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
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 November 17, 2025 has been entered.
RESPONSE TO AMENDMENT
Status of Application/Amendments/claims
3. Applicant’s amendment filed November 17, 2025 is acknowledged. Claims 2-3, 6-11, 13, 21 and 24-29 are canceled. Claims 1 and 14-16 are amended. Claims 1, 4-5, 12, 14-20 and 22-23 are pending in this application. Applicant timely traversed the restriction (election) requirement in the reply filed on November 29, 2024.
4. Claims 1, 4-5, 12, 14-20 and 22-23 are under examination in this office action.
5. Applicant’s arguments filed on November 17, 2025 have been fully considered but they are not deemed to be persuasive for the reasons set forth below.
Claim Rejections/Objections Withdrawn
6. The rejection of claim 13 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite is moot because the claim is canceled.
The rejection of claim 13 under 35 U.S.C. 112(a) or pre-AIA 35 U.S.C. 112, first paragraph, lack of enablement is moot because the claim is canceled.
The rejection of claims 1, 4-5, 12-20 and 22-23 under 35 U.S.C. 103 as being unpatentable over den Hartog et al. (2004) in view of Maihofner et al. (2021), Staff et al. (2019), Kim’2018, Kim’2015, Okada et al. (US7150870), Kartha et al. (2017), Takenaga et al. (2006) and evidentiary references: Bhinge et al. (2012), Rivera et al. (2018), Nomoto et al. (US7700336) and Ikeda et al. (WO200100230 or EP1188445) is withdrawn in response to Applicant’s arguments regarding the effects of PC vs PC-SOD and the effects of SOD vs PC-SOD on p.10-14 of the response filed 11/17/2025 and Dr. Tohru Mizushima’s declaration filed 11/17/2025.
Claim Rejections/Objections Maintained
In view of the amendment filed on November 17, 2025, the following rejections are maintained.
Claim Rejections - 35 USC § 112(b)
7. Claims 1, 4-5, 12, 14-20 and 22-23 stand rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor, or for pre-AIA the applicant regards as the invention. The rejection is maintained for the reasons of record and the reasons set forth below.
Response to Arguments
On p. 8 of the response, Applicant argues that the rejection has been overcome in view of amendment to claim 1.
Applicant's arguments have been fully considered but they are not found persuasive. Contrary to Applicant’s arguments, the examiner asserts that based on MPEP§2171-MPEP§2173, the instant claims 1, 4-5, 12-20 and 22-23 are indefinite because:
i. Claims 1, 4-5, 12-20 and 22-23 stand rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being incomplete for omitting essential elements, such omission amounting to a gap between the elements. See MPEP § 2172.01. The omitted elements are: There is no subject for the step of administering. The subject, such as a subject suffering from cancer and neuropathy or neuropathic pain caused by administration of an anti-cancer agent, is essential element for the step of administering and the claimed method. But no such subject is recited in the claimed method. Thus, the claims are incomplete.
ii. The term “decreasing”, "decreased” or “reduced” in claim 1 or 4 is a relative term which renders the claim indefinite. The term "decreased” or “reduced” is not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention. Applicant fails to set forth the metes and bounds of what is encompassed within the definition of “decreasing”, "decreased” or “reduced”. Since the metes and bounds are unknown, a skilled artisan cannot envision what would be considered as ”decreasing a disorder associated with administration of an anticancer agent”, “decreased nerve fiber density” or “reduced neurites” recited in the claims. Thus the claims are indefinite.
iii. Claim 19 recites both broad and narrow limitations. A broad range or limitation together with a narrow range or limitation that falls within the broad range or limitation (in the same claim) may be considered indefinite if the resulting claim does not clearly set forth the metes and bounds of the patent protection desired. See MPEP § 2173.05(c). In the present instance, claim 19 recites the broad recitation “which is administered in combination with an anticancer agent”, which is any anticancer agent, and the claim also depends from claim 1 that recites specific anticancer agent is at least one selected from….a platinum-based drug….and a proteasome inhibitor”, which is the narrower statement of the range/limitation. The claim(s) are considered indefinite because there is a question or doubt as to whether the feature introduced by such narrower language is (a) merely exemplary of the remainder of the claim, and therefore not required, or (b) a required feature of the claims.
iv. The rest of claims are indefinite as depending from an indefinite.
