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 .
Response to Amendment
Applicant’s remarks and amendments to the claims received 04/16/2026 have been acknowledged. Claim 1 has been amended. Claim 13 has been canceled. The claim amendments overcome rejections made under 35 USC 112(a) written description and 35 USC 102 previously set forth in the Non-Final Rejection of 01/16/2026.
Election/Restrictions
Claim 1 as amended recite several antibodies and antigen-binding fragments targeting Pear1. Upon further examination, the elected species (antibody or antigen-binding fragment that targets Pear1) has been found to be free of the prior art. Thus, the search was extended and stopped upon finding art that read upon another Pear1 agonist: fucoidan. It is noted that other Pear1 agonist species recited in the claims have not been searched or examined on the merits for their patentability in the present Office Action.
Claim Interpretation
The term ‘fucose’ does not appear to be particularly defined in the specification. However, fucoidan – a fucose-rich sulfated polysaccharide – is used as a Pear1 agonist in Example 6. Thus, for the purposes of examination, the term ‘fucose’ is interpreted as encompassing fucose and fucose-containing compounds and fucose derivatives/analogues.
Claim Rejections - 35 USC § 112
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.
Claims 1-2, 11, and 12 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling the use of the fucose-containing compound fucoidan in the treatment of fibrotic disease, does not reasonably provide enablement for …. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
The nature of the invention relates to targeting Pear1 for the treatment of fibrosis-related disease.
The claims are broadly drawn to a method for 1) treating fibrotic disease, 2) downregulating and/or inhibiting fibroblast signaling pathway, and/or 3) inhibiting fibroblast activation, comprising administering a Pear 1 agonist, wherein the Pear1 agonist is fucose.
The specification teaches that the Pear 1 ligand fucoidan inhibits the ability of human lung fibroblasts to synthesize extracellular matrix proteins such as bone membrane protein (Periostin), Col5a3, and Timp1 (Example 6, Figure 5). There is no evidence provided in the specification that fucose in any form can treat fibrotic disease, downregulate fibroblast signaling, and/or inhibit fibroblast activation via Pear 1. Nor is there any guidance on identification of fucose analogues or derivatives thereof that possess anti-fibrotic properties.
The prior art teaches that the biological effects of fucose are highly dependent on its specific form. For example, core fucosylation of glycoproteins—in which a fucose residue is attached via an α1,6-linkage to the core N-acetylglucosamine of N-glycans in mammals—plays a critical role in fibrosis by activating profibrotic signaling pathways such as TGF-β/Smad2/3 and PDGF-β/Erk (Pan et al, Abstract and Sun et al, Abstract and Introduction). In contrast, fucoidan –a fucose-rich sulfated polysaccharide—has demonstrated therapeutic potential in treating various types of fibrosis (lung, liver, and kidney) (see, e.g. Yu et al, Abstract; Li et al, Abstract; and Chen et al, Abstract). These divergent biological effects indicate that the mere presence of fucose does not predict whether a given fucose-containing compound will promote or inhibit fibrosis.
A person of ordinary skill in the art at the time of filing would have had experience in fibrosis research, drug development, and glycobiology. Even at this high level of skill, however, the effect of fucose containing compounds on fibrosis or fibroblast activation not have been readily predicted without additional testing. In Amgen Inc. v. Sanofi, Aventisub LLC, 987 F.3d 1080 (Fed. Cir. 2021), which the Supreme Court affirmed, the Federal Circuit relied on evidence showing that the scope of the claims encompassed millions of antibodies and that it was necessary to screen each candidate antibody in order to determine whether it met the functional limitations of the claim. Id. at 1088. Consequently, the Federal Circuit concluded that there was a lack of enablement (MPEP 2164.06). By analogy, the instant claims encompass fucose and fucose-containing compounds (such as analogues and derivatives of fucose) some of which may not have anti-fibrotic activity. Thus, the level of skill does not obviate the need for substantial experimentation across the full scope of the claimed genus. Claims 2, 11, and 12 incorporate limitations of claim 1 but do not cure the deficiencies of claim 1 and thus are also rejected.
Therefore, the specification is not enabling over the full scope of the claims.
