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 .
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 allowance or after an Office action under Ex Parte Quayle, 25 USPQ 74, 453 O.G. 213 (Comm'r Pat. 1935). 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, prosecution in this application has been reopened pursuant to 37 CFR 1.114. Applicant's submission filed on 1/23/2026 has been entered.
Claim Status
A Corrected Notice of Allowability was mailed on 6/11/2025. In the accompanying interview summary the examiner indicated an amendment to claim 13; however it is not clear this amendment was formally entered.
For clarity of record, the claims pending for examination at this time are: Claims 1, 3, 5, 13-14, 20-26, 28-35, 37, 42-43, 49-52, 58-59 and 76-82, as amended via the Examiner Amendment of 6/6/2025 (remaining claims being cancelled).
And claim 13 is as follows:Claim 13. The method of claim 1, wherein the fibroblasts induce immune modulation in the subject, and wherein the immune modulation comprises enhancing production of a cytokine associated with neuroprotection in the subject.
Upon reconsideration, allowability of the claims is withdrawn.
Claim Objection
Claim 82 lists several agents multiple times. See, for example, PDGF, PD-ECGF, TGF-beta. The claim should be carefully reviewed to remove duplicates.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 26, 76 and 82 are 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 applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Regarding claim 26, the phrase "such as" renders the claim indefinite because it is unclear whether the limitations following the phrase are part of the claimed invention. See MPEP § 2173.05(d). See line 5, “phosphodiesterase inhibitors such as vinpocetine, milrinone, …”
Furthermore, claim 26 recites trademark EXOSURF. Where a trademark or trade name is used in a claim as a limitation to identify or describe a particular material or product, the claim does not comply with the requirements of 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph. See Ex parte Simpson, 218 USPQ 1020 (Bd. App. 1982). The claim scope is uncertain since the trademark or trade name cannot be used properly to identify any particular material or product. A trademark or trade name is used to identify a source of goods, and not the goods themselves. Thus, a trademark or trade name does not identify or describe the goods associated with the trademark or trade name. In the present case, the trademark/trade name is used to identify/describe a synthetic surfactant and, accordingly, the identification/description is indefinite.
Regarding claim 76, it is unclear what amount of metformin will be considered therapeutically effective. The metformin is used for culturing the fibroblasts, it is not administered as an active therapeutic agent. It is recognized that this language was proposed by the previous examiner to place the claim into condition for allowance. However, upon reconsideration at the present time, the current language is considered to render the claim indefinite.
Regarding claim 82, the claim purports it lists angiogenic genes, however the claim does not list any genes, rather the claim lists proteins, cytokines, interleukins, ligands and some general cellular activities (e.g. bFGF inducing activity). This renders the claim indefinite. Furthermore, many of the molecules listed are in fact anti-angiogenic (e.g. endostatin, IFN-gamma, heart derived inhibitor of vascular cell proliferation). Careful review and editing of the claim to limit to molecules known to be angiogenic is required. Recitation of any molecule that is non-angiogenic will render the claim indefinite.
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.
Claims 1, 3, 5, 13, 14, 20-24, 30-32, 49, 50, 58, 59 and 77-81 are rejected under 35 U.S.C. 103 as being unpatentable over Chen et al (J Neuropathol Exp Neurol, 2012), in view of Lim et al (Stem Cell Res & Ther, 2011).
Chen et al disclose treatment of intracerebral hemorrhage (ICH) by administration of 3T3 fibroblast cells (See Chen et al).
Specifically, Chen et al create 3T3 fibroblasts that express eGFP or eGFP and BDNF (3T3-EGFP and 3T3-EGFP-BDNF, respectively) (See Chen et al, Pg 1124, “DNA Transfection and Selection”). Chen et al induce ICH in mice subjects (See Chen et al, Pg 1124 “Animal Preparation” and Pg 1125 “Mouse ICH Model and Cell Implantation”). Chen et al introduce either control PBS, 3T3-EGFP, or 3T3-EGFP-BDNF cells (1 x 106 cells/5 µL PBS) via direct injection into the striatum through a burr hole in the cranium (See Chen et al, Pg 1125 “Mouse ICH Model…”).
