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
RESPONSE TO AMENDMENT
Status of Application/Amendments/claims
2. Applicant’s amendment filed August 07, 2026 is acknowledged. Claims 7-10 are cancelled. Claim 1 is amended. Claims 1-6 and 11-15 are pending in this application. Claims 2-6 are withdrawn without traverse (filed 5/22/2023) from further consideration pursuant to 37 CFR 1.142(b) as being drawn to nonelected inventions, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on May 22, 2023.
3. Claims 1 and 11-15 are under examination with respect to GDF11 peptide, pain and neuropathic pain in this office action.
4. Applicant’s arguments filed on August 07, 2026 have been fully considered but they are not deemed to be persuasive for the reasons set forth below.
Claim Rejections/Objections Maintained
In view of the amendment filed on August 07, 2026, the following rejections are maintained.
Claim Rejections - 35 USC § 102
5. 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 and 11-15 stand rejected under 35 U.S.C. 102(a)(2) as being anticipated by Wagers (US11725033; also published as WO2019144053; the citations of the rejection are based on US11725033) as evidenced by Vadivelu et al. (J. Pain Res. 2016; 9:37-47), Bennett et al. (BMJ Open, 2016; 6:e011616. Doi:10.1136/bmjopen-2016-011616) and Diatchneko et al. (Pain, 2006; 123:226-230). The references of Vadivelu, Bennett and Diatchneko 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 and 11-15 as amended are drawn to a method for treating a TRPV1-mediated disease, comprising administering to a patient with the TRPV1-mediated disease a composition comprising only one active ingredient, wherein the only one active ingredient is a GDF11 peptide consisting of the amino acid sequence set forth in SEQ ID NO:1 (elected), a polynucleotide encoding the GDF11 peptide or an expression vector comprising the polynucleotide; and the composition for treating the TRPV1-mediated disease effectively inhibits TRPV1 activity, and wherein the TRPV1-mediated disease is selected from the group consisting of cancer pain, postoperative pain, idiopathic pain and migraine.
Briefly, Wagers discloses a method for treating different conditions including nerve damage or injuries to the CNS, pain caused by surgery (i.e. postoperative pain) (see col.8, line 25), cancer including CNS metastasis, gliomas, astrocytoma (i.e. cancer pain) (see col. 8, lines30-36), tinnitus (i.e. idiopathic pain) (see col.9, line 5), headache including chronic headache (i.e. idiopathic pain) (col. 9, lines 1-2) or neuropathy causing neuropathic pain or chemotherapy/anti-neoplastic drugs-induced pain or diabetic neuropathic pain or trigeminal neuralgia pain (see col. 9, lines 39-62; col.31, lines 14-col. 32, lines; col. 8, lines 14-col.9, line 7; lines 39-62; claim 20) in a subject in need thereof, comprising administering to the subject a pharmaceutical composition consisting of a GDF11 (col. 22, lines 29-35; col. 24, lines 6-17), wherein the GDF11 peptide consists of the amino acid sequence of SEQ ID NO:3, which is 100% identical to the amino acid sequence of instant SEQ ID NO:1 (see the sequence alignment; claims 1-20; col. 12, lines 20-26; 41-45 ).
The neurological damage due to surgery has postoperative pain as evidenced by Vadivelu et al. (see p.37-38; J. Pain Res. 2016; 9:37-47). The gliomas and astrocytoma disclosed by Wagers have cancer pain as evidenced by Bennett et al. (see p.1, abstract; p. 3, 2nd col., results; p. 5, 1st col, Discussion; BMJ Open, 2016; 6:e011616. Doi:10.1136/bmjopen-2016-011616). The tinnitus and chronic headache disclosed by Wagers is an idiopathic pain as evidenced by Diatchneko et al. (see p.226, 1st col-2nd col.; Pain, 2006; 123:226-230).