Accordingly, the rejection of claims 1, 4-5, 12, 14-20 and 22-23 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite is maintained.
Claim Rejections - 35 USC § 112(a)
8. Claims 1, 4-5, 12, 14-20 and 22-23 stand rejected under 35 U.S.C. 112(a) or pre-AIA 35 U.S.C. 112, first paragraph, as based on a disclosure which is not enabling. The claims recite no subject for the step of administering, which is essential for the claimed method. Thus, the claimed method is not enabling without a subject. The rejection is maintained for the reasons of record and the reasons set forth below.
Response to Arguments
On p. 8 of the response, Applicant argues that the rejection has been overcome in view of amendment to claim 1 by deleting the term “preventing”.
Applicant's arguments related to prevention have been fully considered and they are found persuasive. The rejection based on prevention is withdrawn. However, the instant claims are still not enabling without a subject for the step of administering. The disclosure does not enable one of ordinary skill in the art to practice the invention without a subject for the step of administering. The subject, such as a subject suffering from a cancer and neuropathy or neuropathic pain caused by administration of an anticancer as recited in claim 1, for the step of administering is required by the claimed method, and is critical or essential to the practice of the invention but not included in the claim(s). See In re Mayhew, 527 F.2d 1229, 188 USPQ 356 (CCPA 1976). The claimed method cannot be practiced without a subject for the step of administering. Thus, the claimed method is not enabling without a subject.
Accordingly, the rejection of claims 1, 4-5, 12, 14-20 and 22-23 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, lack of enablement is maintained.
Claim Rejections - 35 USC § 102
9. 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, 4-5, 12, 17-20 and 22-23 stand rejected under 35 U.S.C. 102(a)(1) as being anticipated by den Hartog et al. (Toxicol. App. Pharmacol. 2004; 194:180-188) as evidenced by Bhinge et al. (Int. J. Biochem. Cell Biol.2012; 44:1770-1778. Doi:10.1016/j.biocel.2012.06.010), Rivera et al. (JNCI J. Natl. Cancer Inst. 2018; 110:131-140), Nomoto et al. (US7700336), Ikeda et al. (WO200100230; EP1188445, English-version of WO200100230), Meredith et al. (J. Pharm. Pharmacol. 2016; 68:729-741) and Sishi et al. (Toxicology, 2013; 309:23-29). The references of Meredith et al. and Sishi et al. are necessitated by Applicant’s amendment to the claims. The rejection is maintained for the reasons of record and the reasons set forth below.
Claims 1, 4-5, 12-14, 17-20 and 22-23 as amended are drawn to a method for treating or preventing a disorder associated with administration of an anticancer agent, wherein the disorder associated with administration of an anticancer agent is selected from the group consisting of a peripheral neurological disorder, neuropathy, neuropathic pain, allodynia, hyperalgesia or hypoalgesia, or thermal sensation disorder, myelosuppression, and a combination of one or more thereof, comprising administering to a subject a pharmaceutical composition comprising a lecithinized superoxide dismutase (PC-SOD), wherein the PC-SOD comprises at least one amino group in human-derived SOD subunit coordinated with copper and/or zinc and has a mercapto group in cysteine at position 11 replaced by a hydroxyethylthio group modified with a lecithin residue of the formula (I) directly or via a linker.
Briefly, den Hartog teaches a method of protecting doxorubicin-induced cardiotoxicity, comprising intravenous administering PC-SOD to mice treated with doxorubicin or administering a combination of PC-SOD and doxorubicin to mice, thereby protecting the mice from cardiotoxicity induced by doxorubicin, which meets the limitations recited in claims 1, 4-5, 12-14, 17-20 and 22-23 (See p. 180, abstract; p. 183-187).
The doxorubicin disclosed by den Hartog is an anticancer agent for ovarian cancer, or breast cancer, and administration of doxorubicin to patients with ovarian or breast cancer causes peripheral neuropathy, reduced nerve fiber density, reduced or retracted neurite or damaged dorsal root ganglion neurons and myelosuppression as recited in instant claims 1, 4-5 and 12 as evidenced by Bhinge et al. (see p.1770, abstract; p. 5-7; p.7-8; Bhinge et al., Int. J. Biochem. Cell Biol.2012; 44:1770-1778) and Rivera et al. (see p. 131, abstract; p.133-138, tables 1-2; p. 139; Rivera et al., JNCI J. Natl. Cancer Inst. 2018; 110:131-140).