Chen et al report that the 3T3-EGFP-BDNF treatment group had less brain tissue loss than the other groups (See Chen et al, Pg. 1126 “The 3T3-EGFP-BDNF Treatment Group…”). Chen et al report that both cell types were found around the SVZ and hematoma and both cell types induced migration of DCX-positive neuroblasts to the hematoma from the SVZ (See Chen et al, Pg. 1126, “Cell Transplantation…”). Chen et al report both cell treatment groups showed significant functional improvement over PBS control group (See Chen et al, Pg 1127, “Cell Treatment Promoted …”).
Regarding claim 1: As set forth above, Chen et al administer two types of fibroblasts to ICH subjects and report improvements (less brain tissue loss, recruitment of neuroblasts, and functional improvements) in both cell-treatment groups. Thus Chen et al teaches treating a stroke in a subject in need thereof, comprising providing to the subject… a therapeutically effective amount of a composition comprising fibroblasts.
The method of Chen et al differs from the instant claim in that Chen et al appears to administer the fibroblasts by direct intra-striatal injection, not via intraventricular, intrathecal, or intravenous delivery.
However, at the time the invention was made, one having ordinary skill in the art will recognize that creation of burrs in the skull for direct intra-striatal injection is an invasive procedure. Less invasive procedures would be more desirable for human treatment.
Lim et al test intrathecal and intravenous delivery of hUCB-MSCs as alternatives to intra-striatal injection in stroke models (See Lim et al, Pg 5, “Cell Transplantation”). Lim et al select intrathecal and intravenous delivery as alternatives due to their less invasive nature (See Lim et al, Pg 2, “Introduction”, col. 1-2). Lim et al deliver hUCB-MSCs via intrathecal and intravenous routes following transient MCAO (See Lim et al, Pg 3, “Cell transplantation”). Lim et al report that intrathecally and intravenously delivered cells did locate to the peri-infarct region of the ischemic hemisphere, with intrathecal administration having greater cell numbers (See Lim et al, Pg 4, “Homing of transplanted…”). Lim et al conclude that both intrathecal and intravenous delivery of cells was successful to achieve delivery, engraftment and therapeutic effect of the cells in the brain infarct zone. Different concentrations of cells were required for therapeutic results in each delivery modality (See Lim et al, Pg 8-11).
In an effort to deliver cells via a less invasive method for treatment of human subjects, one would have been motivated to modify the method of Chen eta l to involve intrathecal delivery of the fibroblasts cells for therapeutic purposes instead of direct intra-striatal delivery, particularly when administration is intended for human subjects. One would have had a reasonable expectation of success based on the teachings of Lim et al that cells delivered intrathecally can home to the infarct zone in an infarcted brain. This conclusion of obviousness is based on a teaching, suggestion or motivation in the prior art.
Regarding claim 3: Following the discussion above, the ICH model is a hemorrhagic stroke.
Regarding claim 5: Following the discussion of claim 1 above, fibroblasts are inherently plastic adherent. Chen et al teach 3T3 cells grown on cell culture dishes (See Chen et al, Pg 1124, “Cell Culture”).
Regarding claim 20: Following the discussion of claim 1 above, the fibroblasts are delivered to the subjects following the stroke.
Regarding claims 13, 14, 21-24, 30-32, 77-80: Following the discussion of claims 1 and/or 20 above, it is submitted the fibroblasts administered by Chen et al will inherently achieve each of the effects of the instant claims.
Regarding claim 81: Following the discussion of claim 1 above, at least the 3T3-EGFP-BDNF fibroblasts are transfected with one or more angiogenic genes (BDNF) prior to providing the fibroblasts to the subject.
Regarding claims 49, 50, 58 and 59: Following the discussion of claim 1 above, Chen et al does not teach further administering a mesenchymal stem cell to the ICH subjects. However, Lim et al teaches that MSCs also have therapeutic effect in treating stroke (cerebral ischemia) (See teachings above). Mesenchymal stem cells read on regenerative cells. MSCs inherently express all of CD90, CD105 and CD73.
Because both Chen et al and Lim et al intend to achieve the same effect: protecting brain tissue from further loss and restoration of physiological functional following stroke, it would have been prima facie obvious to apply both therapies to a single patient, for the predictable result of enhancing the protection of brain tissue from further loss and restoration of physiological functioning following a stroke. For the reasons set forth above, it would have been prima facie obvious to have administered both cell therapeutics via intrathecal route.
