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 . 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.
Information Disclosure Statement
The information disclosure statement filed 18 May, 2023 fails to comply with 37 CFR 1.98(a)(2), which requires a legible copy of each cited foreign patent document; each non-patent literature publication or that portion which caused it to be listed; and all other information or that portion which caused it to be listed. There was no copy found in the application file for the citation KR 101222281, so it was not considered.
The information disclosure statement filed 18 May, 2023 fails to comply with 37 CFR 1.98(a)(3)(i) because it does not include a concise explanation of the relevance, as it is presently understood by the individual designated in 37 CFR 1.56(c) most knowledgeable about the content of the information, of each reference listed that is not in the English language. NPL document 4 was not in English, nor was an English language explanation of relevance given. Thus, this reference was not considered.
Election/Restrictions
Applicant’s election of treating a cancer patient with a KRas mutation with SEQ ID 1 and gemcitabine in injectable form in the reply filed on 9 April, 2026 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)).
The requirement is deemed proper and is therefore made FINAL.
Applicant has elected treatment of a cancer patient with a KRas mutation with SEQ ID 1 and gemcitabine in an injectable form. A search was conducted for this invention, and references rendering it obvious were found. As a result, claims 1, 3, 5-9, 20, and 21 were examined and claims 2, 4, 10, 14, and 22 were withdrawn from consideration. Applicant states that they believe claims 4, 10, 14, and 22 read on their elected species, but applicants elected none of the cancers of claim 4, did not specify the ratio of the gemcitabine and SEQ ID 1 in their election, so their election does not read on claim 10. And applicant selected a cancer patient, which is beyond prevention, so claim 14 and 22 are properly withdrawn.
During examination, a reference was found that read on at least one non-elected species. This reference is discussed below.
Claims Status
Claims 1-10, 14, and 20-22 are pending.
Claims 1, 2, 4, 6-10, and 14 have been amended.
Claims 20-22 are new.
Claims 2, 4, 10, 14, and 22 have been withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 9 April, 2026.
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.
Claim(s) 1, 5-7, and 20 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Nishi et al (US 20150307574, cited by applicants). Please note that this rejection does not read on applicant’s elected patient population.
Nishi et al describe galactin-9 variants for treatment of malignant tumors (paragraph 75). These variants are more stable to proteases, and give a higher yield when recombinantly produced (paragraph 3). Specific examples of galactin-9 variants that can be used in the invention include SEQ ID 42 (paragraph 42 and table 3), identical with SEQ ID 1 of the examined claims, and anticipating claims 1 and 20. The material can be formulated with carriers (paragraph 84) for injection (paragraph 83), IV, IM, subQ, ir IP (paragraph 79), anticipating claims 5-7.
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.
first rejection
Claim(s) 1, 3, 5-7, and 20 are rejected under 35 U.S.C. 103 as being unpatentable over Wiersma et al (Autophagy (2015) 11(8) p1373-1388, cited by applicants) in view of Nishi et al (US 20150307574, cited by applicants).
Wiersma et al discuss the effect of galactin-9 on KRas mutant colon cancer (title). The protein is rapidly internalized, killing the cells by halting autophagy (p1374, 1st column, 4th paragraph). This is probably because KRas mutation impairs normal lysosomal composition and function (p1384, 1st column, 2nd paragraph). The invention was also shown to work in an in vivo mouse model, inhibiting tumor growth and increasing overall survivial (p1378, 1st column, 2nd paragraph). Treatment was performed 3x/week, by IP injection (p1387, 1st column, 2nd paragraph).
The difference between this reference and the examined claims is that this reference does not discuss a variant of galactin-9 used in the examined claims.
Nishi et al describe galactin-9 variants for treatment of malignant tumors (paragraph 75). These variants are more stable to proteases, and give a higher yield when recombinantly produced (paragraph 3). Specific examples of galactin-9 variants that can be used in the invention include SEQ ID 42 (paragraph 42 and table 3), identical with SEQ ID 1 of the examined claims. The material can be formulated with carriers (paragraph 84) for injection (paragraph 83), IV, IM, subQ, ir IP (paragraph 79).