The doxorubicin disclosed by den Hartog is a metabolism antagonist as evidenced by Meredith et al. (see p.736-738, section “cell metabolism”; Meredith et al., J. Pharm. Pharmacol. 2016; 68:729-741) and is also a proteasome inhibitor as evidenced by Sishi et al. (see p. 23, abstract; p. 26, 2nd col., section “DXR inhibits proteasome activity”; Sishi et al., Toxicology, 2013; 309:23-29).
The PC-SOD disclosed by de Hartog is the PC-SOD recited in instant claims and has the features, structures, properties and comprises the sequence of instant SEQ ID NO:1 as evidenced by Nomoto et al. (US7700336) and Ikeda et al. (EP1188445 or WO200100230). Nomoto teaches that the PC-SOD comprises at least one amino group in a human-derived SOD subunit coordinated with copper and/or zinc and has a mercapto group in cysteine at position 111 replaced by a hydroxyethylthio group modified with a lecithin residue of formula (I) directly or via a linker as recited in claims 1 and 22 (see abstract; col.1, line 61-col.2, line 61; col.3, line 6-col.6, line 65). The PC-SOD disclosed by Nomoto has the amino acid sequence of SEQ ID NO:1 recited in claim 23 as evidenced by Ikeda (see the sequence alignment above; paragraph [0022] in Ikeda). Ikeda et al. (EP1188445 or WO200100230) teach that the PC-SOD is a lyophilized formulation as in claim 20 (see paragraphs [0003]-[0004];[0013]; [0039]) and comprises at least one amino group in a human-derived SOD subunit coordinated with copper and/or zinc and has a mercapto group in cysteine at position 111 replaced by a hydroxyethylthio group modified with a lecithin residue of formula (I) directly or via a linker as recited in claims1 and 22 (see paragraphs [0023]-[0029]), and the amino acid sequence set forth in SEQ ID NO:1 in claim 23 (see the sequence alignment below; paragraph [0022]). Thus, claims 1, 4-5, 12, 17-18,19-20 and 22-23 are anticipated by den Hartog as evidenced by Bhinge, Rivera, Nomoto, Ikeda, Meredith and Sishi.
Response to Arguments
On p. 8 of the response, Applicant argues that the rejection has been overcome in view of amendment to claim 1 by reciting wherein the anticancer agent is at least one selected from the group consisting of a platinum-based drug, a metabolism antagonist, a taxane drug, a vinca alkaloid drug and a proteasome inhibitor, which is not included in Hartog.
Applicant's arguments have been fully considered but they are not found persuasive. Hower, contrary to Applicant's arguments, the examiner asserts that based on MPEP §2131-2131.01, den Hartog does teach the anticancer agent is a metabolism antagonist or a proteasome inhibitor and does teach the claimed method because doxorubicin disclosed by den Hartog is a metabolism antagonist as evidenced by Meredith et al. (see p.736-738, section “cell metabolism”; Meredith et al., J. Pharm. Pharmacol. 2016; 68:729-741) is also a proteasome inhibitor as evidenced by Sishi et al. (see p. 23, abstract; p. 26, 2nd col., section “DXR inhibits proteasome activity”; Sishi et al., Toxicology, 2013; 309:23-29). Thus, claims 1, 4-5, 12, 17-18,19-20 and 22-23 are anticipated by den Hartog as evidenced by Bhinge, Rivera, Nomoto, Ikeda, Meredith and Sishi.
Accordingly, the rejection of claims 1, 4-5, 12, 17-20 and 22-23 under 35 U.S.C. 102(a)(1) as being anticipated by den Hartog as evidenced by Bhinge, Rivera, Nomoto, Ikeda, Meredith and Sishi is maintained.