The combined effect of the cell-based therapies would have been expected to be greater than the effect of either treatment individually. The reason to combine the different therapies would be to improve overall therapeutic effect following a stroke in a subject. See MPEP 2143(I)(A).
Claims 1, 3, 5, 13, 14, 20-26, 28-35, 37, 49, 50, 58, 59 and 77-80 are rejected under 35 U.S.C. 103 as being unpatentable over Chen et al (J Neuropathol Exp Neurol, 2012), in view of Lim et al (Stem Cell Res & Ther, 2011), and further in view of Ichim et al (US 2018/0071342).
The teachings of Chen et al and Lim et al are set forth above. Briefly, Chen et al and Lim et al render obvious claim 1, specifically intrathecal administration of fibroblasts to a subject following a stroke for the purpose of providing treatment for the stroke.
Ichim et al is also directed to inducing and accelerating neurological recovery following stroke. Ichim et al achieves this recovery through administration of amniotic fluid derived stem cells (See Ichim et al, abstract & ¶0005). The amniotic fluid derived stem cells are mesenchymal stem cells (See Ichim et al, ¶0022).
Regarding claims 49, 50, 58 and 59: Following the discussion of claim 1 above, Chen et al does not teach further administering a mesenchymal stem cell to the ICH subjects. However, Ichim et al teaches that amniotic fluid derived stem cells also have therapeutic effect in treating stroke. Mesenchymal stem cells read on regenerative cells. MSCs inherently express all of CD90, CD105 and CD73.
Because both Chen et al and Ichim et al intend to achieve the same effect: protecting brain tissue from further loss and restoration of physiological functional following stroke, it would have been prima facie obvious to apply both therapies to a single patient, for the predictable result of enhancing the protection of brain tissue from further loss and restoration of physiological functioning following a stroke.
The combined effect of the cell-based therapies would have been expected to be greater than the effect of either treatment individually. The reason to combine the different therapies would be to improve overall therapeutic effect following a stroke in a subject. See MPEP 2143(I)(A).
Regarding claims 25, 26, 28, 29, 33-35 and 37: Following the discussion of claims 49, 50, 58 and 59 above, Ichim et al teaches the amniotic fluid derived cells can further be engineered for enhanced [in] vivo persistence through transfection of a therapeutic [gene] sequence encoding an anti-apoptotic [peptide] (See Ichim et al, ¶0039). Amongst the anti-apoptotic peptides disclosed are: IL-10 (See Ichim et al, ¶0052). IL-10 reads on a TNF-a inhibitor. IL-10 is a spleen derived factor, which is defined by the instant claims as an agent capable of inhibiting responsiveness to TNF-a. (relevant to claims 25, 26, 28, 29 and 33).
TGF-beta (See Ichim et al, ¶0054). TGF-beta reads on a TNF-a inhibitor, as well as an apoptotic agent (relevant to claims 25, 26, 33 and 34)
EGF (See Ichim et al, ¶0068). EGF is an anti-apoptotic agent (relevant to claim 33 and 34).
Inhibitors of caspase 3 (CASP3) and/or caspase 9 (CASP9) (See Ichim et al, ¶0073-0074). (relevant to claims 33-35).
Delivery of the engineered amniotic fluid derived stem cells as part of the method of Chen et al would thereby necessarily delivery the therapeutic peptides discussed above.
Regarding claim 37: Following the discussion of claims 49, 50, 58 and 59 above, Ichim et al teaches the amniotic fluid derived cells can further be engineered to possess enhanced angiogenic activity through transfection with an angiogenic polypeptide (See Ichim et al, ¶0083). Amongst the disclosed angiogenic polypeptides are:
VEGF, leukemia inhibitory factor (LIF), angiopoietin and NGF (See Ichim et al, ¶0084). Delivery of the engineered amniotic fluid derived stem cells as part of the method of Chen et al would thereby necessarily delivery the therapeutic peptides.
Claims 1, 3, 5, 13, 14, 20-24, 30-32, 42, 43, 49-52, and 77-80 are rejected under 35 U.S.C. 103 as being unpatentable over Chen et al (J Neuropathol Exp Neurol, 2012), in view of Lim et al (Stem Cell Res & Ther, 2011), and further in view of Li et al (US 2006/0263332).
