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 .
Applicant's amendments to the claims and arguments filed on 01-13-2026 have been received and entered. Claims 1-5, 9 have been amended. Claims 1-9 are pending in the instant application.
Election/Restrictions
Applicant's election with traverse of Group I, claims 1-6 and 9 in the reply filed on 08-11-2025 is acknowledged. The traversal is on the ground(s) that “claims 1 and 9 have been amended to recite that the receptor-type tyrosine kinase inhibitor used in the method is not an FGF receptor inhibitor. The instant claims exclude the use of an FGF inhibitor as allegedly described by Keller …... The method of the instant claims is not disclosed or suggested by Keller, and claims 7 and 8 (designated as Groups II and III) depend from claim 1. As such, the claims are united by a special technical feature and the restriction requirement should be withdrawn.” (Remarks, page 5).
This is not found persuasive because even though claims 1 and 9 have been amended to recite that the receptor-type tyrosine kinase inhibitor used in the method is not an FGF receptor inhibitor, the previous cited reference Keller et al (WO 2016/131137 A1, International Publication Date: 25 August 2016) specifically teach “incubating the cardiovascular mesoderm cells in a cardiac induction medium comprising a BMP component, optionally BMP4, above a selected amount, and retinoic acid (RA), and optionally one or more of a FGF inhibitor, a WNT inhibitor ……” (see [0098], page 23, line 26). Thus, FGF inhibitor is optional and can be excluded according to the teachings of Keller et al.
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Additionally, the limitations of Group I, claims 1-6 and 9 are not special technical feature as described in the 35 USC§ 103 below.
The requirement is still deemed proper and is therefore made FINAL.
Claims 7-8 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected subject matter, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on.
Claims 1-6 and 9 are under consideration.
Priority
This application is a 371 of PCT/JP2021/011231 filed on 03/18/2021 that claims priority from foreign application JAPAN 2020-050268 filed on 03/19/2020.
Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55.
Should applicant desire to obtain the benefit of foreign priority under 35 U.S.C. 119(a)-(d) prior to declaration of an interference, a certified English translation of the foreign application must be submitted in reply to this action. 37 CFR 41.154(b) and 41.202(e).
Failure to provide a certified translation may result in no benefit being accorded for the non-English application.
Withdrawn-Claim Rejections - 35 USC § 112(b)
Claims 1-6 and 9 were 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. In view of Applicants' amendment of base claim 1 and 9, the previous rejections of claims are hereby withdrawn. Applicants' arguments with respect to the withdrawn rejections are thereby rendered moot.
Withdrawn-Claim Rejections - 35 USC § 112 Improper Markush
Claim 5 was rejected on the basis that it contains an improper Markush grouping of alternatives. In view of Applicants' amendment and arguments, the previous rejections of claims are hereby withdrawn. Applicants' arguments with respect to the withdrawn rejections are thereby rendered moot.
New-Claim Rejections - 35 USC § 112(b)- necessitated by amendments
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 9 is 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.
Claim 9 is directed to “ method for purifying cardiomyocytes”; however, the claim recites “culturing a cell population comprising cardiomyocytes or cardiac progenitor cells, and other cells …… wherein the other cells comprise smooth muscle-like cells, endoderm lineage cells, or endothelium-like cells”, and “the cell population obtained by culturing pluripotent stem cells in a medium for cardiomyocyte differentiation”. Thus, the population is mixture of cardiomyocytes with different types of cells that may or may not have capacity to differentiate into cardiomyocyte, and there is only 1 step of “culturing” a mixture of “cardiomyocytes or cardiac progenitor cells, and other cells”. It is unclear if at the end of the culturing step, there would be only cardiomyocytes for the “ method for purifying cardiomyocytes”.
Maintained in modified form-Claim Rejections - 35 USC § 102- necessitated by amendments
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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, 6, 9 are rejected under 35 U.S.C. 102 (a)(1) (a)(2) as being anticipated by Cao et al (Pub. No.: US 2016/0186141 A1, Pub. Date: Jun. 30, 2016).
Regarding to claims 1, 6 and 9, Cao et al teach “compositions and methods are described herein for chemically inducing cells to change their differentiation state and become cardiac progenitor cells or cardiomyocytes” (Abstract) (for the preamble of claim 1 and 9).