Claim Rejections - 35 USC § 102
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, 2, and 12 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Yu et al (Yu, Hsin-Hsien, et al. "Fucoidan inhibits radiation-induced pneumonitis and lung fibrosis by reducing inflammatory cytokine expression in lung tissues." Marine Drugs 16.10 (2018): 392), hereinafter Yu, as evidenced by Biswas (Biswas, A, “Understanding pulmonary fibrosis: from symptoms to treatments”. Spire Healthcare, Spire Healthcare, 01 May 2025, of record).
Yu teaches the use of fucoidan – which contains high percentages of L-fucose and sulfated ester groups— for the treatment of radiotherapy-induced lung fibrosis. In particular, administration of fucoidan attenuated radiotherapy-induced fibrosis in lung tissues concomitant with a decrease in neutrophil and macrophage accumulation as well as reduced expression of several inflammatory cytokines, including TIMP-1, CXCL1, MCP-1, MIP-2, and interleukin-1Ra (Abstract and 3rd paragraph of Introduction). Pulmonary fibrosis is a type of restrictive lung disease because scarring (fibrosis) in the lung tissue makes the lungs stiff, preventing them from expanding fully, thus making it difficult to breathe as evidenced by Biswas (see entire document, in particular, pages 1-2). Per the instant claims, fucose is a type of Pear1 agonists that enhances its expression and/or activity. The term “fucose” is not particularly defined in the specification and is thus interpreted as encompassing fucose and analogues or derivatives thereof. Thus, the fucose analogue fucoidan can be considered a Pear 1 agonist.
Thus, Yu as evidenced by Biswas meets the limitations of instant claims 1-2 and 12.
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.
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Claims 1, 2, and 12 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-7 and 11-18 of co-pending Application No. 18290817 (reference application) as evidenced by Biswas (Biswas, A., “Understanding pulmonary fibrosis: from symptoms to treatments”. Spire Healthcare, Spire Healthcare, 01 May. 2025). Although the claims at issue are not identical, they are not patentably distinct from each other because the co-pending claims either anticipate or are obvious variants over the instant claims.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
The co-pending claims recite a method for alleviating or fibrotic diseases comprising administering a pharmaceutical composition comprising a Pear1 agonist to a subject in need (co-pending claim 1), wherein a) the fibrotic disease comprises pulmonary fibrosis, liver fibrosis, cardiac fibrosis, renal fibrosis, myelofibrosis (i.e. bone marrow fibrosis), or scars in skin and/or soft tissues (co-pending claim 2); and b) the Pear1 agonist increases the expression and/or activity of Pear 1 and is FcεR1α, dextran sulfate, fucoidan, or an antibody or antigen-binding fragment thereof that specifically activates Pear1 (co-pending claim 3). The antibody can comprise the heavy and light chain CDRs of clones LF2, LF3, LF11, LF15, and LF16 (co-pending claim 11 ; see also Tables 1-2 on Page 25 of co-pending specification). The instant claims also recite clones LF2, LF3, LF7, LF11, LF15, and LF16 in claim 1, parts (1)-(6), respectively (see also Table 3.3 on Pages 27 to 28 of the instant specification):
Clone LF2: heavy chain CDRs of SEQ ID NOs: 26, 27, and 28; and light chain CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46;
Clone LF3 heavy chain CDRs of SEQ ID NOs: 26, 27, and 29; and light chain CDRs of SEQ ID NOs: SEQ ID NO: 45, GAT, and SEQ ID NO: 46;
Clone LF7: heavy chain CDRs of SEQ ID NOs: 26, 30 and 28; and light chain CDRs of SEQ ID NOs: 47, SAS, and SEQ ID NO: 48
Clone LF11: heavy chain CDRs of SEQ ID NOs: 26, 27, and 29; and light chain CDRs of SEQ ID NO: 49, DTS, and SEQ ID NO: 50;
Clone L15: heavy chain CDRs of SEQ ID NOs: 31, 27, and 32; and light chain CDRs of SEQ ID NO: 51, GAT, and SEQ ID NO: 52; or
Clone L16: heavy chain CDRs of SEQ ID NOs: 33, 34, and 35; and light chain CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46.