Therefore, it would be obvious to use the galactin-9 variants of Nishi et al, as they are more stable to proteases and easier to recombinantly produce. As both Nishi et al and Wiersma et al use their compounds to treat cancers, an artisan in this field would attempt this therapy with a reasonable expectation of success.
Wiersma et al discuss treatment of KRas positive cancers with galactin-9. Nishi et al render obvious using SEQ ID 1 of the examined application. Thus, the combination of references renders obvious claims 1, 3, and 20.
Wiersma et al discusses IP injection, which requires a carrier (peptides are solids and cannot be injected), rendering obvious claims 5-7.
second rejection
Claim(s) 1, 3, 5-9, 20, and 21 are rejected under 35 U.S.C. 103 as being unpatentable over Wiersma et al (Autophagy (2015) 11(8) p1373-1388, cited by applicants) in view of Nishi et al (US 20150307574, cited by applicants) and Geller et al (Science (2017) 357 p1156-1160).
Wiersma et al discuss the effect of galactin-9 on KRas mutant colon cancer (title). The protein is rapidly internalized, killing the cells by halting autophagy (p1374, 1st column, 4th paragraph). This is probably because KRas mutation impairs normal lysosomal composition and function (p1384, 1st column, 2nd paragraph). The invention was also shown to work in an in vivo mouse model, inhibiting tumor growth and increasing overall survivial (p1378, 1st column, 2nd paragraph). Treatment was performed 3x/week, by IP injection (p1387, 1st column, 2nd paragraph).
Nishi et al describe galactin-9 variants for treatment of malignant tumors (paragraph 75). These variants are more stable to proteases, and give a higher yield when recombinantly produced (paragraph 3). Specific examples of galactin-9 variants that can be used in the invention include SEQ ID 42 (paragraph 42 and table 3), identical with SEQ ID 1 of the examined claims. The material can be formulated with carriers (paragraph 84) for injection (paragraph 83), IV, IM, subQ, ir IP (paragraph 79).
As noted above, these references render obvious claims 1, 3, 5-7, and 20.
The difference between these references and the remaining claims is that these references do not discuss a second therapeutic.
Geller et al discuss how bacteria mediate tumor resistance to gemcitabine (title), using a colon cancer model (abstract). The bacteria metabolize the drug to an inactive metabolite (1st page, 3d column, 3d paragraph). By killing the bacteria with an antibiotic, gemcitabine was more effective in a murine model of colon cancer (fig 3, 3d page, top of page and 3d page, 3d column, 2nd paragraph, continues to 4th page, 1st column, 1st paragraph). This reference shows that gemcitabine is effective in treating colon cancers, the cancer of Wiersma et al.
Therefore, it would be obvious to add gemcitabine to the therapy of Wiersma et al and Nishi et al, to provide additional therapeutic efficacy. As Geller et al shows that this therapeutic is useful for these cancers, an artisan in this field would attempt this therapy with a reasonable expectation of success. Note that this is a combination of compositions each of which is known to be useful for the same purpose, which is not a patentable distinction (MPEP 2144.06).
Geller et al renders obvious adding gemcitabine to the therapy of Wiersma et al and Nishi et al, rendering obvious claims 8, 9, and 21.
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.
first rejection
Claims 1, 3, 5-9, 20, and 21 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, and 18 of copending Application No. 19/295,090 (US 20260083671) in view of Wiersma et al (Autophagy (2015) 11(8) p1373-1388, cited by applicants) and Geller et al (Science (2017) 357 p1156-1160).
Competing claim 1 describes a formulation of galactin-9 and a buffer (i.e. carrier), while competing claim 2 specifies that the galatcin-9 is SEQ ID 1, identical with SEQ ID 1 of the examined claims. Competing claim 18 specifies an intended use of cancer treatment, anticipating claims 1, 5, and 7.
The difference between the competing claims and the remaining examined claims is that the competing claims do not mention KRas, or a second therapeutic.
Wiersma et al discuss the effect of galactin-9 on KRas mutant colon cancer (title). The protein is rapidly internalized, killing the cells by halting autophagy (p1374, 1st column, 4th paragraph). This is probably because KRas mutation impairs normal lysosomal composition and function (p1384, 1st column, 2nd paragraph). The invention was also shown to work in an in vivo mouse model, inhibiting tumor growth and increasing overall survivial (p1378, 1st column, 2nd paragraph). Treatment was performed 3x/week, by IP injection (p1387, 1st column, 2nd paragraph).
