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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 April 13, 2026 has been entered.
RESPONSE TO AMENDMENT
Status of Application/Amendments/claims
3. Applicant’s amendment filed April 13, 2026 is acknowledged. Claims 11-13 are cancelled. Claims 1-9, 15, 17 and 19 are amended. Claims 1-10 and 14-20 are pending in this application and under examination in this office action.
4. Applicant’s arguments filed on April 13, 2026 have been fully considered but they are not deemed to be persuasive for the reasons set forth below.
Claim Rejections/Objections Withdrawn
5. The rejection of claims 1-10 and 14-20 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, lack of scope of enablement is withdrawn in response to Applicant’s amendment to the claims.
The rejection of claims 1-6 and 9-10 under 35 U.S.C. 102(a)(1) & (a)(2) as being anticipated by Bopardikar et al. (US2017/0029770; issued as US11072776) as evidenced by Fan et al. (Cell Transplantation, 2015; 24:471-485) and Dezawa et al. (US2011/0070647) is withdrawn in response to Applicant’s amendment to the claims.
Claim Rejections/Objections Maintained
In view of the amendment filed on April 13, 2026, the following rejections are maintained.
Claim Rejections - 35 USC § 103
6. Claims 1-10 and 14-20 are rejected under 35 U.S.C. 103 as being unpatentable over Bopardikar (US2017/0029770; issued as US11072776) in view of Dezawa (US2011/0070647), Vawda et al. (Seminars in Fetal & Neonatal Medicine, 2007; 12:259-272) and Ahn et al. (Neonatology, 2016; 109:377-383. DOI:10.1159/000444905), and evidentiary references: Fan (2015), Kirton (see abstract; Stroke, 2013; 44:3265-3271) and Camilo et al. (see abstract; Stroke, 2004; 35:1769-1775). The rejection is maintained for the reasons of record and the reasons set forth below.
Claims 1-10 and 14-20 as amended are drawn to a method for amelioration of a brain disorder associated with fetal growth retardation in a subject in need thereof, comprising administering to the subject a cell preparation comprising autologous or allogeneic cultured Muse cells obtained by
(i) isolating cells that are positive for SSEA-3 or
(ii) exposing cells to external stress treatment,
wherein the cultured Muse cells are isolated from mesenchymal tissue or cultured mesenchymal cells, the cultured Muse cells are in an amount of cells per body weight of approximately 1x105-1x108 cells/kg per subject, and sufficient to ameliorate the brain disorder of the subject, and wherein the cultured Muse cells have the properties of (i)-(v) recited in claim 1; and
wherein the brain disorder associated with fetal growth retardation is at least one selected from the group consisting of abnormal quality of movement and abnormal neurological development, and the fetal growth retardation results from at least one of chronic hypoxemia, circulatory insufficiency and malnutrition caused by placental and umbilical factors.
Briefly, Bopardikar teaches a method for treating cerebral palsy in a subject in need thereof, comprising administering to the subject a composition comprising fetal polymix of mesenchymal stem cells (MSCs) cultured under a hypoxic condition, wherein the fetal polymix-MSCs are SSEA-3+ and CD105+(see paragraphs [0015];[0058];[0104];[0138]; [0148]; [0191]; claims 15 and 20-24), which relates to the claimed method recited instant claims 1-10 and 14-20 because Cerebral palsy is a brain disorder associated with fetal growth retardation as evidenced by Fan et al. (p. 473, 1st col., Risk factors and pathophysiological mechanisms to p. 474, 2nd col.; p. 474-478; Fan et al. Cell Transplantation, 2015; 24:471-485). Patients with cerebral palsy also have abnormal quality of movement, abnormal neurological development, cognitive impairment, and behavior disorder as evidenced by Fan et al. (p. 473, 1st col., Risk factors and pathophysiological mechanisms to p. 474, 2nd col.; p. 474-478; Fan et al. Cell Transplantation, 2015; 24:471-485) and paragraph [0051] of the instant specification.
