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 .
Election/Restrictions
Applicant’s election without traverse of Group I (Claims 1-36; drawn to a method of generating human GATA1+ megakaryocyte/erythroid progenitor cells) in the reply filed on September 25, 2025, is acknowledged.
Claims 37-42 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention (Groups II and III), there being no allowable generic or linking claim.
DETAILED ACTION
The amended claims filed on September 25, 2025, have been acknowledged. Claims 1-4, 8-10, 12, 20-23, 27-33, and 35-36 were amended. In light of the Applicant’s elected invention, claims 37-42 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Claims 1-36 are pending and examined on the merits.
Priority
The applicant claims domestic priority from U.S. provisional application No. 63/287,372, filed on December 8, 2021. Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged. Claims 1-36 receive domestic benefit from U.S. provisional application No. 63/287,372, filed on December 8, 2021.
Information Disclosure Statement
The information disclosure statements (IDS) filed on June 12, 2023, August 15, 2024, and October 29, 2024, have been considered.
Drawings
The drawings are objected to because Figures 1-5 and 7-13 have many parts that are illegible and unreadable. Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Specification
The use of the terms “Lipid MixtureTM”, “Albumax”, and “Chemically Defined Lipid ConcentrateTM”, which are trade names or marks used in commerce, has been noted in this application. The term should be accompanied by the generic terminology; furthermore the term should be capitalized wherever it appears or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the term.
Although the use of trade names and marks used in commerce (i.e., trademarks, service marks, certification marks, and collective marks) are permissible in patent applications, the proprietary nature of the marks should be respected and every effort made to prevent their use in any manner which might adversely affect their validity as commercial marks.
Claim Objections
Claim 26 is objected to because of the following informalities:
Claim 26 recites EB-3D twice in lines 5 and 9, respectively.
Appropriate correction is required.
Claim Rejections - 35 USC § 112
Claims 1-36 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claims contain subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Claims 1 and 32 recite the functional limitations “IL3R pathway agonist”, “TGFβ pathway agonist”, “AHR pathway antagonist”, “RET pathway antagonist”, and “Akt pathway agonist,” but does not describe a structure capable of performing this function. Claim 2 and 32 recites the functional limitations “EPOR agonist” and “AMPK agonist” but does not describe a structure capable of performing this function. Vas-cath Inc. v. Mahurkar, 19USPQ2d 1111, clearly states that Applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the ‘written description’ inquiry, whatever is now claimed.'' (See page 1117) The specification should “clearly allow persons of ordinary skill in the art to recognize that (he or she) invented what is claimed.'' (See Vas-cath at page 1116).
In analyzing whether the written description requirement is met for genus claims, it is first determined whether a representative number of species have been described by their complete structure. To provide adequate written description and evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, methods of making the claimed product, or any combination thereof. The disclosure of a single species is rarely, if ever, sufficient to describe a broad genus, particularly when the specification fails to describe the features of that genus, even in passing. (see In re Shokal 113USPQ283(CCPA1957); Purdue Pharma L.P. vs Faulding Inc. 56 USPQ2nd 1481 (CAFC 2000).
IL3R: In the instant application, the specification teaches that Agonists of the IL3R pathway include agents, molecules, compounds, or substances
capable of stimulating (activating) the IL3R signaling pathway. Applicant identifies 1 example of a non-limiting IL3R agonist compound, IL-3 (page 12, lines 5-11). Figures 1 and 4 of the instant application identifies IL-3 having a positive impact on GATA1 expression, but the specification does not identify whether other types of IL3R pathway agonists (such as agonists that target upstream or downstream of IL-3 and the IL-3 receptor) had similar effects. As such, the applicant provides one example of using an IL3R pathway agonist to differentiate CD34+ cells into GATA1+ cells (Examples 1-4), but has not provided any description or reduction to practice of other IL3R pathway agonists.