Cao et al teach “starting cells are treated for a time and under conditions sufficient to convert the starting cells across lineage and/or differentiation boundaries to form cardiac progenitor cells and/or cardiomyocytes” ([0411], page 15) and “a starting population of cells can be derived from essentially any source, …. include any type of cell from a newborn, including, but not limited to newborn cord blood, newborn stem cells, progenitor cells, and tissue-derived cells” ([0406], page 14), Cao et al also teach reprograming of Human Adult Dermal Fibroblasts (HADFs) into pluripotent stem cell for conversion of into chemically induced cardiomyocytes ([0524], page 24, right column). Cao et al teach “the starting cells can be dispersed in a cell culture medium that contains the reprogramming composition at a density that permits cell expansion” ([0417], page 15). Cao et al teach “the population of reprogrammed cells generated by the methods described herein can include low percentages of non-cardiac cells” ([0440], page 17), and “differentiated non-cardiac cell” is of a cellular lineage other than a cardiac lineage (e.g., fibroblast, a cell of endodermal, mesodermal, epithelial, neuronal, connective, lymphocyte, or other tissue type lineage)” ([0479], page 20) (For step (a) of claim 1 and claims 6, 9).
Cao et al teach that FIG. 1 is a schematic diagram illustrating generation of human cardiomyocytes from starting cells (e.g., fibroblast cells) though treatment with (1) cardiac reprogramming medium (CRM) over 6 days to initiate cell fate conversion followed by (2) exposure to cardiac induction medium 1 (CIM1) for 5 days, and then cardiac induction medium 2 (CIM2) for 30 days or more. The cardiac induction medium used for these experiments contained a combination of nine small-molecule compounds including: CHIR99021, A83-01, SC1, OAC2, Y27632, BIX-01294,AS8351, SU16f, and JNJ- 10198409 ([0013], page 2). The PDGF receptor inhibitors (a receptor-type tyrosine kinase inhibitor) can be SU16f and JNJ-10198409 ([0365]-[0366], page 12 and [0377]-[0378], page 13). Additionally, Cao et al teach “one aspect of the invention is a composition including one or more of the following agents: a WNT agonist, a GSK3 inhibitor, a TGF-beta inhibitor, an inhibitor of extracellular signal-regulated kinase 1 (ERK1), an inhibitor of Ras GTPase-activating protein (Ras-GAP)), an Oct-4 activator, a Rho-associated coiled coil forming protein serine/threonine kinase inhibitor, an iron chelator, a KDM5B inhibitor, a histone methyltransferase inhibitor, a PDGF tyrosine kinase inhibitor, or any combination thereof ([0006], page 1). Thus, Cao et al teach at least one embodiment using only a PDGF tyrosine kinase inhibitor without EGF receptor inhibitors and FGF receptor inhibitors. (For step (b) and (c) of claim 1 and claim 9).
Regarding to claim 4, Cao et al teach platelet-derived growth factor (PDGF) receptor inhibitors ([0363], page 12) and “use of one or more PDGF receptor inhibitors can facilitate conversion of differentiated cells into the cardiac cell lineage” ([0364], page 12).
Thus, claims 1, 4, 6 and 9 are anticipated by Cao et al.
Response to Arguments
Applicant's arguments filed 01-13-2026 have been fully considered but they are not persuasive.
Applicants argue that
In Cao, "starting cells" (fibroblasts exemplified) are cultured in a medium ("CRM") containing a cocktail of nine compounds ("9C") and are reprogrammed into cardiomyocytes. The "9C" cocktail includes SU16f and JNJ-10198409, PDGF receptor tyrosine kinase inhibitors. Then, the starting cells are cultured in a medium (CIM1) containing a GSK3 inhibitor (CHIR99021), BMP4, Activin A, and VEGF, thereby inducing differentiation into cardiomyocyte progenitor cells (Day 6-Day 11 ). Finally, the cardiac progenitor cells are cultured in a medium (CIM2) containing a GSK3 inhibitor (CHIR99021) and VEGF, purportedly allowing maturation and differentiation into cardiomyocytes (Day 11- Day 30).
