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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on July 7, 2026 has been entered.
Claims 1, 11, 16 - 17, 19 are canceled; claims 3 - 5, 14, 20 - 21, 25, 27 - 32 and 35 are pending and have been considered on the merits. All arguments have been fully considered.
Claim Rejections - 35 USC § 112
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.
Claims 3 – 15 are 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.
Claims 3 – 5 fail to depend on a preceding claim previously set forth (MPEP 608.01 (n)(III)).
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 3 – 5, 14, 25, 27 – 32 and 35 are rejected under 35 U.S.C. 102a1 and 102a2 as being anticipated by Jacky et al. (US 2019/0185523) as evidenced by applicant’s specification, p.4; Pappas et al. (2009); Lovaszi et al. (2018); and/or Picardo (2009).
Regarding claim 14, Jacky teaches a method for treating skin conditions comprising administering a clostridial neurotoxin intradermally to a patient the skin condition (0041, 0097, 0122, example 8, 9, 12). Example skin conditions include underactive sebaceous glands, acne which exhibits suppressed levels of fatty acid by more than 20%, (Pappas et al., p. 158); atopic dermatitis, characterized by decreased sebum lipids (Lovaszi et al., p.4); psoriasis; rosacea; and skin dryness (0255, 0269 - 0271), each of which are disclosed by applicant as appropriate and preferred skin conditions associated with decreased sebum lipids (0019, 0152 - 0155 of the instant published application). In further support, Picardo teaches human sebum consists of 12 – 20% squalene, 26 – 30% wax esters, 1.5 – 2.5 cholesterol and 15 – 30% fatty acids (Table 1). Picardo shows that the claimed concentrations of fatty acid and cholesterol concentrations fall overlap with normal ranges, which indicates the claim includes subjects with “normal” sebum lipid levels.
Regarding claims 3 – 4, the method is disclosed as for cosmetic treatment (0007) and promoting skin rejuvenation (0003).
Regarding claim 5, although the reference does not teach the claimed function of inducing secretion of one or more sebaceous lipids to an epidermal layer of skin, e.g., squalene, fatty acid, cholesterol or wax ester, the method steps are in the prior art are administering the same neurotoxin to the same treating population as claimed. Notwithstanding, Jacky teaches the method increases sebum production to reduce skin dryness (0270).
Regarding claim 25, although the reference does not teach the claimed function of inducing retention of a tachykinin peptide in the dermis, the method steps are in the prior art are administering the same neurotoxin to the same treating population as claimed. Thus, the methods of the prior art inherently also induce retention of a tachykinin peptide in the dermis as claimed.
Regarding claims 27 - 31, the neurotoxin is a BoNT/A (0181), chimeric (0204), BoNT/DC, BotNT/X (0201) or a toxin that has a light chain from one botulinum toxin serotype (such as serotype A), and a heavy chain from a different botulinum toxin serotype (such as serotype B) (0117).
Regarding claim 32, Jacky teaches administering therapeutically effective amounts of toxin (0131) such as 1 – 1000 pg/ml (0.000001 – 0.001 ng/ml) and 1 ng/ml (0245), which overlaps with and encompasses the claimed range.
Regarding claim 35, although the reference does not teach the claimed function of inducing secretion of lipids into the stratum corneum, the method steps are in the prior art are administering the same neurotoxin to the same treating population as claimed. Thus, the methods of the prior art inherently also induce secretion of lipids into the stratum corneum as claimed.
Thus, the reference anticipates the claimed subject matter.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
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 14 and 20 – 21 remain rejected under 35 U.S.C. 103 as being unpatentable over Jacky et al. (US 2019/0185523) as evidenced by applicant’s specification, p.4; Pappas et al. (2009); Lovaszi et al. (2018); and/or Picardo (2009).
Regarding claim 14, Jacky teaches a method for treating skin conditions comprising administering a clostridial neurotoxin intradermally to a patient the skin condition (0041, 0097, 0122, example 8, 9, 12). Example skin conditions include underactive sebaceous glands, acne which exhibits suppressed levels of fatty acid by more than 20%, (Pappas et al., p. 158); atopic dermatitis, characterized by decreased sebum lipids (Lovaszi et al., p.4); psoriasis; rosacea; and skin dryness (0255, 0269 - 0271), each of which are disclosed by applicant as appropriate and preferred skin conditions associated with decreased sebum lipids (0019, 0152 - 0155 of the instant published application). In further support, Picardo teaches human sebum consists of 12 – 20% squalene, 26 – 30% wax esters, 1.5 – 2.5 cholesterol and 15 – 30% fatty acids (Table 1). Picardo shows that the claimed concentrations of fatty acid and cholesterol concentrations fall overlap with normal ranges, which indicates the claim includes subjects with “normal” sebum lipid levels.