The limitations “relieves chronic pain through TRPV1 inhibition” in claim 11, “reduces TRPV1-related pain and inflammation and support nerve regeneration” in claim 12, “inhibits a function of a TRPV1 channel” in claim 13, “reduces a TRPV1-mediated Ca2+ influx phenomenon in a concentration-dependent manner” in claim 14 and “reduces a TRPV1-mediated inward current that was induced by capsaicin in a concentration-dependent manner” in claim 15 are inherent results of administration of GDF11 because the material (i.e. GDF11), the active step (i.e. administering GDF11 to patients) and the patients (i.e. cancer pain, postoperative pain, idiopathic pain) disclosed by Wager are identical to those recited instant claims. If the composition recited in instant claims can achieve the effects recited in claims 11-15, the method of Wager using the same GDF11 and the same active step in the same patient population can achieve the same effects as instantly claimed. Further, the limitations recited in claims 11-15 are in a wherein clause and simply express the intended result of administration of GDF11, which is not given weight. Note that
In Hoffer v. Microsoft Corp., 405 F.3d 1326, 1329, 74 USPQ2d 1481, 1483 (Fed. Cir. 2005),…..the court noted (quoting Minton v.Nat’l Ass’n of Securities Dealers, Inc., 336 F.3d 1373, 1381, 67 USPQ2d 1614, 1620 (Fed. Cir. 2003)) that a “‘whereby clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited.’” Id.< See MPEP § 2111.04.
Thus, claims 1 and 11-15 are anticipated by Wagers (US11725033 or WO2019144053).
Response to Arguments
On p. 6-11 of the response, Applicant argues that: i) Wagers does not teach the claimed method because neurological injury associated with surgery is not a postoperative pain, tumors or tumor-associated neurological damage is not cancer pain, headache is not migraine. ii) Wagers does not teach the claimed TRPV1-mediated therapeutic mechanism: TRPV1 inhibition by the claimed composition and does not teach GDF11 as a TRPV1 inhibitor. iii) the office action has not established that administration of GDF11 treat cancer pain, postoperative pain, idiopathic pain or migraine as a TRPV1-mediated disease, inhibit a function of TRPV1 channel, reduces TRPV1-mediated CA2+ influx in a concentration-dependent manner or reduces a capsaicin-induced TRPV1-mdieated inward current in a concentration-dependent manner. iv) Wagers does not teach specific TRPV1 functional effects recited in dependent claims 11-15. Applicant further cites MPEP 2131 and Continental Can Co. USA v. Monsanto Co. in support of the arguments.
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 §2131 and MPEP §2131.01, Wagers does teach the claimed method because:
i. Wagers discloses a method of using the same material (i.e. a pharmaceutical composition consisting of a GDF11 wherein GDF11 consisting of instant SEQ ID NO:1; see sequence alignment; claims 1-20; col. 12, lines 20-26; 41-45; col. 22, lines 29-35; col. 24, lines 6-17)) and the same active step (i.e. administering GDF11 to a subject in need thereof; col. 22, lines 29-35; col. 24, lines 6-17) in the same patient population for treating different conditions including nerve damage or injuries to the CNS, pain caused by surgery (i.e. postoperative pain) (see col.8, line 25), cancer including CNS metastasis, gliomas, astrocytoma (i.e. cancer pain) (see col. 8, lines30-36), tinnitus (i.e. idiopathic pain) (see col.9, line 5), headache including chronic headache (i.e. idiopathic pain) (col. 9, lines 1-2).
The neurological injury or damage due to surgery disclosed by Wagers has postoperative pain as evidenced by Vadivelu et al. (J. Pain Res. 2016; 9:37-47). The gliomas and astrocytoma disclosed by Wagers have cancer pain as evidenced by Bennett et al. (see p.1, abstract; p. 3, 2nd col., results; p. 5, 1st col, Discussion; BMJ Open, 2016; 6:e011616. Doi:10.1136/bmjopen-2016-011616). The tinnitus and chronic headache disclosed by Wagers is an idiopathic pain as evidenced by Diatchneko et al. (see p.226, 1st col-2nd col.; Pain, 2006; 123:226-230).
