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
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office Action.
Status of Claims
Claims 1, 2, 4, 5, 7, 9-26 and 46-48 are currently pending. Claims 1, 4, 7 and 11 have been amended by Applicants’ amendment filed 12-18-2025. Claim 8 has been canceled by Applicants’ amendment filed 12-18-2025. Claim 47 has been added by Applicants’ amendment filed 12-18-2025.
Applicant's election without traverse of Group I, claims 1-13, directed to a method for selecting one or more human hematopoietic stem/progenitor cells from within a heterogenous population of lin- HSPCs; and the election of Species without traverse of:
Species (A): wherein the method of claim 1 further comprising the step of selecting for CD34+ cells (claim 3); and
Species (B): wherein the selecting for the one or more of sLeXhigh cells comprises selecting for cells having the highest 10% of sLeX expression level within the heterogenous population (claim 11); in the reply filed September 24, 2024 was previously acknowledged.
Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election of invention has been treated as an election without traverse (MPEP
§ 818.03(a)).
Regarding newly submitted claim 48, the claim is directed to an invention that is independent or distinct from the invention originally claimed for the following reasons: Newly submitted claim 48 is directed to a method for selecting one or more human hematopoietic stem cells (HSCs) from within a heterogenous population of CD34+ human hematopoietic stem/progenitor cells that have not been modified by fucosylation ("CD34+ unmodified HSPCs") comprising: (1) contacting the heterogenous population of CD34+ unmodified HSPCs with an antibody for sLeX and an antibody for CD38; (2) measuring via flow cytometry an amount of sLeX and CD38 expressed on individual cells in (1); and (3) selecting via FACS one or more of the measured CD34+ unmodified HSPCs of step (2) for cells that are CD38-…thereby selecting the one or more human HSCs (claim 48). Claim 1 of the claims filed February 29, 2024 was directed to a method for selecting one or more human hematopoietic stem/progenitor cells (HSPCs) from within a heterogenous population of lin- HSPCs comprising: contacting the heterogenous population of lin HSPCs with a binding molecule for sialylated Lewis X (sLeX); measuring the amount of sLeX present on individual cells in the heterogenous population of lin- HSPCs; and selecting for one or more of sLeXhigh cells based on the level of sLeX expression of the lin-HSPCs, wherein the sLeXhigh cells are the cells having the highest 15% sLeX expression level within the heterogenous population of sLeX +lin- HSPCs (claim 1). Thus, newly submitted claim 48 requires a search and examination beyond the claims as originally presented, and constructively elected. The different species of methods and/or compositions would require a different field of search; the prior art applicable to one species would not likely be applicable to another species; and/or the species are likely to raise different non-prior art issues under 35 U.S.C. 101 and/or 35 U.S.C. 112(a). For example, the limitations of newly submitted claim 48 recites an independent and distinct cell preparation system comprising different system components as compared to the elected invention of instant claim 1 of the claims filed February 29, 2024.
As noted in MPEP 818.02(a), wherein subsequently presented claims to an invention other than that acted upon should be treated as provided in MPEP § 821.03. As recited in MPEP 821.04 (¶ 8.04), since applicant has received an action on the merits for the originally presented invention, this invention has been constructively elected by original presentation for prosecution on the merits.
Accordingly, newly submitted claim 48 is withdrawn from consideration as being directed to a non-elected invention. See 37 CFR 1.142(b) and MPEP § 821.03.
Please Note (1): in the reply filed September 24, 2024, Applicant elected for Species (A), the method of claim 1, further comprising the step of selecting for CD34+ cells (claim 3). Although amended claim 4 depends from claim 1, instant claim 4 does not recite the elected species. Thus, claim 4 is withdrawn as being directed to a non-elected species.