Regarding claims 20 and 21, Jacky does not specifically teach administering to a non-facial area such as the hands, foot, neck, scalp or back. However, Jacky teaches the methods are used to treat dandruff, acne, seborrheic dermatitis, erythema, rosacea, psoriasis, atopic dermatitis (AD), alopecia (0269, 0271) with the effect of regulating or altering sebum composition. In this regard, it would have been obvious to one practicing the methods of Jacky to administer the active toxin to the location of the condition. Specifically, to the scalp for dandruff, and any body part that exhibits the disclosed conditions. Moreover, at the time the claims were filed, it would have been obvious to one of ordinary skill in the art to administer the toxin of Jacky to the scalp, back, hands, feet or neck with a reasonable expectation of successfully treating dandruff, alopecia, acne, seborrheic dermatitis, erythema, rosacea, psoriasis or atopic dermatitis (AD).
Therefore, the invention as a whole is prima facie obvious over the references, especially in the absence of evidence to the contrary.
Double Patenting
Previous provisional rejections on the ground of nonstatutory double patenting as being unpatentable over claims 33 and 35 of copending Application No. 18/549 871; and 21 and 24 of copending Application No. 18/552 599 are withdrawn.
Applicant argues that the NSDP rejections no longer apply since claim 14 was not rejected.
Applicant's arguments are not persuasive. However, the rejections are withdrawn because application 18/549 871 has been abandoned; and 18/552 599 canceled the claims having overlapping subject matter.
Response to Arguments
Applicant argues that the prior art does not teach a method for treating skin conditions with low levels of lipids in sebum; that Jacky focuses on reducing skin oiliness and inhibiting lipogenesis; and only discloses psoriasis and atopic dermatitis in a laundry list. Applicant argues that example 7 of Jacky inhibits sebum lipid production, reporting cotreatment (oleic acid and polypeptide "substantially similar" to binding domain of BoNT/A) results in reduced sebocyte lipogenesis.
Regarding the argument that Jacky does not teach a method for treating conditions with low levels of lipids in sebum, initially, claim 14 does not require a method for treating skin conditions with low levels of lipids in sebum. Rather, the claim is drawn to a method for treating "a skin condition" where the sebum of the patient comprises fatty acid at a concentration of <50%; wax ester at a concentration of <20%; squalene at a concentration of <10%; and/or cholesterol at a concentration of <4%. As discussed by Picardo, human sebum consists of 15 - 30% fatty acids; 26 - 30% wax esters; 12 - 20% squalene; and 1.5 - 2.5 cholesterol (Table 1). In this regard, the claims are directed to treating patients with sebum having "normal" levels of fatty acid and cholesterol and not low levels of lipids as argued. Notwithstanding, Jacky specifically teaches methods for treating skin disorders associated with sebum dysregulation and/or abnormalities, modulating sebum dysregulation and/or abnormalities (0037, 0040), and disorders caused by underactive sebaceous glands. Example disorders include acne which exhibits suppressed levels of fatty acid by more than 20%, (Pappas et al., p. 158); atopic dermatitis, characterized by decreased sebum lipids (Lovaszi et al., p.4); psoriasis; rosacea; and skin dryness (0255, 0269 - 0271), each of which are disclosed by applicant as appropriate and preferred skin conditions (0152 - 0155 of the instant published application).
Regarding the argument that Jacky focuses on reducing skin oiliness and inhibiting lipogenesis, "The use of patents as references is not limited to what the patentees describe as their own inventions or to the problems with which they are concerned. They are part of the literature of the art, relevant for all they contain." In re Heck, 699 F.2d 1331, 1332-33, 216 USPQ 1038, 1039 (Fed. Cir. 1983) (quoting In re Lemelson, 397 F.2d 1006, 1009, 158 USPQ 275, 277 (CCPA 1968)). A reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill in the art, including nonpreferred embodiments. Disclosed examples and preferred embodiments do not constitute a teaching away from a broader disclosure or nonpreferred embodiments. In re Susi, 440 F.2d 442, 169 USPQ 423 (CCPA 1971) (MPEP 2123).
Regarding the argument that psoriasis and atopic dermatitis are disclosed in a laundry list, these conditions are listed as 2 of 8 specific skin conditions (0271, claim 37). In this regard, the teachings are specific and finite as to what conditions can be treated with BoNT/A. Moreover, Jacky clearly names these conditions as treatable within the genus of skin disorders to be treated (MPEP 2131.02 (II)).
