by mass or greater.
Claim 2 of ‘585 recites the anti-aging composition for skin according to claim 1, wherein the inositol is myo-inositol.
Claim 3 of ‘585 recites the anti-aging composition for skin according to claim 1, further comprising a pharmaceutically acceptable carrier.
The anti-aging composition claimed by ‘585 satisfies all limitations of claims 1-9 of the present application. Regarding the requirement that the composition acts as an autophagy activator, as evidenced by the present specification described above, the composition claimed by ‘585 is believed to be an inherent activator of autophagy, absent evidence to the contrary.
Claims 1, 9, and 11-13 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3 and 7 of U.S. patent 10,918,585 (reference patent, hereafter ‘585) in view of Duarte (Duarte, T. L.; et al. Free Radical Biology and Medicine 2008, vol. 46, pp. 78-87; cited in PTO-892) and Hata (Hata, R; et al. European Journal of Biochemistry 1988, vol. 173, pp. 261-267; cited in PTO-892).
Claims 1-3 of ‘585 claim as described in the above nonstatutory double patenting rejection. Claim 7 of ‘585 claims a method of promoting expression of collagen genes or elastin genes in human fibroblast, comprising administering an effective amount of the anti-aging composition according to claim 1 to a human subject.
The claims of ‘585 do not claim the composition for activating autophagy according to
claim 9, further comprising at least one vitamin derivative or a salt thereof selected from a group consisting of vitamin C derivatives, vitamin E derivatives, and vitamin P derivatives as recited in claim 11, the specific vitamin derivatives recited in claim 12, or the total content of the vitamin derivative or a salt thereof is 0.01 to 15% by mass relative to a total amount of the composition for activating autophagy, as recited in claim 13.
Duarte and Hata teach as described in the above rejections under 35 U.S.C. 103.
It would therefore have been prima facie obvious to prepare a pharmaceutical composition comprising the anti-aging composition claimed by ‘585 with ascorbic acid-2-phosphate in view of Duarte teaching the benefits of AA2P in promoting fibroblast proliferation, migration, and replication, which has the effect of protecting skin. Accordingly, one of ordinary skill in the art would have contemplated the composition claimed by ‘585 with AA2P, because AA2P’s role for protecting human skin cells would have been expected to enhance the anti-aging effect of said composition.
Regarding the specific amount of ascorbic acid-2-phosphate in the composition, because Hata demonstrates the concentration-dependent effect of ascorbic acid in promoting collagen synthesis and stimulating fibroblast growth, one of ordinary skill in the art would have identified the optimal concentration of AA2P, a stable ascorbic acid derivative, for enhancing the anti-aging effect of said composition. See MPEP 2144.05 II at A.
Claims 1-13 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3, 7-9, and 12 of copending U.S. patent application 19/085041 (reference patent, hereafter ‘041). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of ‘041 anticipate the claimed invention.
The present application and ‘041 are each assigned to Resonac Corporation and include Yuko Nakagami as an inventor.
Claim 1 of ‘041 claims a method for suppressing cancer cell proliferation, comprising administering an inositol derivative in which a sugar is bound to inositol to a mammal. Claim 2 claims the sugar is glucose or an oligosaccharide containing glucose as a constitutional unit, and claim 3 claims the inositol is myo-inositol.
Claim 7 of ‘041 claims the inositol derivative is administered as a composition comprising the inositol derivative and a pharmaceutically acceptable carrier, claim 8 claims a total content of the inositol derivative in the composition is 0.1% to 2% by mass, claim 9 claims the composition further comprises a tocopherol phosphate ester or a salt thereof, and claim 12 claims a total content of the tocopherol phosphate ester or the salt thereof is 0.1% to 2% by mass.
The inositol derivative and composition comprising said inositol derivative required by the claims of ‘041 satisfies all limitations of claims 1-13 of the present application. Regarding the requirement that the inositol derivative and composition acts as an autophagy activator, as evidenced by the present specification described above, the composition claimed by ‘041 is believed to be an inherent activator of autophagy, absent evidence to the contrary.
This is a provisional nonstatutory double patenting rejection because the patentably distinct claims have not been patented.
Conclusion
No claims are allowed.
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/B.M.B./ Examiner, Art Unit 1693
/ANDREA OLSON/ Primary Examiner, Art Unit 1693