The limitations “wherein the composition relieves chronic pain through TRPV1 inhibition” in claim 11, “wherein the composition reduces TRPV1-related pain and inflammation and support nerve regeneration” in claim 12, “wherein the composition inhibits a function of a TRPV1 channel” in claim 13, “wherein the composition reduces a TRPV1-mediated Ca2+ influx phenomenon in a concentration-dependent manner” in claim 14 and “wherein the composition reduces a TRPV1-mediated inward current that was induced by capsaicin in a concentration-dependent manner” in claim 15 are in a wherein clause and simply express the intended results of administration of GDF11.
The limitations recited in claims 11-15 are inherent results of administration of GDF11 because the material (i.e. GDF11), the active step (i.e. administering GDF11 to patients) and the patients (i.e. cancer pain, postoperative pain, idiopathic pain) disclosed by Wager are identical to those recited instant claims. If the GDF11 consisting of instant SEQ ID NO:1 recited in instant claims can achieve the effects recited in claims 11-15, the same GDF11 disclosed and used in the method of Wager for treating the same patient population can achieve the same effects as instantly claimed. Further, the limitations recited in claims 11-15 are in a wherein clause and simply express the intended result of administration of GDF11, which is not given weight. Note that
In Hoffer v. Microsoft Corp., 405 F.3d 1326, 1329, 74 USPQ2d 1481, 1483 (Fed. Cir. 2005),…..the court noted (quoting Minton v.Nat’l Ass’n of Securities Dealers, Inc., 336 F.3d 1373, 1381, 67 USPQ2d 1614, 1620 (Fed. Cir. 2003)) that a “‘whereby clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited.’” Id.< See MPEP § 2111.04.
Moreover, “The discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer.” Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342,1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977)“. See MPEP § 2112.01.
Accordingly, the rejection of claims 1 and 11-15 under 35 U.S.C. 102(a)(2) as being anticipated by Wagers (US11725033 or WO2019144053) as evidenced by Vadivelu, Bennett and Diatchneko is maintained.
Conclusion
6. NO CLAIM IS ALLOWED.
Sequence alignment
SEQ ID NO:2 1 MVLAAPLLLGFLLLALELRPRGEAAEGPAAAAAAAAAAAAAGVGGERSSRPAPSVAPEPD 60
SEQ ID NO:1 ------------------------------------------------------------
SEQ ID NO:2 61 GCPVCVWRQHSRELRLESIKSQILSKLRLKEAPNISREVVKQLLPKAPPLQQILDLHDFQ 120
SEQ ID NO:1 ------------------------------------------------------------
SEQ ID NO:2 121 GDALQPEDFLEEDEYHATTETVISMAQETDPAVQTDGSPLCCHFHFSPKVMFTKVLKAQL 180
SEQ ID NO:1 ------------------------------------------------------------
SEQ ID NO:2 181 WVYLRPVPRPATVYLQILRLKPLTGEGTAGGGGGGRRHIRIRSLKIELHSRSGHWQSIDF 240
SEQ ID NO:1 ------------------------------------------------------------
SEQ ID NO:2 241 KQVLHSWFRQPQSNWGIEINAFDPSGTDLAVTSLGPGAEGLHPFMELRVLENTKRSRRNL 300
SEQ ID NO:1 1 -----------------------------------------------------------NL 2
SEQ ID NO:2 301 GLDCDEHSSESRCCRYPLTVDFEAFGWDWIIAPKRYKANYCSGQCEYMFMQKYPHTHLVQ 360
SEQ ID NO:1 3 GLDCDEHSSESRCCRYPLTVDFEAFGWDWIIAPKRYKANYCSGQCEYMFMQKYPHTHLVQ 62
SEQ ID NO:2 361 QANPRGSAGPCCTPTKMSPINMLYFNDKQQIIYGKIPGMVVDRCGCS 407
SEQ ID NO:1 63 QANPRGSAGPCCTPTKMSPINMLYFNDKQQIIYGKIPGMVVDRCGCS 109
7. The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
Wagers (US11725033 or WO2019144053) under the 102 rejection teaches a method of treating different conditions including pain caused by nerve damages to the CNS or other conditions using the GDF-11 of instant SEQ ID NO:1 (see the sequence alignment below).