Regarding applicant's discussion of example 7, Jacky teaches "overproduction of sebum was significantly attenuated" (0194). While Example 7 shows that BoNT/A polypeptides reduce overproduction of sebum when cotreated with oleic acid (e.g. a 6 - 8 fold increase in sebum lipogenesis), the example further shows that treatment with BoNT/A alone does not affect sebum lipogenesis (0283). Moreover, example 7 shows that BoNT/A has a regulatory effect on sebum overproduction rather than a straightforward inhibition on sebum lipid production as argued by applicant. It is noted that reducing lipid overproduction is not equivalent to reducing "normal" or "underactive" lipid production. This is further supported by example 10, which shows BoNT/A polypeptide modulates skin sebum production and composition to affect skin oiliness and dryness (0293)
Applicant argues Picardo fails to motivate or provide the reasonable expectation to successfully treat reduced sebum lipids, but only provides normal sebum composition data; that combined, the prior art does not provide a reasonable expectation of success to treat reduced sebum lipid levels with a clostridial neurotoxin; and the combined references teach away from the claimed invention.
Regarding applicant's argument that Picardo fails to motivate one to treat reduced sebum lipids, it is iterated that claim 14 does not require a method for treating reduced serum lipids. As such, this argument is not commensurate in scope with the claimed invention. Notwithstanding, Picardo is not cited to motivate or provide reasonable expectation for successfully treating reduced sebum lipids. Rather, Jacky is relied upon to teach treating such conditions with clostridial neurotoxin. Ins
It is agreed that Picardo teaches normal sebum composition data. It is, in fact, why Picardo is cited and relied upon to further evidence the composition of "normal" sebum lipids compared to those with psoriasis and atopic dermatitis. Moreover, applicant's specification identifies patients with these conditions have lower levels of sebum lipids than patients without the conditions (p.4, via Shale et al.) and Picardo further supports patients with psoriasis or atopic dermatitis have lipid levels as recited in claim 14.
Regarding the argument that the combined references do not provide a reasonable expectation for successfully treating reduced sebum lipid levels with a clostridial neurotoxin, it is iterated that claim 14 does not require a method for treating reduced serum lipids. As such, this argument is not commensurate in scope with the claimed invention. Notwithstanding, Jacky clearly teaches methods for treating skin disorders associated with sebum dysregulation and/or abnormalities, modulating sebum dysregulation and/or abnormalities (0037, 0040), and disorders caused by underactive sebaceous glands. Example disorders include acne which exhibits suppressed levels of fatty acid by more than 20%, (Pappas et al., p. 158); atopic dermatitis, characterized by decreased sebum lipids (Lovaszi et al., p.4); psoriasis; rosacea; and skin dryness (0255, 0269 - 0271), each of which are disclosed by applicant as appropriate and preferred skin conditions (0152 - 0155 of the instant published application).
Regarding the argument that one in the art would be discouraged from the claimed invention, Jacky specifically teaches methods for treating skin disorders associated with sebum dysregulation and/or abnormalities, modulating sebum dysregulation and/or abnormalities (0037, 0040), and disorders caused by underactive sebaceous glands. Example disorders include acne which exhibits suppressed levels of fatty acid by more than 20%, (Pappas et al., p. 158); atopic dermatitis, characterized by decreased sebum lipids (Lovaszi et al., p.4); psoriasis; rosacea; and skin dryness (0255, 0269 - 0271), each of which are disclosed by applicant as appropriate and preferred skin conditions (0152 - 0155 of the instant published application).
Applicant argues the claimed method is unexpected and surprising in that intradermal administration of clostridial neurotoxin increases sebaceous lipids in the sebum without changing overall sebum levels; that clostridial neurotoxins were known to decrease sebum levels; and that applicant shows that intradermal BoNT/A administration leads to increased levels or secretion of sebum lipids which is unexpected in view of the cited references.
Regarding applicant's assertions of unexpected results, applicant refers to paragraphs 0609 - 0616 (examples 1 - 6) of the published application in support of the unexpected result. However, these examples are not commensurate in scope with the claimed invention. Specifically, the subjects do not have the claimed reduced concentrations of sebum lipids and the examples are drawn to administering a single BoNT/A, Dysport. Moreover, the examples are drawn to treating mice having "normal" sebum lipid composition with Dysport. In this regard, the examples do not support applicant's assertion of unexpected results. Furthermore, since the claims are drawn to treating "a skin condition" with specifically lower than normal sebum lipid concentrations, neither the argument nor the evidence are commensurate in scope with the claimed invention. Still further, the claims do not require increasing sebaceous lipids in the sebum without changing overall sebum levels as argued.
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to RUTH A DAVIS whose telephone number is (571)272-0915. The examiner can normally be reached Monday - Friday (8am - 4pm).
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/RUTH A DAVIS/Primary Examiner, Art Unit 1699
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