Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
DETAILED ACTION
Applicant’s arguments, filed 3/25/2026, have been fully considered but they are not deemed to be persuasive. Rejections and/or objections not reiterated from previous office actions are hereby withdrawn. The following rejections and/or objects are either reiterated or newly applied. They constitute the complete set presently being applied to the instant application.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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 55 and 83 are rejected under 35 U.S.C. 103 as being unpatentable over Walston (Sarcopenia in older adults, Curr Opin Rheumatol. 2012 November ; 24(6): 623–627) in view of Yonekawa (Sialyllactose ameliorates myopathic phenotypes in symptomatic GNE myopathy model mice, Brain 2014: 137; 2670–2679). Walston teaches that Sarcopenia is age related, involuntary loss of skeletal muscle mass and strength (Introduction).
Watson fails to teach a method of treating sarcopenia by administering a composition comprising the presently claimed of 6’-sialyllactose.
Yonekawa teaches methods of treatment of muscle loss including skeletal muscle loss by administration of 6’-sialyllactose (corresponding to the presently claimed sialyllactose) (Abstract; Results). It further teaches that by applying this method to all treatment groups, it was found that a high dose of 6’-sialyllactose remarkably prevented further deterioration of motor performance. The findings support the use of this less invasive and reliable tool in the evaluation of other models of myopathy (page 2678, left column, first full paragraph), and further teaches low dose treatment ameliorated the contractile properties of gastrocnemius and tibialis anterior muscles and in the NeuAc group, sialic acid levels in skeletal muscle were increased to the level in the low dose group (page 2678, left column, third full paragraph), and enhanced sialylation for recovery of skeletal muscle function (page 2678, right column, last paragraph). Administration may be by a sustained-release preparation (page 2671, left column, first paragraph).
It would have been obvious to one of ordinary skill in the art at the time the invention was filed to treat the skeletal muscle mass loss caused by sarcopenia by administering 6’-sialyllactose. The motivation for this is that it was known to treat skeletal muscle mass loss using 6’-sialyllactose, and by administering 6’-sialyllactose, the skeletal muscle mass loss caused by sarcopenia may be treated. Regarding present claim 83, as the method rendered obvious by Walston and Yonekawa has the same patient population and same compound being administered, the method would result in the same effects as the present invention, that is, increase PCG-1alpha expression in the subject.
Applicant’s arguments have been fully considered but are not found persuasive. Regarding applicant’s arguments that there would be no motivation or reasonable expectation of success to combine, the examiner’s response is that 6’-sialyllactose was known at the time of the invention for treatment of muscle loss. The artisan, in seeking treatment for muscle loss in the form of sarcopenia, would not dismiss the teaching that 6’-sialyllactose was known at the time of the invention for treatment of muscle loss, as applicant argues. It would have been obvious to treat the skeletal muscle mass loss caused by sarcopenia by administering 6’-sialyllactose. The motivation for this is that it was known to treat skeletal muscle mass loss using 6’-sialyllactose, and by administering 6’-sialyllactose, the skeletal muscle mass loss caused by sarcopenia may be treated, and further, as the method rendered obvious by Walston and Yonekawa has the same patient population and same compound being administered, the method would result in the same effects as the present invention, that is, increase PCG-1alpha expression in the subject. In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). Regarding applicant’s argument that the examiner has used improper hindsight reasoning, the examiner examiner’s response is that they have no relied on improper hindsight reasoning but have relied only on the teachings of the references and what they would have conveyed to the ordinary artisan at the time of filing. Regarding applicant’s argument that the subject matter of claim 55 has been allowed in other countries, the examiner’s response is that (1) applicant has provided no evidence of this; and (2) the patent office is not bound to the opinion of the patent offices cited by applicant.
Claims 55-57, 74-75, and 83 are rejected under 35 U.S.C. 103 as being unpatentable over Walston (Curr Opin Rheumatol. 2012) in view of Yonekawa (Brain 2014) in further view Kang, Role of PGC-1a in muscle function and aging, Journal of Sport and Health Science 2 (2013) 81e86. The relevant portions of Walston and Yoneawa are given above.