SEQ ID NO:1
BGP16908
ID BGP16908 standard; protein; 109 AA.
XX
AC BGP16908;
XX
DT 05-SEP-2019 (first entry)
XX
DE Human mature growth and differentiation factor 11 (GDF11) SEQ ID 3.
XX
KW BMP11 protein; Bone morphogenetic protein-11 ligand; GDF11 protein;
KW Growth and Differentiation Factor 11; aging; alexander disease;
KW alzheimers disease; angiogenesis stimulation; ataxia telangiectasia;
KW canavan disease; cell proliferation; cerebroprotective;
KW cerebrovascular disease; cockayne syndrome; creutzfeldt jakob disease;
KW degeneration; exercise endurance capacity; gene expression;
KW globoid cell leukodystrophy; guillain barre syndrome; ischemic stroke;
KW kuru; lewy body dementia; motor neurone disease; multiple sclerosis;
KW multiple system atrophy; muscle injury; muscular-gen.;
KW musculoskeletal-gen.; myotonic dystrophy; neurodegenerative disease;
KW neuroprotective; prophylactic to disease; protein engineering;
KW protein therapy; spinocerebellar ataxia; stem cell; therapeutic;
KW vasotropic; vulnerary.
XX
OS Homo sapiens.
XX
CC PN WO2019144053-A1.
XX
CC PD 25-JUL-2019.
XX
CC PF 18-JAN-2019; 2019WO-US014363.
XX
PR 19-JAN-2018; 2018US-0619683P.
PR 06-APR-2018; 2018US-0654303P.
XX
CC PA (HARD ) HARVARD COLLEGE.
XX
CC PI Wagers AJ, Goldstein J, Walker RG;
XX
DR WPI; 2019-646671/60.
XX
CC PT New growth differentiation factor (GDF) 11 variant comprising a
CC PT modification to the C-terminus region of a native GDF 11 protein is used
CC PT to e.g. increase levels of circulating GDF 11 protein, increase
CC PT angiogenesis and neurogenesis.
XX
CC PS Claim 4; SEQ ID NO 3; 130pp; English.
XX
CC The present invention relates to a novel growth and differentiation
CC factor 11 (GDF11) variant useful for treating or preventing neurovascular
CC or neurodegenerative disorders. The GDF11 variant is encoded by a
CC nucleotide sequence shown in SEQ ID 19 (see BGP16924). The invention
CC further relates to: (1) a composition comprising a GDF11 variant, where
CC the GDF11 variant comprises inclusion of at least two amino acids at the
CC C-terminus region as compared to a native GDF 11 protein, and a carrier;
CC (2) a method for increasing the levels of circulating GDF11 protein in a
CC subject, comprising administering to the subject a GDF11 variant
CC polypeptide; (3) a method for increasing angiogenesis or neurogenesis in
CC a subject; (4) a method for treating or preventing a neurovascular
CC disorder or a neurodegenerative disorder in a subject; (5) a method for
CC rejuvenating skeletal muscle stem cells in a subject; and (6) a method
CC for increasing the strength or exercise endurance capacity in a subject
CC diagnosed with a skeletal muscle condition due to aging. The
CC neurodegenerative disorder comprises myotonic dystrophy, spinocerebellar
CC ataxia type 8 and type 12, Alexander disease, Alzheimer, amyotrophic
CC lateral sclerosis (ALS), ataxia telangiectasia, Canavan disease, Cockayne
CC syndrome, corticobasal degeneration, Creutzfeldt-Jakob disease, Guillain-
CC Barre syndrome, ischemia stroke, Krabbe disease, kuru, Lewy body
CC dementia, multiple sclerosis, and multiple system atrophy.