Alternatively, the antibody comprises the VH and VL chains of clones hLF101, hLF-N55S, hLF-N55D, hLF-N55Q, hLF-G56A, and hLF-G56V (co-pending claim 11, see also Tables 3 and 4 on pages 25-26 of the co-pending specification). The instant claims recite the CDRs of the aforementioned clones in claim 1, parts (7)-(12), respectively (as shown below) (see also Table 5 on Pages 29-30 of the instant specification):
Clone hLF101: VH chain of SEQ ID NO: 7 comprising the CDRs of SEQ ID NOs: 39, 27, and 28; VL chain of SEQ ID NO: 22 comprising the CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46;
Clone hLF-N55S: VH chain of SEQ ID NO: 11 comprising the CDRs of SEQ ID NOs: 39, 40, and 28; VL chain of 22 comprising the CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46;
Clone hLF-N55D: VH chain of SEQ ID NO: 12 comprising the CDRs of SEQ ID NOs: 39, 41, and 28; VL chain of SEQ ID NO: 22 comprising the CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46;
Clone hLF-N55Q: VH chain of SEQ ID NO: 13 comprising the CDRs of SEQ ID NOs: 39, 42, and 28; VL chain of SEQ ID NO: 22 comprising the CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46;
Clone hLF-G56A: VH chain of SEQ ID NO: 14 comprising the CDRs of SEQ ID NOs: 39, 43, and 28; VL chain of SEQ ID NO: 22 comprising the CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46; or
Clone hLF-G56V: VH chain of SEQ ID NO: 15 comprising the CDRs of SEQ ID NOs: 39, 44, and 28; VL chain of SEQ ID NO: 22 comprising the CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46.
Pulmonary fibrosis is a type of restrictive lung disease because the scarring (fibrosis) in the lung tissue makes the lungs stiff, preventing them from expanding fully, thus making it difficult to breath as evidenced by Biswas (see entire document, in particular, pages 1-2).
Thus, the co-pending claims meet the limitations of instant claims 1, 2, and 12.
Claim 11 is provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-7 and 11-18 of co-pending Application No. 18290817, as applied to claims 1, 2, and 12 above, in view of Raghu et al (Raghu, Ganesh, et al. "Incidence and prevalence of idiopathic pulmonary fibrosis." American journal of respiratory and critical care medicine 174.7 (2006): 810-816, of record), hereinafter Raghu.
This is a provisional nonstatutory double patenting rejection.
The teachings of the co-pending claims have been discussed above and differ from the instantly claimed invention in that it is not specifically taught that the pulmonary fibrosis is idiopathic pulmonary fibrosis.
However, Raghu teaches that idiopathic pulmonary fibrosis is a progressive life-threatening disease of unknown etiology characterized by scarring of the lungs and shortness of breath. Of the over 150 recognized types of interstitial lung disease, IPF is the most common and one of the most deleterious with a prevalence of 3 to 6 cases per 100,000 persons in the United States alone and a median survival rate of 3 to 5 years (Abstract and Introduction on Page 810).
It would have been obvious to one of ordinary skill in the art to modify the method of the co-pending claims such that the pulmonary fibrosis treated by a Pear1 agonist is idiopathic pulmonary fibrosis. One of ordinary skill in the art would have been motivated do to so since idiopathic pulmonary fibrosis is the most common and one of the most deleterious interstitial lung diseases with a prevalence of 3 to 6 cases per 100,000 persons in the United States and a median survival rate of 3 to 5 years as taught by Raghu. As such, patients with idiopathic pulmonary fibrosis represent a patient population that would receive therapeutic benefit treatment with the anti-fibrotic Pear1 agonists of the co-pending claims. Therefore, one of ordinary skill in the art would reasonably expect a Pear1 agonist can be used to effectively treat idiopathic pulmonary fibrosis in a subject according to the method of the co-pending claims.