While Bopardikar does not teach the claimed Muse cells, an amount of cells per body weight of approximately 1x105-1x108 cells/kg per subject recited in claim 1, or 1x106-1x107 cells/kg per target subject recited in claim 8 or human neonate or infant recited in claims 7-8 and 14, Dezawa, Vawda and Ahn teach these limitations and provide motivation and an expectation of success in using Muse cells in an amount of cells per body weight of approximately 1x105-1x108 cells/kg per subject in the Bopardikar’s method for treating Cerebral palsy which is a brain disorder associated with fetal growth retardation because: i) Dezawa teaches a therapeutic method for treatment of a degenerative or traumatic neurologic disorders including damages to brain, damages to the CNS, ischemia, brain infarction, comprising administering to a patient in need thereof a therapeutically effective dose of a cell preparation comprising a cell preparation comprising cultured SSEA-3+/CD105+ Muse cells isolated from mesenchymal tissue of or cultured mesenchymal cells (see abstract; paragraphs [0142]-[0146]; [0132]-[0134]; [0016]-[0019]; [0019]-[0023], [0078]-[0079], [0206]-[0219]; p. 22, claims 1-24, in particular); wherein the cultured SSEA-3+/CD105+ Muse cells are isolated by the steps recited in claim 1 and have the properties (i)-(v) recited in claim 1 and are CD117(-) and CD146(-) as in claim 3; CD117(-), CD146(-), NG2(-), CD34(-), vWF(-) and CD271(-) as in claim 4 and CD117(-), CD146(-), NG2(-), CD34(-), vWF(-), Sox10(-), Snail(-), Slug(-), Tyrp-1 (-) and Dct(-) as in claim 5 (see paragraphs [0019]-[0023]; [0103]-[0109]; [0208], [0211], [0233];in particular); and capable of engrafting into the brain tissue as in claim 6 (see paragraph [0132]); and the effective dose is approximately 1x105 cells/individual (see paragraphs [0221], example 2). The damages to brain, ischemia, brain infarction disclosed in the Dezawa’s method causes cerebral palsy or epilepsy as evidenced by Kirton et al. (see abstract; Stroke, 2013; 44:3265-3271) and Camilo et al. (see abstract; Stroke, 2004; 35:1769-1775). ii) Vawda teaches treating perinatal brain injuries or damages by administering to a neonate patient in need thereof a therapeutically effective dose of SSEA-3+ pluripotent stem cells or CD105+ stem cells isolated from mesenchymal tissue of or cultured mesenchymal cells; and wherein the perinatal brain injuries or damages include hypoxia-ischemia due to cerebral palsy, developmental disabilities, infection, extended labor or repeated asphyxia after birth, pediatric traumatic brain injury (TBI), blunt head injury, hypoxic ischemic encephalopathy, epilepsy, seizure, metabolic diseases including lysosomal, peroxisomal mitochondrial and amino acid disorders to neurodegenerative diseases and muscle diseases, and white matter diseases including hypo or dysmyelination during development or demyelination in the postnatal (see abstract; p. 259-267, in particular). iii) Ahn teaches a therapeutic method for treating neonatal brain disorders including neonatal brain injury caused by intraventricular hemorrhage or hypoxic-ischemic encephalopathy injuries or neonatal stroke, comprising intraventricularly administering to a patient in need thereof a therapeutically effective dose of pluripotent stem cells from umbilical cord blood-derived mesenchymal stem cells (MSCs), wherein the effective dose is at least 5x105 cells per dose, 1x106 cells per dose or 5x106 cells/kg per dose or 1x107 cells/kg per dose as recited in claims 1, 7-8 and 14 (see abstract; p. 378-381, in particular).
A person of ordinary skill in the art would have recognized that selecting and applying the known Muse cells that are SSEA-3+/CD105+ and having the properties (i)-(v) recited in claim 1 and features recited in claims 3-6, the known amount of cells per body weight of approximately 1x105-1x108 cells/kg per subject, the known methods of treating brain injuries or damages or disorders or perinatal brain injuries or damages associated fetal growth retardation and the known technique disclosed by Dezawa, Vawda and Ahn to the Bopardikar’s method would have yielded the predictable result of ameliorating a brain disorder or perinatal brain damage associated with fetal growth retardation in a human neonate subject in need thereof, and resulted in an improved method.
Using the known Muse cells that are SSEA-3+/CD105+ and having the properties (i)-(v) recited in claim 1 and features recited in claims 3-6, the know amount of cells per body weight of approximately 1x105-1x108 cells/kg per subject, the known methods of treating brain injuries or damages or disorders or perinatal brain injuries or damages associated fetal growth retardation in the Bopardikar’s method would ameliorate brain injuries or damages or disorders including cerebral palsy or perinatal brain damage associated with fetal growth retardation in a human neonate subject in need thereof, and expand application of the Bopardikar’s method, and would increase patient’s satisfaction with the treatment of brain injuries or damages or disorders including cerebral palsy or perinatal brain damage associated fetal growth retardation in a perinatal, neonate or infant in need thereof using cultured Muse cell therapy because SSEA-3+/CD105+-Muse cells having the properties recited (i)-(v) of claim 1 and claims 2-6 have been shown to be effective to treat brain damage caused by ischemia or brain infarction or cerebral palsy or perinatal brain damage associated with fetal growth retardation or fetal growth restriction, thereby improves intellectual disability or mental development delay, learning disability or memory learning and visual cognitive memory due to perinatal brain damage.