XX
SQ Sequence 109 AA;
Query Match 100.0%; Score 628; DB 29; Length 109;
Best Local Similarity 100.0%;
Matches 109; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 NLGLDCDEHSSESRCCRYPLTVDFEAFGWDWIIAPKRYKANYCSGQCEYMFMQKYPHTHL 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 NLGLDCDEHSSESRCCRYPLTVDFEAFGWDWIIAPKRYKANYCSGQCEYMFMQKYPHTHL 60
Qy 61 VQQANPRGSAGPCCTPTKMSPINMLYFNDKQQIIYGKIPGMVVDRCGCS 109
|||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 VQQANPRGSAGPCCTPTKMSPINMLYFNDKQQIIYGKIPGMVVDRCGCS 109
Shen (US10987427) cited under the 103 rejection teaches a method of treating and reducing pain and/or inflammation in a subject in need thereof, comprising administering to the subject a composition or device comprising a GDF11 of SEQ ID NO:1 (see the sequence alignment below).
SEQ ID NO:1
US-16-405-594-20
; Sequence 20, Application US/16405594
; Patent No. 10987427
; GENERAL INFORMATION
; APPLICANT: THE CALIFORNIA INSTITUTE FOR BIOMEDICAL RESEARCH
; APPLICANT:THE SCRIPPS RESEARCH INSTITUTE
; TITLE OF INVENTION: MODIFIED THERAPEUTIC AGENTS AND COMPOSITIONS THEREOF
; FILE REFERENCE: 41135-709.301
; CURRENT APPLICATION NUMBER: US/16/405,594
; CURRENT FILING DATE: 2019-05-07
; PRIOR APPLICATION NUMBER: US 14/917,689
; PRIOR FILING DATE: 2016-03-09
; PRIOR APPLICATION NUMBER: PCT/US2014/055457
; PRIOR FILING DATE: 2014-09-12
; PRIOR APPLICATION NUMBER: US 61/877,799
; PRIOR FILING DATE: 2013-09-13
; PRIOR APPLICATION NUMBER: US 61/917,816
; PRIOR FILING DATE: 2013-12-18
; NUMBER OF SEQ ID NOS: 73
; SOFTWARE: PatentIn version 3.5
; SEQ ID NO 20
; LENGTH: 109
; TYPE: PRT
; ORGANISM: Artificial Sequence
; FEATURE:
; OTHER INFORMATION: Description of Artificial Sequence: Synthetic polypeptide
US-16-405-594-20
Query Match 100.0%; Score 628; DB 3; Length 109;
Best Local Similarity 100.0%;
Matches 109; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 NLGLDCDEHSSESRCCRYPLTVDFEAFGWDWIIAPKRYKANYCSGQCEYMFMQKYPHTHL 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 NLGLDCDEHSSESRCCRYPLTVDFEAFGWDWIIAPKRYKANYCSGQCEYMFMQKYPHTHL 60
Qy 61 VQQANPRGSAGPCCTPTKMSPINMLYFNDKQQIIYGKIPGMVVDRCGCS 109
|||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 VQQANPRGSAGPCCTPTKMSPINMLYFNDKQQIIYGKIPGMVVDRCGCS 109
Wagers (WO2015070076) teach a method for treating neuromuscular junction fragmentation including muscle atrophy or amyotrophic lateral sclerosis in a subject in need thereof, comprising administering to the subject a composition comprising a GDF11 peptide consisting SEQ ID NO:3, which is 100% identical to instant SEQ ID NO:1 (see the sequence alignment below).
SEQ ID NO:1
BCA17047
ID BCA17047 standard; protein; 109 AA.
XX
AC BCA17047;
XX
DT 02-JUL-2015 (first entry)
XX
DE Human growth and differentiation factor 11 mature protein, SEQ ID 3.
XX
KW Bone morphogenetic protein-11 ligand; GDF11 protein;
KW Growth and differentiation factor 11; atrophy; motor neurone disease;
KW muscle disease; prophylactic to disease; protein therapy; therapeutic.