Conclusion
12. NO CLAIM IS ALLOWED.
13. The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
den Hartog et al. (Toxicol. App. Pharmacol. 2004; 194:180-188) under 102 rejection teaches a method of protecting doxorubicin-induced cardiotoxicity, comprising intravenous administering PC-SOD to mice treated with doxorubicin or administering a combination of PC-SOD and doxorubicin to mice, thereby protecting the mice from cardiotoxicity induced by doxorubicin, wherein the PC-SOD comprises the amino acid sequence of SEQ ID NO:1 (see the sequence alignment below) and doxorubicin is an anticancer agent and is a metabolism antagonist.
SEQ ID NO:1
AAB46775
(NOTE: this sequence has 37 duplicates in the database searched.
See complete list at the end of this report)
ID AAB46775 standard; protein; 153 AA.
XX
AC AAB46775;
XX
DT 15-JUN-2007 (revised)
DT 19-APR-2001 (first entry)
XX
DE Human superoxide-dismutase protein fragment.
XX
KW Superoxide-dismutase; SOD; human; drug composition; lecithin-modified;
KW neuroprotective; nootropic; antiulcer; motorneuron disease;
KW ulcerative gastrointestinal disorder.
XX
OS Homo sapiens.
XX
CC PN WO200100230-A1.
XX
CC PD 04-JAN-2001.
XX
CC PF 23-JUN-2000; 2000WO-JP004138.
XX
PR 24-JUN-1999; 99JP-00178227.
XX
CC PA (SEGK ) SEIKAGAKU CORP.
CC PA (LTTL-) LTT INST CO LTD.
XX
CC PI Ikeda Y, Satou H;
XX
DR WPI; 2001-112391/12.
DR PC:NCBI; gi31615344.
XX
CC PT Freeze-dryable drug composition for treating e.g. motoneuron disease and
CC PT ulcerative gastrointestinal disorder comprising lecithin-modified
CC PT superoxide dismutase with specific properties and stability.
XX
CC PS Disclosure; Page 33-34; 37pp; Japanese.
XX
CC This invention describes a novel drug composition comprising a lecithin-
CC modified superoxide dismutase of a specific formula (I). The invention
CC also describes (1) a remedy for treating diseases made from the drug
CC composition; and (2) an agent for inhibiting the lowering of superoxide
CC dismutase or suppressing the appearance of peaks assignable to superoxide
CC dismutase analogs in column chromatography containing particularly
CC sucrose as an active ingredient for formulation of a lecithin-modified
CC superoxide dismutase. The products of the invention have neuroprotective,
CC nootropic and antiulcer activity. The drug compositions are applicable in
CC treating e.g. motorneuron disease and ulcerative gastrointestinal
CC disorder. The drug compositions are freeze-dryable, with specific
CC properties and stability but without lowering activity even after long-
CC term storage or decomposition
CC
CC Revised record issued on 15-JUN-2007 : Enhanced with precomputed
CC information from BOND.
XX
SQ Sequence 153 AA;
Query Match 100.0%; Score 816; Length 153;
Best Local Similarity 100.0%;
Matches 153; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 ATKAVCVLKGDGPVQGIINFEQKESNGPVKVWGSIKGLTEGLHGFHVHEFGDNTAGCTSA 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 ATKAVCVLKGDGPVQGIINFEQKESNGPVKVWGSIKGLTEGLHGFHVHEFGDNTAGCTSA 60
Qy 61 GPHFNPLSRKHGGPKDEERHVGDLGNVTADKDGVADVSIEDSVISLSGDHCIIGRTLVVH 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GPHFNPLSRKHGGPKDEERHVGDLGNVTADKDGVADVSIEDSVISLSGDHCIIGRTLVVH 120
Qy 121 EKADDLGKGGNEESTKTGNAGSRLACGVIGIAQ 153
|||||||||||||||||||||||||||||||||
Db 121 EKADDLGKGGNEESTKTGNAGSRLACGVIGIAQ 153
Belotte et al. (Clin. Cancer Res., 2015; 21:B01. Doi.org/10.1158/1557-3265.PMS14-B01, abstract) teach that treatment of epithelial ovarian cancer cell lines SKOV-3 and MDAH-2774 with the combination of SOD with cisplatin provides a protecting effect against chemoresistance in ovarian cancer cells and reduces development of cisplatin resistance in epithelial ovarian cancer cell lines SKOV-3 and MDAH-2774 (see abstract).