Geller et al discuss how bacteria mediate tumor resistance to gemcitabine (title), using a colon cancer model (abstract). The bacteria metabolize the drug to an inactive metabolite (1st page, 3d column, 3d paragraph). By killing the bacteria with an antibiotic, gemcitabine was more effective in a murine model of colon cancer (fig 3, 3d page, top of page and 3d page, 3d column, 2nd paragraph, continues to 4th page, 1st column, 1st paragraph). This reference shows that gemcitabine is effective in treating colon cancers, the cancer of Wiersma et al.
Therefore, it would be obvious to use the therapeutic of the competing claim to treat the colon cancer of Wiersma et al, as a substitution of one known element (the cancer of the competing claims) for another (the KRas mutated colon cancer of Wiersma et al) yielding expected results (treatment of cancer). As both the competing claims and Wiersma et al discuss treating cancer with galactin-9, an artisan in this filed would make this substitution with a reasonable expectation of success.
Furthermore, it would be obvious to add gemcitabine to the therapy of Wiersma et al, to provide additional therapeutic efficacy. As Geller et al shows that this therapeutic is useful for these cancers, an artisan in this field would attempt this therapy with a reasonable expectation of success. Note that this is a combination of compositions each of which is known to be useful for the same purpose, which is not a patentable distinction (MPEP 2144.06).
second rejection
Claims 1, 3, 5-9, 20, and 21 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3, 6, and 7 of copending Application No. 19/332,507 (US 20260015394) in view of Shady et al (Oncotarget (2017) 8(39) p66117-66127) and Geller et al (Science (2017) 357 p1156-1160).
Competing claim 1 describes a method of treatment of bone disease with a polypeptide of SEQ ID 1, identical with SEQ ID 1 of the examined claim, while competing claim 3 specifies a Markush group including metastatic bone disease (interpreted as including bone metastases). Competing claim 6 specifies a pharmaceutically acceptable carrier, and competing claim 7 describes a number of administration routes, including oral, IM, IV, IP, and subQ. This anticipates examined claims 1, 5-7, and 20.
The difference between the competing claims and the remaining examined claims is that the competing claims do not discuss KRas status, or a second therapeutic.
Shady et al discuss Kras status in the context of colorectal cancer (title). Colorectal metastases patients have a shorter survival time with Kras mutations (abstract). About 16% of the Kras positive patients also had bone metastases (p66122, 1st column, 1st paragraph). This reference discusses a patient cohort that reads on the competing claims comprising a KRas positive bone metastasis.
Geller et al discuss how bacteria mediate tumor resistance to gemcitabine (title), using a colon cancer model (abstract). The bacteria metabolize the drug to an inactive metabolite (1st page, 3d column, 3d paragraph). By killing the bacteria with an antibiotic, gemcitabine was more effective in a murine model of colon cancer (fig 3, 3d page, top of page and 3d page, 3d column, 2nd paragraph, continues to 4th page, 1st column, 1st paragraph). This reference shows that gemcitabine is effective in treating colon cancers, the cancer of Shady et al.
Therefore, it would be obvious to use the method of the competing claims, as a substitution of one element (the cancers of Shady et al) for another (the cancers of the competing claims) yielding expected results (treatment of cancers). As the cancers of Shady et al are a subgenus of the cancers of the competing claims, an artisan in this field would attempt this therapy with a reasonable expectation of success.
Furthermore, it would be obvious to add gemcitabine to the therapy of the Shandy et al, to provide additional therapeutic efficacy. As Geller et al shows that this therapeutic is useful for these cancers, an artisan in this field would attempt this therapy with a reasonable expectation of success. Note that this is a combination of compositions each of which is known to be useful for the same purpose, which is not a patentable distinction (MPEP 2144.06).
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to FRED REYNOLDS whose telephone number is (571)270-7214. The examiner can normally be reached M-Th 9-3:30.
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/FRED H REYNOLDS/Primary Examiner, Art Unit 1658
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