Based on the applicant's specification, the skilled artisan cannot envision the detailed chemical structure of the IL3R pathway agonist encompassed by the claims. The one IL3R pathway agonist specifically disclosed in examples 1-4 (IL-3) is not representative of the genera, because there are multiple types of agonists that bind to different molecular targets along the IL3R pathway. It is unclear whether targeting other molecules that are part of the IL3R signaling pathway is sufficient to generate GATA1+ cells.
Accordingly, given that the specification only teaches the complete structure of a single species of the exceptionally broadly-defined “IL3R pathway agonist” genus, this limited information is not deemed sufficient to reasonably convey to one skilled in the art that the applicant is in possession of the required starting materials, that is a IL3R pathway agonist, at the time the application was filed.
TGFβ: In the instant application, the specification teaches that Agonists of the TGFβ pathway include agents, molecules, compounds, or substances capable of stimulating (activating) the TGFβ signaling pathway. Applicant identifies 4 examples of non-limiting IL3R agonist compounds, alantolactone, Activin A, TGFβ1, and Nodal (page 12, lines 12-19). Figures 1 and 4 of the instant application identifies alantolactone having a positive impact on GATA1 expression, but the specification does not identify whether other types of TGFβ pathway agonists (such as agonists that target upstream or downstream of the alantolactone target molecule) had similar effects. As such, the applicant provides one example of using an TGFβ pathway agonist to differentiate CD34+ cells into GATA1+ cells (Examples 1-4), but has not provided any description or reduction to practice of other TGFβ pathway agonists.
Based on the applicant's specification, the skilled artisan cannot envision the detailed chemical structure of the TGFβ pathway agonist encompassed by the claims. The one TGFβ pathway agonist specifically disclosed in examples 1-4 (alantolactone) is not representative of the genera, because there are multiple types of agonists that bind to different molecular targets along the TGFβ pathway. It is unclear whether targeting other molecules that are part of the TGFβ signaling pathway is sufficient to generate GATA1+ cells.
Accordingly, given that the specification only teaches the complete structure of a single species of the exceptionally broadly-defined “TGFβ pathway agonist” genus, this limited information is not deemed sufficient to reasonably convey to one skilled in the art that the applicant is in possession of the required starting materials, that is a TGFβ pathway agonist, at the time the application was filed.
AHR: In the instant application, the specification teaches that Antagonists of the AHR (aryl hydrocarbon receptor) pathway include agents, molecules, compounds, or substances capable of inhibiting (downregulating) the AHR signaling pathway. Applicant identifies 9 examples of non-limiting AHR pathway antagonist compounds, SR1, GNF351, AHR antagonist 5 hemimaleate, AHR antagonist 1, PDM2, BAY 2416964, CH- 223191, AHR antagonist 2, and AHR antagonist 4 (page 12, lines 20-29). Figures 1 and 4 of the instant application identifies SR1 having a positive impact on GATA1 expression, but the specification does not identify whether other types of AHR pathway antagonists (such as antagonists that target upstream or downstream of the SR1 target molecule) had similar effects. As such, the applicant provides one example of using an AHR pathway antagonist to differentiate CD34+ cells into GATA1+ cells (Examples 1-4), but has not provided any description or reduction to practice of other AHR pathway antagonists.
Based on the applicant's specification, the skilled artisan cannot envision the detailed chemical structure of the AHR pathway antagonist encompassed by the claims. The one AHR pathway antagonist specifically disclosed in examples 1-4 (SR1) is not representative of the genera, because there are multiple types of antagonists that bind to different molecular targets along the AHR pathway. It is unclear whether targeting other molecules that are part of the AHR signaling pathway is sufficient to generate GATA1+ cells.
Accordingly, given that the specification only teaches the complete structure of a single species of the exceptionally broadly-defined “AHR pathway antagonist” genus, this limited information is not deemed sufficient to reasonably convey to one skilled in the art that the applicant is in possession of the required starting materials, that is a AHR pathway antagonist, at the time the application was filed.