Thus, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to select and apply the known cultured Muse cells that are SSEA-3+/CD105+ and have the properties (i)-(v) recited in claim 1 and features recited in claims 2-6, the known amount of cells per body weight of approximately 1x105-1x108 cells/kg per subject, the known methods of treating brain injuries or damages or disorders or perinatal brain injuries or damages associated fetal growth retardation and the known technique disclosed by Dezawa, Vawda and Ahn to the Bopardikar’s method, and yield the predictable result of ameliorating a brain disorder or perinatal brain damage associated with fetal growth retardation in a human including human neonate or infant in need thereof for improving intellectual disability or mental development delay, learning disability or memory learning and visual cognitive memory or treating cerebral palsy, developmental disabilities, infection, extended labor or repeated asphyxia after birth, pediatric traumatic brain injury (TBI), blunt head injury, hypoxic ischemic encephalopathy, epilepsy, seizure. See KSR International Co. V. Teleflex Inc. 82 USPQ2d 1385 (2007) In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980); In re Crockett, 279 F.2d 274, 126 USPQ 186 (CCPA 1960); Ex parte Quadranti, 25 USPQ2d 1071 (Bd. Pat. App. & Inter. 1992), Sinclair & Carroll Co. v. Interchemical Corp., 325 U.S. 327, 65 USPQ 297 (1945) and In re Kahn, 441 F.3d 977, 986, 78 USPQ2d 1329, 1335 (Fed. Cir. 2006) and also see MPEP § 2143. 01-I, MPEP § 2144.06 and MPEP §2144.07.
Response to Arguments
On p.8-9 of the response, Applicant argues that: i) Bopardikar does not teach Muse cells; ii) none of Fan, Kirton and Camilo cure the deficiencies of Bopardikar because none of Fan, Kirton Camilo teach Muse cells; ii) relates to mechanisms of cerebral palsy but does not provide guidance to a specific treatment using a cell preparation comprising a therapeutically effective amount of specific cells; iv) Kirton and Camilo only provide general information related to stroke and seizures, not a treatment of brain disorder associated with fetal growth retardation, which is different from cerebral palsy, cerebral hemorrhage and cerebral infarction; v) Vawda and Ahn relate to brain injuries/disorders but do not address brain disorder associated with fetal growth retardation resulting from at least one of chronic hypoxemia, circulatory insufficiency and malnutrition caused by placental and umbilical factors; vi) Sanberg teaches dosages but is related to neurodegenerative diseases such as stroke, which is a different disease and is not applicable to infants.
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 §2141, MPEP2141-I, rationales identified by the Court in KSR (KSR International Co. v. Teleflex Inc. (KSR), 550 U.S. 398, 82 USPQ2d 1385 (2007)), MPEP2141-II, the basic factual inquires of Graham v. John Deere Co.(Graham v. John Deere Co., 383 U.S. 1, 148 USPQ 459 (1966)),and MPEP §2141.01-2147.03, the cited references do render the claimed invention obvious because:
i. Applicant cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). Dezawa is cited to support the limitation “Muse cells” and the use of muse cells for treating damages to brain, damages to the CNS, ischemia, brain infarction, which cause cerebral palsy. Fan, Kirton Camilo are cited to support that i) Cerebral palsy disclosed in the Bopardikar’s method is a brain disorder associated with fetal growth retardation and patients with cerebral palsy also have abnormal quality of movement, abnormal neurological development, cognitive impairment, and behavior disorder (see p. 473, 1st col., Risk factors and pathophysiological mechanisms to p. 474, 2nd col.; p. 474-478 in Fan, and paragraph [0051] of the instant specification); ii) The damages to brain, ischemia, brain infarction disclosed in the Dezawa’s method causes cerebral palsy or epilepsy (see abstract in Kirton and see abstract in Camilo).