The teachings of Chen et al and Lim et al are set forth above. Briefly, Chen et al and Lim et al render obvious claim 1, specifically intrathecal administration of fibroblasts to a subject following a stroke for the purpose of providing treatment for the stroke.
Li et al is also focused on repairing brain damage, including brain damage from cerebral ischemia (strokes), comprising administering peripheral blood hematopoietic stem cells in combination with G-CSF (See Li et al, ¶0007-0008 and claim 1).
Regarding claims 42 and 43: Administration of G-CSF will inherently mobilize endothelial progenitor cells in the subject.
Because both Chen et al and Li et al are focused on improving therapeutic outcome following stroke, it would have been prima facie obvious to apply both therapies (intrathecal administration of fibroblasts, and administration of G-CSF) to a single patient, for the predictable result of enhancing recovery and functional outcome following a stroke.
The combined effect of the two therapies would have been expected to be greater than the effect of either treatment individually. The reason to combine the different therapies would be to improve overall therapeutic effect following a stroke in a subject. See MPEP 2143(I)(A).
Regarding claims 49-52: Li et al teach administration of peripheral blood hematopoietic stem cells. Peripheral blood hematopoietic stem cells (PBSCs) are CD34+ (See Li et al, ¶0059). As above, because both Chen et al and Li et al are focused on improving therapeutic outcome following stroke, it would have been prima facie obvious to apply both therapies (intrathecal administration of fibroblasts, and administration of PBSCs) to a single patient, for the predictable result of enhancing recovery and functional outcome following a stroke.
The combined effect of the two therapies would have been expected to be greater than the effect of either treatment individually. The reason to combine the different therapies would be to improve overall therapeutic effect following a stroke in a subject. See MPEP 2143(I)(A).
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.
Claims 1, 3, 5, 13, 14, 20-26, 28-35, 37, 42, 43, 49-52, 58, 59, and 76-82 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-30 of copending Application No. 19/331852 (reference application), in view of Ichim et al (US 2018/0071342).
Although the claims at issue are not identical, they are not patentably distinct from each other because the copending claims are drawn to the same method as the instant claim, but require administration of conditioned media from the fibroblasts, as opposed to the fibroblasts, per se. However, at the time the application was filed it was generally recognized that paracrine effects of cells are achievable by delivering the cells per se, or by delivering conditioned media thereof (see Ichim et al, abstract).
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 1, 3, 5, 13, 20-24, 30-32, and 77-80 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims of U.S. Patent Application No. 17/309178 (reference application).
Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the reference application anticipates the instant claims.
Regarding claims 1 and 20: The reference application claims are drawn to methods of inducing regeneration and/or healing response in a brain of an individual following stroke (see reference application claims 1, 5, 27 and 28). Reference application claim 19 states the fibroblasts are administered intrathecally. This anticipates claims 1 and 20.
Regarding claim 3: Reference application claim 5 states the stroke can be an ischemic or hemorrhagic stroke.
Regarding claim 5: Fibroblasts are inherently plastic adherent.
Regarding claims 13, 14, 21-24, 30-32, 77-80: Following the discussion of claim 1 above, it is submitted the fibroblasts will inherently achieve each of the effects of the instant claims.
This is a provisional rejection because the copending claims have not yet been patented.
Claims 1, 3, 5, 13, 14, 20-26, 28-35, 37, 49, 50, 58, 59 and 77-80 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims of U.S. Patent Application No. 17/309178 (reference application), in view of Ichim et al (US 2018/0071342).
Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the reference application, in view of Ichim et al renders obvious the instant claims.
The teachings of Ichim et al are set forth above. Briefly, Ichim et al is also directed to inducing and accelerating neurological recovery following stroke. Ichim et al achieves this recovery through administration of amniotic fluid derived stem cells (See Ichim et al, abstract & ¶0005). The amniotic fluid derived stem cells are mesenchymal stem cells (See Ichim et al, ¶0022).
Regarding claims 49, 50, 58 and 59: Following the discussion of claim 1 above, the reference application does not teach further administering a mesenchymal stem cell to the stroke subjects. However, reference application claim 21 does teach providing additional therapies for the stroke.
Because both the reference application claims and Ichim et al intend to achieve the same effect: protecting brain tissue from further loss and restoration of physiological functional following stroke, it would have been prima facie obvious to apply both therapies to a single patient, for the predictable result of enhancing the protection of brain tissue from further loss and restoration of physiological functioning following a stroke.