Claim 1 is provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-4 and 6-16 of co-pending Application No. 18290815 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the co-pending claims either anticipate or are obvious variants over the instant claims.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
The co-pending claims recite a method for preventing, alleviating, or treating adhesive diseases comprising administering a Pear1 agonist to a subject in need (co-pending claim 1), wherein the Pear1 agonist increases the expression and/or activity of Pear 1 and is FcεR1α, dextran sulfate, fucoidan, or an antibody or antigen-binding fragment thereof that specifically activates Pear1 (co-pending claims 3 and 11). The Pear1 agonist is also used to inhibit fibroblast proliferation or activation at a lesion site (co-pending claim 4). The Pear1 agonist can be an antibody or antigen-binding fragment thereof that specifically activates Pear1, wherein the antibody comprises the heavy and light chain CDRs of clones LF2, LF3, LF11, LF15, and LF16 (co-pending claim 7 ; see also Table 2 on page 21 of co-pending specification). The instant claims also recite clones LF2, LF3, LF7, LF11, LF15, and LF16 in claim 1, parts (1)-(6), respectively (see also Table 3.3 on Pages 27 to 28 of the instant specification):
1) Clone LF2: heavy chain CDRs of SEQ ID NOs: 26, 27, and 28; and light chain CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46;
2) Clone LF3 heavy chain CDRs of SEQ ID NOs: 26, 27, and 29; and light chain CDRs of SEQ ID NOs: SEQ ID NO: 45, GAT, and SEQ ID NO: 46;
3) Clone LF7: heavy chain CDRs of SEQ ID NOs: 26, 30 and 28; and light chain CDRs of SEQ ID NOs: 47, SAS, and SEQ ID NO: 48
4) Clone LF11: heavy chain CDRs of SEQ ID NOs: 26, 27, and 29; and light chain CDRs of SEQ ID NO: 49, DTS, and SEQ ID NO: 50;
5) Clone L15: heavy chain CDRs of SEQ ID NOs: 31, 27, and 32; and light chain CDRs of SEQ ID NO: 51, GAT, and SEQ ID NO: 52; or
6) Clone L16: heavy chain CDRs of SEQ ID NOs: 33, 34, and 35; and light chain CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46.
Alternatively, the antibody comprises the VH and VL chains of clones hLF101, hLF-N55S, hLF-N55D, hLF-N55Q, hLF-G56A, and hLF-G56V (co-pending claim 8, see also Tables 3 and 4 on pages 21-22 of the co-pending specification). The instant claims recite the CDRs of the aforementioned clones in claim 1, parts (7)-(12), respectively (as shown below) (see also Table 5 on Pages 29-30 of the instant specification):
7) Clone hLF101: VH chain of SEQ ID NO: 7 comprising the CDRs of SEQ ID NOs: 39, 27, and 28; VL chain of SEQ ID NO: 22 comprising the CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46;
8) Clone hLF-N55S: VH chain of SEQ ID NO: 11 comprising the CDRs of SEQ ID NOs: 39, 40, and 28; VL chain of 22 comprising the CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46;
9) Clone hLF-N55D: VH chain of SEQ ID NO: 12 comprising the CDRs of SEQ ID NOs: 39, 41, and 28; VL chain of SEQ ID NO: 22 comprising the CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46;
10) Clone hLF-N55Q: VH chain of SEQ ID NO: 13 comprising the CDRs of SEQ ID NOs: 39, 42, and 28; VL chain of SEQ ID NO: 22 comprising the CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46;
11) Clone hLF-G56A: VH chain of SEQ ID NO: 14 comprising the CDRs of SEQ ID NOs: 39, 43, and 28; VL chain of SEQ ID NO: 22 comprising the CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46; or
12) Clone hLF-G56V: VH chain of SEQ ID NO: 15 comprising the CDRs of SEQ ID NOs: 39, 44, and 28; VL chain of SEQ ID NO: 22 comprising the CDRs of SEQ ID NO: 45, GAT, and SEQ ID NO: 46.
Thus, the co-pending claim meets the limitation of instant claim 1.
