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 .
Applicant’s amendments filed 7/8/2026 have been entered.
Claims 1-18 are pending.
Claims 1-12 and 14-16 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected invention, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 1/2/2026.
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.
Claim(s) 13, 17-18 is/are rejected under 35 U.S.C. 103 as being unpatentable over Yokoyama et al., Biol Pharm Bull 41,979-984 (2018).
Yokoyama et al. teaches “transthyretin (TTR)-related amyloidosis is caused by mutations in the TTR gene. The muta tions destabilize the tetramer and/or monomer of TTR, and thus the stabilization of TTR is a key strategy for the treatment of TTR-related amyloidosis” (see the abstract). Yokoyama et al. teaches “TTR causes transthyretin-related amyloidosis (ATTR), including familial amyloid polyneuropathy (FAP), familial amyloid cardiomyopathy (FAC), central nervous system se lective amyloidosis (CNSA), and senile systemic amyloidosis (SSA).” (see page 979, col. 1, Section 2, TTR-related amyloidosis). Yokoyama et al. teaches “In 1996, it was elucidated that the binding of T4 stabilizes the TTR tetramer and inhibits the amyloid fibril formation of TTR. By this discovery, the search for TTR stabilizers that bind to the T4 binding site of TTR and stabilize the TTR tetramer became an efficient strategy for TTR amyloidosis therapy” (see page 981, col. 1, last paragraph). Yokoyama et al. teaches “glabridin, which is a prenylated isoflavan from licorice, is an inhibitor of TTR amyloidogenesis, and the inhibitory potency of glabridin is similar to that of diflunisal” (see page 982, col. 1, last paragraph).
Yokoyama et al. does not expressly teach the dosage of the licorice extract.
It would have been obvious to one of ordinary skill in the art at the time of filing to adjust the dosage of the licorice extract.
One of ordinary skill in the art would have been motivated to adjust the dosage of the licorice extract. The optimization of result effect parameters (dosage range, dosing regimens) is obvious as being within the skill of the artisan. The optimization of known effective amounts of known active agents to be administered, is considered well in the competence level of an ordinary skilled artisan in pharmaceutical science, involving merely routine skill in the art. It has been held that it is within the skill in the art to select optimal parameters, such as amounts of ingredients, in a composition in order to achieve a beneficial effect. See In re Boesch, 205 USPQ 215 (CCPA 1980). It is also noted that “[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). It is known that glabridin is an inhibitor of TTR amyloidogenesis and the inhibitory potency of glabridin is similar to that of diflunisal. According to Table 1, the compound concentration of diflunisal for inhibiting TTR amyloidogenesis. Accordingly, the dosage of licorice extract would be similar to that of diflunisal. Adjusting the dosage or amount of licorice extract to exhibit the inhibitory effect on TTR amyloidogenesis and treat amyloidosis thereby.
No claims are allowed.
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/SAN MING R HUI/Primary Examiner, Art Unit 1627
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