The combined effect of the cell-based therapies would have been expected to be greater than the effect of either treatment individually. The reason to combine the different therapies would be to improve overall therapeutic effect following a stroke in a subject. See MPEP 2143(I)(A).
Regarding claims 25, 26, 28, 29, 33-35 and 37: Following the discussion of claims 49, 50, 58 and 59 above, Ichim et al teaches the amniotic fluid derived cells can further be engineered for enhanced [in] vivo persistence through transfection of a therapeutic [gene] sequence encoding an anti-apoptotic [peptide] (See Ichim et al, ¶0039). Amongst the anti-apoptotic peptides disclosed are: IL-10 (See Ichim et al, ¶0052). IL-10 reads on a TNF-a inhibitor. IL-10 is a spleen derived factor, which is defined by the instant claims as an agent capable of inhibiting responsiveness to TNF-a. (relevant to claims 25, 26, 28, 29 and 33).
TGF-beta (See Ichim et al, ¶0054). TGF-beta reads on a TNF-a inhibitor, as well as an apoptotic agent (relevant to claims 25, 26, 33 and 34)
EGF (See Ichim et al, ¶0068). EGF is an anti-apoptotic agent (relevant to claim 33 and 34).
Inhibitors of caspase 3 (CASP3) and/or caspase 9 (CASP9) (See Ichim et al, ¶0073-0074). (relevant to claims 33-35).
Delivery of the engineered amniotic fluid derived stem cells as part of the method of the reference application would thereby necessarily delivery the therapeutic peptides discussed above.
Regarding claim 37: Following the discussion of claims 49, 50, 58 and 59 above, Ichim et al teaches the amniotic fluid derived cells can further be engineered to possess enhanced angiogenic activity through transfection with an angiogenic polypeptide (See Ichim et al, ¶0083). Amongst the disclosed angiogenic polypeptides are:
VEGF, leukemia inhibitory factor (LIF), angiopoietin and NGF (See Ichim et al, ¶0084). Delivery of the engineered amniotic fluid derived stem cells as part of the method of the reference application would thereby necessarily delivery the therapeutic peptides.
This is a provisional rejection because the copending claims have not yet been patented.
Claims 1, 3, 5, 13, 14, 20-24, 30-32, 42, 43, 49-52, 58, 59 and 77-80 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims of U.S. Patent Application No. 17/309178 (reference application), in view of Li et al (US 2006/0263332).
Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the reference application, in view of Li et al renders obvious the instant claims.
The teachings of Li et al are set forth above. Briefly, Li et al is also focused on repairing brain damage, including brain damage from cerebral ischemia (strokes), comprising administering peripheral blood hematopoietic stem cells in combination with G-CSF (See Li et al, ¶0007-0008 and claim 1).
Regarding claims 42 and 43: Administration of G-CSF will inherently mobilize endothelial progenitor cells in the subject.
Because both the reference application claims and Li et al are focused on improving therapeutic outcome following stroke, it would have been prima facie obvious to apply both therapies (intrathecal administration of fibroblasts, and administration of G-CSF) to a single patient, for the predictable result of enhancing recovery and functional outcome following a stroke.
The combined effect of the two therapies would have been expected to be greater than the effect of either treatment individually. The reason to combine the different therapies would be to improve overall therapeutic effect following a stroke in a subject. See MPEP 2143(I)(A).
Regarding claims 49-52: Li et al teach administration of peripheral blood hematopoietic stem cells. Peripheral blood hematopoietic stem cells (PBSCs) are CD34+ (See Li et al, ¶0059). As above, because both reference application claims and Li et al are focused on improving therapeutic outcome following stroke, it would have been prima facie obvious to apply both therapies (intrathecal administration of fibroblasts, and administration of PBSCs) to a single patient, for the predictable result of enhancing recovery and functional outcome following a stroke.
The combined effect of the two therapies would have been expected to be greater than the effect of either treatment individually. The reason to combine the different therapies would be to improve overall therapeutic effect following a stroke in a subject. See MPEP 2143(I)(A).
This is a provisional rejection because the copending claims have not yet been patented.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ALLISON M FOX whose telephone number is (571)272-2936. The examiner can normally be reached M-F 10-6 EST.
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/ALLISON M FOX/Primary Examiner, Art Unit 1633