Response to Arguments
With respect to double patenting rejections, Applicant's arguments filed 04/16/2026 have been fully considered but they are not persuasive. Regarding the rejection over co-pending application 18/290,817, Applicant argues that the pending claims are patentably distinct by virtue of the mechanistic limitations. The co-pending claims are directed to methods for treating fibrotic disease but do not require the specific mechanistic outcomes that define the instant claims: downregulation of fibroblast signaling pathway and inhibition of fibroblast signaling. Applicant contends that a method claim defined by a specific mechanism of action is patentably distinct from a method claim directed to the therapeutic use alone using the same agent, where the mechanism is not a claim element. Further, Applicant argues that the secondary references over Biswas and Raghu do not cure these deficiencies.
In response to Applicant arguments, the Examiner notes that per the instant claims, a Pear 1 agonist (FcεR1α, fucose, or an antibody or antigen-binding fragment thereof targeting Pear1 having the recited CDRs) can 1) treat fibrotic disease, 2) downregulate fibroblast activation signaling pathway, and/or 3) inhibit fibroblast activation. As such, the co-pending claims reciting the same Pear 1 agonists having the same structure would possess the same mechanism of action involved in treating a fibrotic disease. Thus, the double patenting rejection over co-pending application 18/290,817 is maintained.
Regarding the double patenting rejection over co-pending application 18/290,815, Applicant argues that are directed to method of preventing, alleviating, or treating adhesive diseases comprising administering a Pear1 agonist, wherein the Pear1 agonist inhibits fibroblast proliferation or activation at the lesion site. Applicant contends that -unlike fibrotic diseases-adhesive diseases involve abnormal tissue adhesion typically localized post-surgical or inflammatory sequelae where normally separate tissues become bound together. While both may involve fibroblasts, Applicant argues that they differ substantially in etiology, pathophysiology, clinical presentation, and therapeutic approach. Applicant asserts that ‘inhibiting fibroblast proliferation or activation at a lesion sit’ does not meet the limitation of claim 1 because localized fibroblast inhibition at a discrete lesion site is mechanistically and therapeutically distinct from the systemic downregulation of the fibroblast activation signaling pathway in the context of progressive fibrotic organ disease.
In response to Applicant’s argument, the Examiner notes that the instant claims recite a method for 1) treating fibrotic disease, 2) downregulation fibroblast activation signaling pathway, and/or 3) inhibiting fibroblast activation. The phrase “and/or” encompasses embodiments of the method having at least one of the recited functional properties or any combination thereof. Thus, the co-pending claims reciting a method of treating adhesive diseases comprising administering a Pear1 agonist, wherein the Pear1 agonist inhibits fibroblast proliferation or activation at the lesion site meets at least one of the limitations of the instantly claimed method (i.e. inhibiting fibroblast activation). Further, Applicant has not provided any evidence to support the assertion that “localized fibroblast inhibition at a discrete lesion site is mechanistically and therapeutically distinct from the systemic downregulation of the fibroblast activation signaling pathway in the context of progressive fibrotic organ disease”. Arguments presented by applicant cannot take the place of evidence in the record. See In re De Blauwe, 736 F.2d 699, 705, 222 USPQ 191, 196 (Fed. Cir. 1984); In re Schulze, 346 F.2d 600, 602, 145 USPQ 716, 718 (CCPA 1965); In re Geisler, 116 F.3d 1465, 43 USPQ2d 1362 (Fed. Cir. 1997) (“An assertion of what seems to follow from common experience is just attorney argument and not the kind of factual evidence that is required to rebut a prima facie case of obviousness.”) (MPEP 2145). Nevertheless, the Examiner notes that the instantly claimed method is not limited to inhibiting fibroblast at any particular location and thus encompass inhibiting fibroblast activation at a lesion site. Therefore, the double patenting rejection over co-pending application 18/290,815 is maintained.
Applicant’s arguments with respect to the rejections of claims under 35 USC 112(a) and 35 USC 102 have been fully considered and are persuasive. Therefore, the rejection has been withdrawn. However, upon further consideration, a new ground(s) of rejection under 35 USC 112(a) enablement and 35 USC 102 is made in view of extended prior art search of Pear1 agonist species which was stopped upon finding art that read upon the Pear1 agonist fucoidan.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/LIA E TAYLOR/Examiner, Art Unit 1641
/MISOOK YU/Supervisory Patent Examiner, Art Unit 1641
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