At best, Cao discloses application of PDGF receptor inhibitor to "starting cells" (only fibroblasts in the Examples), not a population of cells comprising cardiomyocytes, cardiomyocyte progenitor cells, and other cells as required in the instant claims. Cao applies the PDGF receptor inhibitor to "starting cells" to induce development into cardiomyocyte progenitor cells. This is distinct from the method of the instant claims where a receptor-type tyrosine kinase inhibitor is applied to a population of cells comprising cardiomyocytes, cardiomyocyte progenitor cells, and other cells. The "starting cells" are not differentiated and, as such, do not include cardiomyocytes or cardiomyocyte progenitor cells. The cells treated with a tyrosine kinase inhibitor are different in the method of Cao vs. the instantly claimed method (Remarks, page 8-9).
Response to Arguments
Applicants argue that Cao discloses application of PDGF receptor inhibitor to "starting cells" not a population of cells comprising cardiomyocytes, cardiomyocyte progenitor cells, and other cells as required in the instant claims and the "starting cells" are not differentiated and, as such, do not include cardiomyocytes or cardiomyocyte progenitor cells. This is not persuasive because Cao et al teach in FIG. 1 with schematic diagram illustrating generation of human cardiomyocytes from starting cells though treatment with cardiac induction medium 1 (CIM1) cardiac induction medium 2 (CIM2): The cardiac induction medium (CIM1 and CIM2) used for these experiments contained a combination of nine small-molecule compounds including: CHIR99021, A83-01, SC1, OAC2, Y27632, BIX-01294,AS8351, SU16f, and JNJ- 10198409 ([0013], page 2). SU16f, and JNJ- 10198409 are receptor-type tyrosine kinase inhibitor: Cao et al teach the PDGF receptor inhibitors (a receptor-type tyrosine kinase inhibitor) can be SU16f and JNJ-10198409 ([0365]-[0366], page 12 and [0377]-[0378], page 13). Since cardiac induction medium (CIM1 and CIM2) was used for entire process of differentiation to cardiomyocyte, Cao et al teach contacting cardiomyocyte/ cardiac progenitor cells with a PDGF receptor-type tyrosine kinase inhibitor SU16f and JNJ-10198409.
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Additionally, Cao et al teach “one aspect of the invention is a composition including one or more of the following agents: a WNT agonist, a GSK3 inhibitor, a TGF-beta inhibitor, an inhibitor of extracellular signal-regulated kinase 1 (ERK1), an inhibitor of Ras GTPase-activating protein (Ras-GAP)), an Oct-4 activator, a Rho-associated coiled coil forming protein serine/threonine kinase inhibitor, an iron chelator, a KDM5B inhibitor, a histone methyltransferase inhibitor, a PDGF tyrosine kinase inhibitor, or any combination thereof ([0006], page 1). Thus, Cao et al teach at least one embodiment using only a PDGF tyrosine kinase inhibitor without EGF receptor inhibitors and FGF receptor inhibitors. (For step (b) and (c) of claim 1 and claim 9).
Maintained-Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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 2-3 are rejected under 35 U.S.C. 103 as being unpatentable over Cao et al (Pub. No.: US 2016/0186141 A1, Pub. Date: Jun. 30, 2016) in view of Keller et al (WO 2016/131137 A1, 25 August 2016).
The teachings of Cao et al above are incorporated herein in their entirety.
Cao et al do not teach “the cell population is contacted with the receptor-type tyrosine kinase inhibitor on or after 4 days from the start of differentiation induction of pluripotent stem cells.”. Keller et al cure the deficiency.
Regarding to claims 2-3, Keller et al teach “a method of producing a population of cardiomyocytes from human pluripotent stem cells (hPSCs), the steps comprising: a. incubating the hPSCs in an embryoid body medium … for a period of time to generate embryoid bodies; b. incubating the embryoid bodies in a mesoderm induction medium …. to generate cardiovascular mesoderm cells c. incubating the cardiovascular mesoderm cells ……to generate a population of cardiomyocytes” ([0008], page 2). The hPSCs are induced pluripotent stem cells (iPSCs) ([00101], page 24).