ii. In this case, Bopardikar teaches a method for treating cerebral palsy in a subject in need thereof, comprising administering to the subject a composition comprising fetal polymix of mesenchymal stem cells (MSCs) cultured under a hypoxic condition, wherein the fetal polymix-MSCs are SSEA-3+ and CD105+(see paragraphs [0015];[0058];[0104];[0138]; [0148]; [0191]; claims 15 and 20-24). Cerebral palsy is a brain disorder associated with fetal growth retardation as evidenced by Fan et al. (p. 473, 1st col., Risk factors and pathophysiological mechanisms to p. 474, 2nd col.; p. 474-478). Patients with cerebral palsy also have abnormal quality of movement, abnormal neurological development, cognitive impairment, and behavior disorder as evidenced by Fan et al. (p. 473, 1st col., Risk factors and pathophysiological mechanisms to p. 474, 2nd col.; p. 474-478) and paragraph [0051] of the instant specification.
While Bopardikar does not teach the claimed Muse cells, Dezawa teaches a therapeutic method of using cultured SSEA-3+/CD105+ Muse cells for treatment of a degenerative or traumatic neurologic disorders including damages to brain, damages to the CNS, ischemia, brain infarction, wherein the cultured SSEA-3+/CD105+ Muse cells are isolated from mesenchymal tissue of or cultured mesenchymal cells (see abstract; paragraphs [0142]-[0146]; [0132]-[0134]; [0016]-[0019]; [0019]-[0023], [0078]-[0079], [0206]-[0219]; p. 22, claims 1-24, in particular) by the steps recited in claim 1 and have the properties (i)-(v) recited in claim 1 and are CD117(-) and CD146(-) as in claim 3; CD117(-), CD146(-), NG2(-), CD34(-), vWF(-) and CD271(-) as in claim 4 and CD117(-), CD146(-), NG2(-), CD34(-), vWF(-), Sox10(-), Snail(-), Slug(-), Tyrp-1 (-) and Dct(-) as in claim 5 (see paragraphs [0019]-[0023]; [0103]-[0109]; [0208], [0211], [0233];in particular); and capable of engrafting into the brain tissue as in claim 6 (see paragraph [0132]); and the effective dose is approximately 1x105 cells/individual (see paragraphs [0221], example 2). The damages to brain, ischemia, brain infarction disclosed in the Dezawa’s method causes cerebral palsy or epilepsy as evidenced by Kirton et al. (see abstract; Stroke, 2013; 44:3265-3271) and Camilo et al. (see abstract; Stroke, 2004; 35:1769-1775).
While Bopardikar does not teach an amount of cells per body weight of approximately 1x105-1x108 cells/kg per subject recited in claim 1 or human neonate or infant recited in claims 7-8 and 14, Vawda teaches treating perinatal brain injuries or damages by administering to a neonate patient in need thereof a therapeutically effective dose of SSEA-3+ pluripotent stem cells or CD105+ stem cells isolated from mesenchymal tissue of or cultured mesenchymal cells; and wherein the perinatal brain injuries or damages include hypoxia-ischemia due to cerebral palsy, developmental disabilities, infection, extended labor or repeated asphyxia after birth, pediatric traumatic brain injury (TBI), blunt head injury, hypoxic ischemic encephalopathy, epilepsy, seizure, metabolic diseases including lysosomal, peroxisomal mitochondrial and amino acid disorders to neurodegenerative diseases and muscle diseases, and white matter diseases including hypo or dysmyelination during development or demyelination in the postnatal (see abstract; p. 259-267, in particular) and Ahn teaches a therapeutic method for treating neonatal brain disorders including neonatal brain injury caused by intraventricular hemorrhage or hypoxic-ischemic encephalopathy injuries or neonatal stroke, comprising intraventricularly administering to a patient in need thereof a therapeutically effective dose of pluripotent stem cells from umbilical cord blood-derived mesenchymal stem cells (MSCs), wherein the effective dose is at least 5x105 cells per dose, 1x106 cells per dose or 5x106 cells/kg per dose or 1x107 cells/kg per dose as in claims 7-8 and 14 (see abstract; p. 378-381, in particular).
A person of ordinary skill in the art would have recognized that selecting and applying the known SSEA-3+/CD105+ Muse cells having the properties (i)-(v) recited in claim 1 and features recited in claims 3-6, the known amount of cells per body weight of approximately 1x105-1x108 cells/kg per subject, the known methods of treating brain injuries or damages or disorders or perinatal brain injuries or damages associated fetal growth retardation and the known technique disclosed by Dezawa, Vawda and Ahn to the Bopardikar’s method would have yielded the predictable result of ameliorating a brain disorder or perinatal brain damage associated with fetal growth retardation in a human neonate subject in need thereof, and resulted in an improved method.