RET: In the instant application, the specification teaches that Antagonists of the RET pathway include agents, molecules, compounds, or substances capable of inhibiting (downregulating) the RET signaling pathway. Applicant identifies 28 examples of non-limiting RET pathway antagonist compounds, RETki, Lenvatinib, Regorafenib, Pralsetinib, Selpertinib, Lenvatinib mesylate, RET-IN-4, RPI-1, JNJ38158471, Amuvatinib, TG101209, Regorafenib Hydrochloride, Ilorasertib hydrochloride, AST487, PF477736, BBT594, AD80, GSK3179106,SPP86, RET-IN-3, WF-47-JSO3, RET V804M-IN-1, Trans-pralsetinib, PZ1, Regorafenib D3, RET-IN-1, ML786 dihydrochloride, and WHI-P 180 hydrochloride (page 12, line 30-page 13, line 11). Figures 1 and 4 of the instant application identifies RETki having a positive impact on GATA1 expression, but the specification does not identify whether other types of RET pathway antagonists (such as antagonists that target upstream or downstream of the RETki target molecule) had similar effects. As such, the applicant provides one example of using a RET pathway antagonist to differentiate CD34+ cells into GATA1+ cells (Examples 1-4), but has not provided any description or reduction to practice of other RET pathway antagonists.
Based on the applicant's specification, the skilled artisan cannot envision the detailed chemical structure of the RET pathway antagonist encompassed by the claims. The one RET pathway antagonist specifically disclosed in examples 1-4 (RETki) is not representative of the genera, because there are multiple types of antagonists that bind to different molecular targets along the RET pathway. It is unclear whether targeting other molecules that are part of the RET signaling pathway is sufficient to generate GATA1+ cells.
Accordingly, given that the specification only teaches the complete structure of a single species of the exceptionally broadly-defined “RET pathway antagonist” genus, this limited information is not deemed sufficient to reasonably convey to one skilled in the art that the applicant is in possession of the required starting materials, that is a RET pathway antagonist, at the time the application was filed.
AKT: In the instant application, the specification teaches that Antagonists of the AKT (rearranged during transfection) pathway include agents, molecules, compounds, or substances capable of inhibiting (downregulating) the AKT signaling pathway. Applicant identifies 30 examples of non-limiting AKT pathway antagonist compounds, MK2206, GSK690693, Perifosine (KRX-0401), Ipatasertib (GDC-0068), Capivasertib (AZD5363), PF-04691502, AT 7867, Triciribine (NSC154020), ARQ751, Miransertib (ab235550), Borussertib, Cerisertib, Aktil/2, CCT128930, A 674563, PHT 427, Miltefosine, AT 13148, ML 9, BAY 1125976, Oridonin, TIC10, Pectolinarin, Acti IV, 10-DEBC, API-1,SC 66,FPA 124, API-2, Urolithin A (page 13, lines 12-24). Figures 1 and 4 of the instant application identifies MK2206 having a positive impact on GATA1 expression, but the specification does not identify whether other types of AKT pathway antagonists (such as antagonists that target upstream or downstream of the MK2206 target molecule) had similar effects. As such, the applicant provides one example of using an AKT pathway antagonist to differentiate CD34+ cells into GATA1+ cells (Examples 1-4), but has not provided any description or reduction to practice of other RET pathway antagonists.
Based on the applicant's specification, the skilled artisan cannot envision the detailed chemical structure of the AKT pathway antagonist encompassed by the claims. The one AKT pathway antagonist specifically disclosed in examples 1-4 (MK2206) is not representative of the genera, because there are multiple types of antagonists that bind to different molecular targets along the AKT pathway. It is unclear whether targeting other molecules that are part of the AKT signaling pathway is sufficient to generate GATA1+ cells.
Accordingly, given that the specification only teaches the complete structure of a single species of the exceptionally broadly-defined “AKT pathway antagonist” genus, this limited information is not deemed sufficient to reasonably convey to one skilled in the art that the applicant is in possession of the required starting materials, that is a AKT pathway antagonist, at the time the application was filed.