The hPSCs are incubated in the embryoid body medium to generate embryoid bodies from about 6 hours to about 2 days (step a) ([00125], page 27). The embryoid bodies are incubated in the mesoderm induction medium to generate cardiovascular mesoderm cells for about 1 to about 4 days (step b) ([00126], page 27). The cardiovascular mesoderm cells are incubated in the cardiac induction medium to generate cardiovascular progenitor cells for about 1 to about 4 days ([00127], page 27). The cardiovascular progenitor cells are incubated in the basic medium to generate cardiomyocytes for about 4 or more days (step c) ([00128], page 28).
Given that inhibitors such as WNT inhibitor, activin/nodal inhibitor, a FGF inhibitor etc. are optionally added in step c. for generation of a population of cardiomyocytes (see [0008], page 2, lines 30-31) which is after generation of embryoid bodies (2 days) and after generation of cardiovascular mesoderm cells (4 days); Thus, it is taught by the prior art that the inhibitors can be added on or after 4 days from the start of differentiation induction of pluripotent stem cells to as required by the claim. Further, it is indicating that the timing for adding the inhibitor was recognized in the prior art to be a result-effective variable. A person of ordinary skill in the art would have been motivated to perform the incubation with different time periods a plurality of times out of the course of routine optimization before adding the inhibitor in order to increase efficiency of the differentiation.
Therefore, it would have been prima facie obvious for a person of ordinary skill in the art before the effective filing date of the rejected claims to combine the teachings of prior art to modify the method of Cao et al by adding the inhibitors on or after 4 days from the start of differentiation induction of pluripotent stem cells as taught by Keller et al as instantly claimed, with a reasonable expectation of success. Said modification amounting to combining prior art elements according to known methods to yield predictable results. One of ordinary skill in the art would have been motivated to do so because Keller et al teach that combined treatment of cardiovascular mesoderm cells with BMP4 and RA between days 3 and 5 increases the sinoatrial node-like pacemaker cardiomyocytes (SANLCM) differentiation process ([00140], page 29). Efficient cardiomyocyte differentiation was achieved with three different combinations of pathway agonists ([00217], page 42, lines 36-38). Furthermore, Keller et al stated that “The improved RA/BMP-induced pacemaker expression profile was associated with a significant increase in the beating rate of the cells (138 ± 7 bpm) (Fig. 3G). These rates are within the range of the human fetal heartbeat which is at 120-160 bpm” ([00221], page 44). One of ordinary skill in the art would have had a reasonable expectation of success in doing so because Keller et al were successful in generation of cardiomyocytes from iPSC differentiation with detailed instructions and working examples.
Claim 5 are rejected under 35 U.S.C. 103 as being unpatentable over Cao et al (Pub. No.: US 2016/0186141 A1, Pub. Date: Jun. 30, 2016) in view of Awazu et al (Cancer Sci | April 2013 | vol. 104 | no. 4 | 486–494, doi: 10.1111/cas.12101).
The teachings of Cao et al above are incorporated herein in their entirety.
Although Cao et al teach platelet-derived growth factor (PDGF) receptor inhibitors ([0363] – [0365], page 12) and “use of one or more PDGF receptor inhibitors can facilitate conversion of differentiated cells into the cardiac cell lineage” ([0364], page 12), Cao et al do not teach the specific inhibitors such as N-[5-({2-[(cyclopropanecarbonyl)amino]imidazo[1 ,2-b]pyridazin-6-yl}oxy)-2-
methylphenyl]-1 ,3-dimethyl-1 H-pyrazole-5-carboxamide as recited in claim 5. Awazu et al cure the deficiency.
Awazu et al reported that “TAK-593, a novel imidazo[1,2-b]pyridazine derivative, is a highly potent and selective inhibitor of the vascular endothelial growth factor (VEGF) and platelet derived growth factor (PDGF) receptor tyrosine kinase families …. TAK-593 is an extremely potent VEGFR/PDGFR kinase inhibitor” (Abstract). Awazu et al teach that TAK-593 is N-[5-({2-[(cyclopropylcarbonyl) amino]imidazo[1,2-b]pyridazin-6-yl}oxy}- 2-methylphenyl)-1,3- dimethyl-1H-pyrazole-5-carboxamide (page 486, right column, last para.).
Since Cao et al teach the use of platelet-derived growth factor (PDGF) receptor inhibitors ([0363] – [0365], page 12) to facilitate conversion of differentiated cells into the cardiac cell lineage ([0364], page 12), it is obvious for a person of ordinary skill in the art to look for highly potent and selective inhibitor of platelet derived growth factor (PDGF) receptor tyrosine kinase such as TAK-593 as taught by Awazu et al to facilitate conversion of differentiated cells into the cardiac cell lineage.