Using the known SSEA-3+/CD105+ Muse cells having the properties (i)-(v) recited in claim 1 and features recited in claims 3-6, the know amount of cells per body weight of approximately 1x105-1x108 cells/kg per subject, the known methods of treating brain injuries or damages or disorders or perinatal brain injuries or damages associated fetal growth retardation in the Bopardikar’s method would ameliorate brain injuries or damages or disorders including cerebral palsy or perinatal brain damage associated with fetal growth retardation in a human neonate subject in need thereof, and expand application of the Bopardikar’s method, and would increase patient’s satisfaction with the treatment of brain injuries or damages or disorders including cerebral palsy or perinatal brain damage associated fetal growth retardation in a perinatal, neonate or infant in need thereof using cultured Muse cell therapy because SSEA-3+/CD105+-Muse cells having the properties recited (i)-(v) of claim 1 and claims 2-6 have been shown to be effective to treat brain damage caused by ischemia or brain infarction or cerebral palsy or perinatal brain damage associated with fetal growth retardation or fetal growth restriction, thereby improves intellectual disability or mental development delay, learning disability or memory learning and visual cognitive memory due to perinatal brain damage.
Thus, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to select and apply the known cultured SSEA-3+/CD105+ Muse cells having the properties (i)-(v) recited in claim 1 and features recited in claims 2-6, the known amount of cells per body weight of approximately 1x105-1x108 cells/kg per subject, the known methods of treating brain injuries or damages or disorders or perinatal brain injuries or damages associated fetal growth retardation and the known technique disclosed by Dezawa, Vawda and Ahn to the Bopardikar’s method, and yield the predictable result of ameliorating a brain disorder or perinatal brain damage associated with fetal growth retardation in a human including human neonate or infant in need thereof for improving intellectual disability or mental development delay, learning disability or memory learning and visual cognitive memory or treating cerebral palsy, developmental disabilities, infection, extended labor or repeated asphyxia after birth, pediatric traumatic brain injury (TBI), blunt head injury, hypoxic ischemic encephalopathy, epilepsy, seizure. See KSR International Co. V. Teleflex Inc. 82 USPQ2d 1385 (2007) In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980); In re Crockett, 279 F.2d 274, 126 USPQ 186 (CCPA 1960); Ex parte Quadranti, 25 USPQ2d 1071 (Bd. Pat. App. & Inter. 1992), Sinclair & Carroll Co. v. Interchemical Corp., 325 U.S. 327, 65 USPQ 297 (1945) and In re Kahn, 441 F.3d 977, 986, 78 USPQ2d 1329, 1335 (Fed. Cir. 2006) and also see MPEP § 2143. 01-I, MPEP § 2144.06 and MPEP §2144.07.
Accordingly, the rejection of claims 1-10 and 14-200 under 35 U.S.C. 103 as being unpatentable over Bopardikar in view of Dezawa, Vawda and Ahn, and evidentiary references: Fan, Kirton and Camilo is maintained.
Claim Rejections - 35 USC § 103
7. Claims 1 and 8 are rejected under 35 U.S.C. 103 as being unpatentable over Bopardikar (US2017/0029770; issued as US11072776) in view of Dezawa (US2011/0070647), Vawda (2007) and Ahn (2016) and evidentiary references: Fan (2015), Kirton (2013) and Camilo (2004) as applied to claims 1-10 and 14-20 above, and further in view of Sanberg (US2013/0045189). The rejection is maintained for the reasons of record and the reasons set forth below.
Response to Arguments
On p.10 of the response, Applicant argues that: i) for the reasons set forth above, claim 1 is not obvious over Bopardikar in view of Dezawa, Vawda and Ahn and evidentiary references: Fan, Kirton and Camilo; ii) Sanberg fails to teach Muse cells or mesenchymal-derived cells.