XX
OS Homo sapiens.
XX
CC PN WO2015070076-A2.
XX
CC PD 14-MAY-2015.
XX
CC PF 07-NOV-2014; 2014WO-US064648.
XX
PR 08-NOV-2013; 2013US-0901875P.
XX
CC PA (HARD ) HARVARD COLLEGE.
XX
CC PI Wagers AJ;
XX
DR WPI; 2015-30272K/35.
DR REFSEQ; NP_005802.
XX
CC PT Rejuvenating neuromuscular junction, treating, preventing, or delaying
CC PT onset of, neuromuscular junction fragmentation or related disorder by
CC PT administering composition that increases level of growth differentiation
CC PT factor-11 polypeptide.
XX
CC PS Claim 15; SEQ ID NO 3; 84pp; English.
XX
CC The present invention relates to a novel method for rejuvenating
CC neuromuscular junctions in a subject in need. The method involves:
CC administering to the subject a composition which increases the level of
CC GDF11 (growth and differentiation factor 11) polypeptide in the subject.
CC The invention also provides: (1) a method for treating, preventing, or
CC delaying the onset of, neuromuscular junction fragmentation or a related
CC disorder such as muscle atrophy, and amyotrophic lateral sclerosis in a
CC subject; and (2) a pharmaceutical composition which comprises a GDF11
CC polypeptide or its functional fragment or its variant, and a carrier. The
CC composition causes one or more of a decrease in fragmentation of
CC neuromuscular junctions, an increase or maintenance of neuromuscular
CC innervation, a decrease of neuromuscular denervation, preservation or
CC restoration of motor units, an increase in the size of postsynaptic
CC endplates, an increases in the number of postsynaptic endplates, an
CC increase in the length of postsynaptic endplates, an increase in the
CC density of postsynaptic folds, normalization of neuromuscular junction
CC morphology, a decrease in denervation of fast-twitch fibers, an increase
CC in the number of nerve terminal branches per endplate, an increase in the
CC number of terminal sprouts, an increase or maintenance of synaptic
CC vesicles, mitochondrial content, or nerve terminal area in presynaptic
CC terminals, reversal of age-related changes in the quantal content of
CC neurotransmitter release measured by decreases in amplitude of evoked
CC endplate potentials (EPP), a reversal of age-related decline in axonal
CC transport, preservation or restoration of muscle fibers, an increase in
CC acetylcholine receptor number, a decrease in partially innervated or
CC completed denervated neuromuscular junctions, an increase in the number
CC of functional motor units in fast twitch muscle, enhanced neuromuscular
CC recovery, enhanced physical performance, an increase in neuromuscular
CC junction area, an increase in muscle size, and their combinations. The
CC present sequence is a human growth and differentiation factor 11 mature
CC protein, used in the composition of the invention for treating,
CC preventing, or delaying the onset of, neuromuscular junction
CC fragmentation or a related disorder.
XX
SQ Sequence 109 AA;
Query Match 100.0%; Score 628; DB 22; Length 109;
Best Local Similarity 100.0%;
Matches 109; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 NLGLDCDEHSSESRCCRYPLTVDFEAFGWDWIIAPKRYKANYCSGQCEYMFMQKYPHTHL 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 NLGLDCDEHSSESRCCRYPLTVDFEAFGWDWIIAPKRYKANYCSGQCEYMFMQKYPHTHL 60
Qy 61 VQQANPRGSAGPCCTPTKMSPINMLYFNDKQQIIYGKIPGMVVDRCGCS 109
|||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 VQQANPRGSAGPCCTPTKMSPINMLYFNDKQQIIYGKIPGMVVDRCGCS 109
Shen et al. (WO2015038938) teaches a method of treating a cardiovascular disease, acute heart failure and pain using a modified therapeutic agent comprising a GDF-11 peptide having the amino acid sequence of SEQ ID NO:1 (see the sequence alignment below).