Walston and Yonekawa fail to teach “further comprising, before the administering step, measuring the expression level of PGC-1a in cells from a sample isolated from the subject) (present claim 56), and “wherein it is observed whether or not the expression level of PGC-1a is decreased compared with a control group, and then, if decreased, the administering step is performed on the subject, wherein the control group shows no disease or symptom associated with a decrease in PGC-1a expression.
Kang teaches that PGC-1a regulates cellular oxidant-antioxidant homeostasis by stimulating the gene expression of superoxide dismutase-2, catalase, glutathione peroxidase 1, and uncoupling protein. Recent reports from muscle-specific PGC-1a overexpression underline the benefit of PGC-1a in muscle atrophy and sarcopenia, during which PGC-1a enhanced mitochondrial biogenic pathway and reduced oxidative damage. Kang further teaches that muscle atrophy caused by prolonged IM appears to be a highly ordered and regulated process which is characterized by decreased muscle fiber cross-sectional area, reduced force production, increased fatigability and insulin resistance (Section 2.2), and PGC-1a plays a critical role in maintaining muscle metabolic function and controls numerous genes that affect a broad range of muscle morphology and physiological function. Inactivity and aging are two important negative factors that down-regulate PGC-1a gene expression and subsequent down-regulation of mitochondrial biogenesis. Therefore, increased expression of pathways associated with these coactivators could provide effective improvements of mitochondrial dysfunction during aging (Conclusion).
It would have been obvious to one of ordinary skill in the art at the time the invention was made to, before the administering step, measure the expression level of PGC-1alpha in cells from a sample isolated from the subject. The motivation for this would be to assess the muscle loss status in the patient. It would have been further obvious to observe whether or not or not the expression level of PGC-1a is decreased compared with a control group, and then, if decreased, the administering step is performed on the subject, wherein the control group shows no disease or symptom associated with decrease PGC-1a expression, with the motivation of comparing the result to a baseline for analysis and to assess the current muscle loss state of the patient.
Applicant’s arguments have been fully considered but are not found persuasive. Regarding applicant’s arguments that there would be no motivation or reasonable expectation of success to combine, the examiner’s response is that 6’-sialyllactose was known at the time of the invention for treatment of muscle loss. The artisan, in seeking treatment for muscle loss in the form of sarcopenia, would not dismiss the teaching that 6’-sialyllactose was known at the time of the invention for treatment of muscle loss, as applicant argues. It would have been obvious to treat the skeletal muscle mass loss caused by sarcopenia by administering 6’-sialyllactose. The motivation for this is that it was known to treat skeletal muscle mass loss using 6’-sialyllactose, and by administering 6’-sialyllactose, the skeletal muscle mass loss caused by sarcopenia may be treated, and further, as the method rendered obvious by Walston and Yonekawa has the same patient population and same compound being administered, the method would result in the same effects as the present invention, that is, increase PCG-1alpha expression in the subject. In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). Regarding applicant’s argument that the examiner has used improper hindsight reasoning, the examiner examiner’s response is that they have no relied on improper hindsight reasoning but have relied only on the teachings of the references and what they would have conveyed to the ordinary artisan at the time of filing. Regarding applicant’s argument that the subject matter of claim 55 has been allowed in other countries, the examiner’s response is that (1) applicant has provided no evidence of this; and (2) the patent office is not bound to the opinion of the patent offices cited by applicant.
Conclusion
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
Any inquiry concerning this communication or earlier communications from the examiner should be directed to PAUL W DICKINSON whose telephone number is (571)270-3499. The examiner can normally be reached on M-F 9 AM to 7:30 PM.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Michael Hartley can be reached on 571-272-0616. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/PAUL W DICKINSON/Primary Examiner, Art Unit 1618
April 7, 2026