JP09110717 teaches human SOD having the amino acid sequence of instant SEQ ID NO:1 (see the sequence alignment below).
SEQ ID NO:1
AAW22113
ID AAW22113 standard; protein; 153 AA.
XX
AC AAW22113;
XX
DT 15-JUN-2007 (revised)
DT 12-SEP-1997 (first entry)
XX
DE Human Cu/ZnSOD.
XX
KW Superoxide dismutase; human; Cu/ZnSOD; lupus nephritis; lecithin.
XX
OS Homo sapiens.
XX
FH Key Location/Qualifiers
FT Modified-site 1
FT /note= "Optionally modified"
FT Modified-site 3
FT /note= "Optionally modified"
FT Modified-site 9
FT /note= "Optionally modified"
FT Modified-site 23
FT /note= "Optionally modified"
FT Modified-site 30
FT /note= "Optionally modified"
FT Modified-site 36
FT /note= "Optionally modified"
FT Disulfide-bond 57..146
FT Modified-site 70
FT /note= "Optionally modified"
FT Modified-site 75
FT /note= "Optionally modified"
FT Modified-site 91
FT /note= "Optionally modified"
FT Modified-site 122
FT /note= "Optionally modified"
FT Modified-site 128
FT /note= "Optionally modified"
FT Modified-site 136
FT /note= "Optionally modified"
XX
CC PN JP09110717-A.
XX
CC PD 28-APR-1997.
XX
CC PF 21-OCT-1995; 95JP-00297668.
XX
PR 21-OCT-1995; 95JP-00297668.
XX
CC PA (SAMU-) SAMU KENKYUSHO KK.
XX
DR WPI; 1997-294867/27.
DR PC:NCBI; gi31615344.
XX
CC PT Lupus nephritis treating agent - containing modified amino acid residues.
XX
CC PS Disclosure; Fig 1; 17pp; Japanese.
XX
CC This sequence represents human superoxide dismutase (Cu/ZnSOD). This
CC protein was used in a lupus nephritis treating agent, chemically combined
CC by lecithin, preferably through chemical crosslinking, as the active
CC agent. The treating agent allows effective treatment of lupus nephritis
CC
CC Revised record issued on 15-JUN-2007 : Enhanced with precomputed
CC information from BOND.
XX
SQ Sequence 153 AA;
Query Match 100.0%; Score 816; Length 153;
Best Local Similarity 100.0%;
Matches 153; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 ATKAVCVLKGDGPVQGIINFEQKESNGPVKVWGSIKGLTEGLHGFHVHEFGDNTAGCTSA 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 ATKAVCVLKGDGPVQGIINFEQKESNGPVKVWGSIKGLTEGLHGFHVHEFGDNTAGCTSA 60
Qy 61 GPHFNPLSRKHGGPKDEERHVGDLGNVTADKDGVADVSIEDSVISLSGDHCIIGRTLVVH 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GPHFNPLSRKHGGPKDEERHVGDLGNVTADKDGVADVSIEDSVISLSGDHCIIGRTLVVH 120
Qy 121 EKADDLGKGGNEESTKTGNAGSRLACGVIGIAQ 153
|||||||||||||||||||||||||||||||||
Db 121 EKADDLGKGGNEESTKTGNAGSRLACGVIGIAQ 153
JP10338645 teaches human SOD having the amino acid sequence of instant SEQ ID NO:1 (see the sequence alignment below).
SEQ ID NO:1
AAW89197
ID AAW89197 standard; protein; 153 AA.
XX
AC AAW89197;
XX
DT 15-JUN-2007 (revised)
DT 16-MAR-1999 (first entry)
XX
DE Superoxide dismutase (SOD).
XX
KW SOD; superoxide dismutase; improver; functional disorder; lecithin;
KW cerebral vessel disorder; PC-SOD; drug; human.
XX
OS Unidentified.
XX
CC PN JP10338645-A.
XX
CC PD 22-DEC-1998.
XX
CC PF 06-JUN-1997; 97JP-00149787.
XX
PR 06-JUN-1997; 97JP-00149787.
XX
CC PA (SAMU-) SAMU KENKYUSHO KK.
XX
DR WPI; 1999-114796/10.
DR PC:NCBI; gi31615344.
XX
CC PT New improver for a functional disorder - contains superoxide dismutase
CC PT and lecithin.