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 §2141, MPEP2141-I, rationales identified by the Court in KSR (KSR International Co. v. Teleflex Inc. (KSR), 550 U.S. 398, 82 USPQ2d 1385 (2007)), MPEP2141-II, the basic factual inquires of Graham v. John Deere Co.(Graham v. John Deere Co., 383 U.S. 1, 148 USPQ 459 (1966)),and MPEP §2141.01-2147.03, the cited references do render the claimed invention obvious because:
i. For the reasons set forth above, Bopardikar, Dezawa, Vawda and Ahn and evidentiary references: Fan, Kirton and Camilo do teach the limitations recited in claims 1-10 and 14-10 and render the method recited in claims 1-10 and 14-20 obvious.
ii. Applicant cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
While Bopardikar, Dezawa, Vawda and Ahn do not teach a cell dose range that is exactly identical to the claimed range of 1x105-1x108 cells/kg/subject or 1x105-1x108cells/kg per target individual as in claims 1 and 8, Dezawa teaches a dose range of approximately 1x105 cells/individual (see paragraphs [0221], example 2), Ahn teaches at least 5x105 cells per dose or 1x106 cells per dose, or 5x106 cells/kg per dose or 1x107 cells/kg (see abstract; p. 380-381, in particular) for treating brain damage, ischemia, perinatal brain damage including cerebral palsy, developmental disabilities, infection, extended labor or repeated asphyxia after birth, and Sanberg teaches the use of human neural stem cells in an amount of the range of about 1x104 to about 1x109 cells, about 1x105 to about 1x107 or about 2x105 to about 8x106 for treating neurodegenerative diseases including traumatic brain injury, ischemia and stroke, which are brain damage causing cerebral palsy (see abstract; paragraphs [0046]-[0047], [0037]; p. 8-9, claims 1-23).
A person of ordinary skill in the art would have recognized that selecting and applying the known dose ranges and technique disclosed by Dezawa and Sanberg to the method of Bopardikar, Dezawa, Vawda and Ahn would have yielded the predictable result of ameliorating and/treating a brain disorder or perinatal brain damage associated with fetal growth retardation in a subject including a human neonate or infant in need thereof for improving intellectual disability or mental development delay, learning disability or memory learning and visual cognitive memory and resulted in an improved method because different dose ranges including 1x105 cells/individual, at least 5x105 cells per dose, 1x106 cells per dose, or 5x106 cells/kg per dose or 1x107 cells/kg or about 1x104 to about 1x109 cells have been shown to successfully treat brain injury or damage including cerebral palsy, developmental disabilities, infection, extended labor or repeated asphyxia after birth or pediatric traumatic brain injury (TBI), hypoxic ischemic encephalopathy which causes cerebral palsy.
Further, routine optimization of Dezawa’s dose ranges, Ahn’s dose ranges, and Sanberg’s dose ranges would have led to the claimed range of 1x105-1x108 cells/individual or 1x105-1x108 cells/kg per target individual because Sanberg teaches the use of different dose ranges including 1x105 cells/individual, at least 5x105 cells per dose, 1x106 cells per dose, or 5x106 cells/kg per dose or 1x107 cells/kg or about 1x104 to about 1x109 cells for treating brain injury or damage including cerebral palsy, developmental disabilities, extended labor or repeated asphyxia after birth or pediatric traumatic brain injury (TBI), hypoxic ischemic encephalopathy. The person of ordinary skill in the art would have found it obvious to optimize within the range taught by Sanberg because Sanberg teaches that this entire range treat brain damages and also teaches how to optimize the cell dose ranges. It is obvious and not inventive to discover the optimum or workable ranges by routine experimentation because the results are expected. Note that “[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation.” In re Aller, 220 F.2d 454, 456, 105USPQ 233, 235 (CCPA 1955)” See MPEP 2144.05-II.
Thus, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to select and apply the known dose ranges and technique disclosed by Sanberg, Dezawa and Ahn to the method of the method of Bopardikar, Dezawa, Vawda and Ahn to ameliorate or treat brain injuries or damages or disorders including cerebral palsy, developmental disabilities, extended labor or repeated asphyxia after birth, or perinatal brain damage associated fetal growth retardation in a subject including a human neonate or infant in need thereof and yield the predictable result of ameliorating or treating brain injuries or damages or disorders including cerebral palsy, developmental disabilities, extended labor or repeated asphyxia after birth or perinatal brain damage associated fetal growth retardation in a subject including a human neonate or infant in need thereof and improving intellectual disability or mental development delay, learning disability or memory learning and visual cognitive memory.
Accordingly, the rejection of claims 1 and 8 under 35 U.S.C. 103 as being unpatentable over Bopardikar in view of Dezawa, Vawda, Ahn as applied to claims 1-10 and 14-20, and further in view of Sanberg, and evidentiary references: Fan, Kirton and Camilo is maintained.
Conclusion
8. NO CLAIM IS ALLOWED.
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.
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Chang-Yu Wang
September 26, 2026
/CHANG-YU WANG/Primary Examiner, Art Unit 1675