SEQ ID NO:1
BBW23942
ID BBW23942 standard; protein; 109 AA.
XX
AC BBW23942;
XX
DT 07-MAY-2015 (first entry)
XX
DE Growth differentiation factor (GDF11) protein, SEQ ID 20.
XX
KW Bone morphogenetic protein-11 ligand; GDF11;
KW Growth differentiation factor; analgesic;
KW angiotensin converting enzyme inhibitor; antiinflammatory;
KW cardiac failure; cardiant; cardiovascular disease; cardiovascular-gen.;
KW enzyme inhibition; fibrosis; neuropathic pain; pain; pharmaceutical;
KW protein therapy; therapeutic.
XX
OS Unidentified.
XX
CC PN WO2015038938-A1.
XX
CC PD 19-MAR-2015.
XX
CC PF 12-SEP-2014; 2014WO-US055457.
XX
PR 13-SEP-2013; 2013US-0877799P.
PR 18-DEC-2013; 2013US-0917816P.
XX
CC PA (CALC-) CALIFORNIA INST BIOMEDICAL RES.
CC PA (SCRI ) SCRIPPS RES INST.
XX
CC PI Shen W, Schultz PG, Muppidi A, Crameri A, Ahmad I, Yang P;
XX
DR WPI; 2015-191433/23.
DR N-PSDB; BBW23930.
XX
CC PT Modified therapeutic agent used for treating a cardiovascular disorder,
CC PT acute heart failure, fibrosis, and pain comprises a therapeutic agent and
CC PT half-life extending moieties.
XX
CC PS Claim 14; SEQ ID NO 20; 170pp; English.
XX
CC The present invention relates to a novel modified therapeutic agent
CC (mTA). The mTA comprises a therapeutic agent (TA) and half-life extending
CC moieties, where the TA is a peptide that is covalently attached to each
CC of the half-life extending moieties via a cysteine residue on the
CC peptide, and which is selected from a group consisting of an anti-
CC inflammatory drug, a statin, a diuretic, a beta- blocker, an angiotensin
CC converting enzyme inhibitor, an angiotensin II receptor blocker or their
CC combination. The invention further provides: (1) a pharmaceutical
CC composition comprising the mTA; (2) a lipid conjugate (LC) comprising
CC lipids selected from sterols, sterol derivatives, bile acids, vitamin E
CC derivatives, fatty di-acids, fatty acids, fatty amides, fatty amines, and
CC fatty alcohols, and their derivatives, and the TA; and (3) a method for
CC treating a disease or a condition in a subject, by administering a
CC composition comprising the mTA or the LC, where the disease or the
CC condition is cardiovascular disorder, acute heart failure, fibrosis, and
CC pain (e.g., neuropathic pain or inflammatory pain). The present sequence
CC represents a Growth differentiation factor (GDF11) protein, which is used
CC in the therapeutic agent for treating the above-mentioned diseases.
XX
SQ Sequence 109 AA;
Query Match 100.0%; Score 628; DB 22; Length 109;
Best Local Similarity 100.0%;
Matches 109; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 NLGLDCDEHSSESRCCRYPLTVDFEAFGWDWIIAPKRYKANYCSGQCEYMFMQKYPHTHL 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 NLGLDCDEHSSESRCCRYPLTVDFEAFGWDWIIAPKRYKANYCSGQCEYMFMQKYPHTHL 60
Qy 61 VQQANPRGSAGPCCTPTKMSPINMLYFNDKQQIIYGKIPGMVVDRCGCS 109
|||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 VQQANPRGSAGPCCTPTKMSPINMLYFNDKQQIIYGKIPGMVVDRCGCS 109
Shen et al. (WO2016149501) teaches a method of treating a cardiovascular disease, acute heart failure and pain using a modified therapeutic agent comprising a GDF-11 peptide having the amino acid sequence of SEQ ID NO:1 (see the sequence alignment below).
SEQ ID NO:1
BDE95383
ID BDE95383 standard; protein; 109 AA.