EPOR: In the instant application, the specification teaches that Agonists of the EPOR pathway include agents, molecules, compounds, or substances
capable of stimulating (activating) the erythropoietin receptor (EPOR) signaling pathway. As such, although claims 2 and 32 do not specifically recite that the EPOR agonist is a pathway agonist, based on the definition recited in the specification, the EPOR agonist of the claims are considered EPOR pathway agonists Applicant identifies 2 examples of a non-limiting EPOR agonist compound, EPO or a EPOR-binding analog (page 14, lines 1-7). Figures 3 and 8 of the instant application identifies EPO having a positive impact on HBA1 expression and differentiating GATA1+ cell into CD71+ CD235+ CD34- cells, but the specification does not identify whether other types of EPOR pathway agonists (such as agonists that target upstream or downstream of EPO and the EPO receptor) had similar effects. As such, the applicant provides one example of using an EPOR pathway agonist to differentiate GATA1+ cells into CD71+ CD235+ CD34- cells (Examples 1-4), but has not provided any description or reduction to practice of other EPOR pathway agonists.
Based on the applicant's specification, the skilled artisan cannot envision the detailed chemical structure of the EPOR pathway agonist encompassed by the claims. The one EPOR pathway agonist specifically disclosed in examples 1-4 (EPO) is not representative of the genera, because there are multiple types of agonists that bind to different molecular targets along the EPOR pathway. It is unclear whether targeting other molecules that are part of the EPOR signaling pathway is sufficient to generate CD71+ CD235+ CD34- cells.
Accordingly, given that the specification only teaches the complete structure of a single species of the exceptionally broadly-defined “EPOR pathway agonist” genus, this limited information is not deemed sufficient to reasonably convey to one skilled in the art that the applicant is in possession of the required starting materials, that is a EPOR pathway agonist, at the time the application was filed.
AMPK: In the instant application, the specification teaches that Agonist of the AMPK (AMP activated protein kinase) pathway include agents,
molecules, compounds, or substances capable of stimulating (activating) the AMPK signaling pathway. As such, although claims 2 and 32 do not specifically recite that the AMPK agonist is a pathway agonist, based on the definition recited in the specification, the AMPK agonist of the claims are considered AMPK pathway agonists Applicant identifies 54 examples of a non-limiting EPOR agonist compound, AICAR, Metformin, BC1618, Malvidin-3-0-arabinoside chloride, A-769662, MK8722, Bempedoic acid, AICAR phosphate, Phenformin hydrochloride, EX229, gingerol, Kazinol B, PF06409577, Flufenamic acid, GSK621, Urolithin B, MK3903, chitosan oligosaccharide, palmitelaidic acid, 0-304, Amarogentin, 7-Methoxyisoflavone, EB-3D, Buformin hydrochloride, Platycodin D, ZLNO24 hydrochloride, Danthron, Ampkinone, ginkolide C, Gomisin J,
Demethylenebemerine, ASP4132, IM156, Vacarin, MOTS-c(human) acetate, Kahweol, AMPK activator 4, Marein, Euphorbiasteroid, Cimiracemoside C, Metformin D6 hydrochloride, MT6378, RSVA405, Nepodin, 3a-Hydroxymogrol, AMPK activator 1, YLF-466D, Buformin, IQZ23, Galegine hydrochloride, Karanjin, COH-SR4, HL271, and ZLNO24 (page 14, lines 8-25). Figures 3 and 8 of the instant application identifies AICAR having a positive impact on HBA1 expression and differentiating GATA1+ cell into CD71+ CD235+ CD34- cells, but the specification does not identify whether other types of AMPK pathway agonists (such as agonists that target upstream or downstream of the AICAR target molecule) had similar effects. As such, the applicant provides one example of using an AMPK pathway agonist to differentiate GATA1+ cells into CD71+ CD235+ CD34- cells (Examples 1-4), but has not provided any description or reduction to practice of other AMPK pathway agonists.