Therefore, it would have been prima facie obvious for a person of ordinary skill in the art before the effective filing date of the rejected claims to combine the teachings of prior art to modify the method of Cao et al by using PDGFR kinase inhibitor such as TAK-593 as taught by Awazu et al as instantly claimed, with a reasonable expectation of success. Said modification amounting to combining prior art elements according to known methods to yield predictable results. One of ordinary skill in the art would have been motivated to do so because Awazu et al reported that TAK-593 is a highly selective small molecular weight inhibitor of the PDGFRb tyrosine kinases that has been shown to exhibit a markedly long residence time on its targets (page 486, right column, 3rd para.). Awazu et al concluded that “TAK-593 had dual potent inhibition of both VEGF and PDGF signaling. The strong activities of TAK-593 on tumor growth and angiogenesis results in marked tumor regression combined with good tolerability” (page 492, right column, 3rd para.). One of ordinary skill in the art would have had a reasonable expectation of success in doing so because Awazu et al provide teachings of TAK-593 chemical structure and instructions for using TAK-593 in cell cultures with working examples.
Response to Arguments
Applicant's arguments filed 01-13-2026 have been fully considered but they are not persuasive.
Applicants argue that
The instantly claimed method is fundamentally different than that of Cao. Cao applies PDGF receptor tyrosine kinase inhibitors to "starting cells" prior to differentiation of the starting cells to cardiomyocytes or cardiomyocyte progenitor cells. Indeed, PDGF receptor tyrosine kinase inhibitors are discussed in Cao in terms of "programming" cells to differentiate into cardiomyocytes. See, e.g., Cao Table 1. Cao fails to teach or suggest applying a receptor-type tyrosine kinase inhibitor to an already differentiated cell population comprising cardiomyocytes or cardiomyocyte progenitor cells and other cells.
Applicant conducted intensive studies and discovered that the ratio of cardiomyocytes in a cell population (e.g., also comprising smooth muscle-like cells, endoderm lineage cells or endothelium-like cells) may be increased by suppressing the proliferation of other cells using inhibitors against receptor type tyrosine kinase. See, e.g., paragraph [0006]. This advantage could not have been predicted from the cited references. (Remarks, page 10)
Response to Arguments:
As described above, Cao et al teach the use of SU16f, and JNJ- 10198409 (PDGF receptor tyrosine kinase inhibitors) in cardiac induction medium (CIM1 and CIM2) for generation of human cardiomyocytes ([0013], page 2). Thus, Cao et al teach applying a receptor-type tyrosine kinase inhibitor to an already differentiated cell population comprising cardiomyocytes or cardiomyocyte progenitor cells.
The use of tyrosine kinase inhibitor such as PDGF tyrosine kinase inhibitor has been routinely used in the art as described above. Cao et al teach FIG. 3 illustrates the conversion efficiency into cardiomyocyte cells using the compositions and methods described herein ([0015], page 2). Thus, the prior art reference recognizes the use of PDGF tyrosine kinase inhibitor in differentiation process to generate cardiomyocytes or cardiomyocyte progenitor cells. As per MPEP 2112 (II), inherent feature need not be recognized at the relevant time: There is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference. Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003) (rejecting the contention that inherent anticipation requires recognition by a person of ordinary skill in the art before the critical date and allowing expert testimony with respect to post-critical date clinical trials to show inherency); see also Toro Co. v. Deere & Co., 355 F.3d 1313, 1320, 69 USPQ2d 1584, 1590 (Fed. Cir. 2004) ("[T]he fact that a characteristic is a necessary feature or result of a prior-art embodiment (that is itself sufficiently described and enabled) is enough for inherent anticipation, even if that fact was unknown at the time of the prior invention.").
Conclusion
No claim is allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to KHOA NHAT TRAN whose telephone number is (571)270-0201. The examiner can normally be reached M-F (9-5).
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/KHOA NHAT TRAN/Examiner, Art Unit 1632
/PETER PARAS JR/Supervisory Patent Examiner, Art Unit 1632
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