XX
AC BDE95383;
XX
DT 17-NOV-2016 (first entry)
XX
DE Growth differentiation factor 11 (GDF 11) polypeptide, SEQ ID 20.
XX
KW GDF 11 protein; Growth differentiation factor 11; analgesic;
KW antiinflammatory; autoimmune disease; cardiac failure; cardiant;
KW cardiovascular disease; cardiovascular-gen.;
KW central nervous system disease; fibrosis; immunosuppressive;
KW inflammatory disease; metabolic disorder; metabolic-gen.;
KW neuropathic pain; neuroprotective; pain; prophylactic to disease;
KW protein kinetics; protein therapy; therapeutic.
XX
OS Unidentified.
XX
CC PN WO2016149501-A2.
XX
CC PD 22-SEP-2016.
XX
CC PF 17-MAR-2016; 2016WO-US022880.
XX
PR 18-MAR-2015; 2015US-0134939P.
XX
CC PA (CALC-) CALIFORNIA INST BIOMEDICAL RES.
XX
CC PI Shen W, Muppidi A, Schultz PG;
XX
DR WPI; 2016-595955/67.
DR N-PSDB; BDE95371.
XX
CC PT Modified therapeutic agent comprises therapeutic agent comprising relaxin
CC PT A-chain amino acid, and half-life extending moiety.
XX
CC PS Disclosure; SEQ ID NO 20; 164pp; English.
XX
CC The present invention relates to a novel modified therapeutic agent
CC comprising a half-life extending moiety and a therapeutic agent, where
CC the therapeutic agent is covalently attached to the half-life extending
CC moiety via a cysteine residue. The therapeutic agent comprises a relaxin
CC A-chain selected from SEQ ID NO: 54 (see BDE95417), SEQ ID NO: 55 (see
CC BDE95418), SEQ ID NO: 59 (see BDE95422) and SEQ ID NO: 60 (see BDE95423)
CC and a relaxin B-chain selected from SEQ ID NO: 16 (see BDE95379), SEQ ID
CC NO: 40 (see BDE95403), SEQ ID NO: 48-52 (see BDE95411-BDE95415), SEQ ID
CC NO: 56 (see BDE95419), SEQ ID NO: 58 (see BDE95421) and SEQ ID NO: 61
CC (see BDE95424). The invention further provides: (1) a pharmaceutical
CC composition comprising the modified therapeutic agent; (2) a method for
CC treating a disease or condition in a subject by administering the
CC pharmaceutical composition to the subject; and (3) a method and a
CC composition for extending the half-life of the therapeutic agent. The
CC modified therapeutic agent of the present invention can be used in the
CC pharmaceutical composition for preventing and treating cardiovascular
CC disorder, acute heart failure, fibrosis, autoimmune disorder,
CC inflammatory disease, metabolic disease, central nervous system (CNS)
CC disorder or pain, where the pain is neuropathic pain or inflammatory
CC pain. The present sequence represents a growth differentiation factor 11
CC (GDF 11) polypeptide which can be used as a therapeutic agent for
CC treating the above-mentioned diseases.
XX
SQ Sequence 109 AA;
Query Match 100.0%; Score 628; DB 23; Length 109;
Best Local Similarity 100.0%;
Matches 109; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 NLGLDCDEHSSESRCCRYPLTVDFEAFGWDWIIAPKRYKANYCSGQCEYMFMQKYPHTHL 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 NLGLDCDEHSSESRCCRYPLTVDFEAFGWDWIIAPKRYKANYCSGQCEYMFMQKYPHTHL 60
Qy 61 VQQANPRGSAGPCCTPTKMSPINMLYFNDKQQIIYGKIPGMVVDRCGCS 109
|||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 VQQANPRGSAGPCCTPTKMSPINMLYFNDKQQIIYGKIPGMVVDRCGCS 109
8. THIS ACTION IS MADE FINAL. 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.
9. 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
October 13, 2026
/CHANG-YU WANG/Primary Examiner, Art Unit 1675