Based on the applicant's specification, the skilled artisan cannot envision the detailed chemical structure of the AMPK pathway agonist encompassed by the claims. The one AMPK pathway agonist specifically disclosed in examples 1-4 (AICAR) is not representative of the genera, because there are multiple types of agonists that bind to different molecular targets along the AMPK pathway. It is unclear whether targeting other molecules that are part of the AMPK signaling pathway is sufficient to generate CD71+ CD235+ CD34- cells.
Accordingly, given that the specification only teaches the complete structure of a single species of the exceptionally broadly-defined “AMPK pathway agonist” genus, this limited information is not deemed sufficient to reasonably convey to one skilled in the art that the applicant is in possession of the required starting materials, that is a AMPK pathway agonist, at the time the application was filed.
As such, the ordinary artisan would have to perform a trail-and-error assessment of different “IL3R pathway agonists”, “TGFβ pathway agonists”, “AHR pathway antagonists”, “RET pathway antagonists”, and “Akt pathway agonists” to assess their efficacy in differentiating CD34+ cells into GATA1+ cells and a trail-and-error assessment of different “EPOR agonists” and “AMPK agonists” to assess their efficacy in differentiating GATA1+ cells into CD71+ CD235+ CD34- cells with unpredictable results.
Thus, for the reasons outlined above, it is concluded that the claims do not meet the requirements for written description under 35 U.S.C. 112, first paragraph.
Applicant is reminded that MPEP 2163 - 35 U.S.C. 112(a) and the first paragraph of pre-AIA 35 U.S.C. 112 require that the “specification shall contain a written description of the invention ....” This requirement is separate and distinct from the enablement requirement. Ariad Pharm., Inc. v. Eli Lilly & Co., 598 F.3d 1336, 1340, 94 USPQ2d 1161, 1167 (Fed. Cir. 2010) (en banc).
The court explained that “reading a claim in light of the specification, to thereby interpret limitations explicitly recited in the claim, is a quite different thing from ‘reading limitations of the specification into a claim,’ to thereby narrow the scope of the claim by implicitly adding disclosed limitations which have no express basis in the claim.” The court found that applicant was advocating the latter, i.e., the impermissible importation of subject matter from the specification into the claim.). See also In re Morris, 127 F.3d 1048, 1054-55, 44 USPQ2d 1023, 1027-28 (Fed. Cir. 1997).
The claims fail to recite, and the specification fails to disclose, a nexus between a structure and the corresponding recited functional property of “IL3R pathway agonists”, “TGFβ pathway agonists”, “AHR pathway antagonists”, “RET pathway antagonists”, “Akt pathway agonists”, “EPOR agonists”, and “AMPK agonists”.
Without a correlation between structure and function, the claim does little more than define the claimed invention by function. That is not sufficient to satisfy the written description requirement. See Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406 (“definition by function … does not suffice to define the genus because it is only an indication of what the gene does, rather than what it is”).
Claims 2-31 are also rejected because of their dependency on claim 1. Although claims 5-19 identify specific compounds that correspond to “IL3R pathway agonists”, “TGFβ pathway agonists”, “AHR pathway antagonists”, “RET pathway antagonists”, and “Akt pathway agonists”, they fail to overcome the 112a rejection of claim 1 because at least one pathway does not have specific compounds identified. Claims 20-31 are also rejected because of their dependency on claim 2 for the same reason. Claims 33-36 are also rejected because of their dependency on claim 32 for the same reason.
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 29-31 and 35-36 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.
Claim 29 contains the trademark/trade names “Lipid MixtureTM”, “AlbumaxTM”, and “Chemically Defined Lipid ConcentrateTM” and claims 30-31, and 35-36 contains the trademark/trade name “AlbumaxTM”. 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 “Lipid MixtureTM”, “AlbumaxTM”, and “Chemically Defined Lipid ConcentrateTM” and, accordingly, the identification/description is indefinite.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to KEENAN A BATES whose telephone number is (571)270-0727. The examiner can normally be reached M-F 7:30-5:00.
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, Doug Schultz can be reached at (571) 272-0763. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/KEENAN A BATES/Examiner, Art Unit 1631