XX
CC PS Example; Page 8; 9pp; Japanese.
XX
CC This sequence represents a superoxide dismutase (SOD). The invention
CC relates to a new improver for a functional disorder accompanied to
CC cerebral vessel disorder. The improver contains SOD combined chemically
CC with lecithin (PC-SOD) as the active component. The drug is effective in
CC humans
CC
CC Revised record issued on 15-JUN-2007 : Enhanced with precomputed
CC information from BOND.
XX
SQ Sequence 153 AA;
Query Match 100.0%; Score 816; Length 153;
Best Local Similarity 100.0%;
Matches 153; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 ATKAVCVLKGDGPVQGIINFEQKESNGPVKVWGSIKGLTEGLHGFHVHEFGDNTAGCTSA 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 ATKAVCVLKGDGPVQGIINFEQKESNGPVKVWGSIKGLTEGLHGFHVHEFGDNTAGCTSA 60
Qy 61 GPHFNPLSRKHGGPKDEERHVGDLGNVTADKDGVADVSIEDSVISLSGDHCIIGRTLVVH 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GPHFNPLSRKHGGPKDEERHVGDLGNVTADKDGVADVSIEDSVISLSGDHCIIGRTLVVH 120
Qy 121 EKADDLGKGGNEESTKTGNAGSRLACGVIGIAQ 153
|||||||||||||||||||||||||||||||||
Db 121 EKADDLGKGGNEESTKTGNAGSRLACGVIGIAQ 153
Maihofner et al. (Supportive Care in Cancer, 2021; 29:4223-4238) teach chemotherapeutic agents including a platinum-based drug, a metabolism antagonist, a taxane drug, a vinca alkaloid drug, and a proteasome inhibitor as in claims 13-15 induce peripheral neurotoxicity or peripheral neuropathy (p. 4226, table 1).
Staff et al. (J. Peripher. Nerv. Syst. 2019; 24: S26-S39) teach chemotherapy regimens including oxalipatin (i.e. FOLFOX and XELOX) or a platinum-based drug induced peripheral neurotoxicity or peripheral neuropathy as in claims 15-16 (p. 4; p.7-8).
Kim’2018 (Drug and Chem. Toxicol. 2018; 41: 476-485) teaches a method of treating neuropathy or peripheral neurotoxicity or mechanical and thermal sensation disorder and neuronal damage induced by a taxane chemotherapeutic agent including docetaxel, comprising administering phosphatidylcholine (PC) to rats treated with docetaxel to attenuate neuropathy or peripheral neurotoxicity or mechanical and thermal sensation disorder and neuronal damage induced by docetaxel, which is a taxane chemotherapeutic agent for head and neck cancer, metastatic breast cancer, ovarian cancer, gastric cancer, prostate cancer and non-small cell lung cancer (see abstract; p. 478-484).
Kim’2015 (Life Science, 2015; 130:81-87) teaches a method of treating oxaliplatin-induced peripheral neuropathy, peripheral neurotoxicity or mechanical and thermal sensation disorder and neuronal damage, comprising administering phosphatidylcholine (PC) to rats treated with oxaliplatin to attenuate peripheral neuropathy, peripheral neurotoxicity or mechanical and thermal sensation disorder and neuronal damage induced by oxaliplatin, which is a platinum-based chemotherapeutic agent for advanced colorectal cancer and adjuvant therapy for different cancers (see p.81, abstract; p. 84-87).
Okada et al. (US7150870) teaches a method of treating or inhibiting a tumor growth and malignant progression including different tumors: brain, lung, colon, gastric, uterus tumor in a subject, comprising administering to the subject a pharmaceutically effective amount superoxide dismutase (SOD) wherein the SOD is coated with a protein, gliadin, or a lipid (see abstract; col. 2, line 60; claims 1-4).
14. Any inquiry concerning this communication or earlier communications from the examiner should be directed to CHANG-YU WANG whose telephone number is (571)272-4521. The examiner can normally be reached Monday-Thursday, 7:00am-5:00pm EST.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Jeffrey Stucker can be reached at 571-272-0911. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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Chang-Yu Wang
September 30, 2026
/CHANG-YU WANG/Primary Examiner, Art Unit 1675