Please Note (2): in the response filed September 24, 2024, Applicant elected for Species (B), wherein the selecting for the one or more of sLeXhigh cells comprises selecting for cells having the highest 10% of sLeX expression level within the heterogenous population (claim 11). As previously noted, claim 47 recites that sLexhigh comprises selecting by FACS, such that claim 47 is withdrawn from further consideration as being directed to a non-elected species.
Claims 14-26 and 46 were previously withdrawn, and claim 48 is newly withdrawn, from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a non-elected invention, there being no
allowable generic or linking claim.
Claims 2, 5, 6, 10, 12, 13 and 47 were previously withdraw from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a non-elected species, there being no allowable generic or linking claim.
The restriction requirement was deemed proper and was made FINAL.
The claims will be examined insofar as they read on the elected species.
A complete reply to the final rejection must include cancellation of nonelected claims or other appropriate action (37 CFR 1.144) See MPEP § 821.01.
Therefore, claims 1, 7 and 11 are under consideration to which the following grounds of rejection are applicable.
Priority
The instant application filed February 29, 2024 is a CON of PCT/US2024/011599, filed January 16, 2024 (now abandoned), which claims priority to US Provisional Patent Application 63479853, filed
January 13, 2023.
Applicant has not complied with one or more conditions for receiving the benefit of an earlier filing date under 35 U.S.C. 120 as follows:
The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original nonprovisional application or provisional application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of the first paragraph of 35 U.S.C. 112. See Transco Products, Inc. v. Performance Contracting, Inc., 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994).
The disclosure of the prior-filed application, Application 63/479,853, filed January 13, 2023, fails to provide adequate support or enablement in the manner provided by the first paragraph of 35 U.S.C. 112 for one or more claims of this application. The specific method steps recited in independent claim 1 does not have support for; “one or more human hematopoietic stem cells (HSCs) from within a heterogenous population of CD34+ human hematopoietic stem/progenitor cells (HSPCs) that have not been modified by fucosylation”; “contacting the heterogenous population of CD34+ HSPCs of step (1)”; “sLeXhigh cells have the highest 15% sLeX expression level within the heterogenous population of CD34+ HSPCs”; and “thereby obtaining the one or more human HSCs”. Therefore, the priority date for the presently claimed invention is January 16, 2024, the filing date of International Application WO2024152043, filed January 16, 2024.
Applicants are invited to specifically indicate the location of the cited phrases pertinent to claim 1 of the instant application.
Response to Arguments
Applicant’s arguments filed December 18, 2025 have been fully considered and are not found persuasive. Applicants essentially assert that: (a) support for claim 1 is found in at least the examples disclosed in the provisional application (Applicant Remarks, pg. 9, first full paragraph).
Regarding (a), Applicant did not specifically point out where the specific method steps can be found in the Examples disclosed in the provisional application. The Examiner respectfully requests that Applicant specifically point to the page, paragraphs and/or lines where support can be found in International Application WO2024152043 and US Provisional Patent Application 63/479,853 for each of the limitations as recited in claim 1. The priority date for the presently claimed invention remains January 16, 2024.
Withdrawn Objections/Rejections
Claim Rejections - 35 USC § 112(d)
The rejection of claims 7 and 11 is withdrawn under 35 U.S.C. 112(d) as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends due to Applicant’s amendment of the claims, in the reply filed 12-18-2025.
Claim Rejections - 35 USC § 102
The rejection of claims 1, 7, 8 and 11 is withdrawn under 35 U.S.C. 102(a1)/102(a2) as being anticipated by Rossi et. al. (hereinafter “Rossi”) (US Patent Application Publication No. 20190119642, published April 25, 2019; International Application WO2017201537, filed March 15, 2017; effective filing date March 15, 2016).
Rossi is not the best reference for this rejection.
In view of the withdrawn rejection, Applicant’s arguments are rendered moot.
Claim Rejections - 35 USC § 103
The rejection of claims 1, 7, 8 and 11 is withdrawn under 35 U.S.C. 103 as being unpatentable over Rossi et. al. (hereinafter “Rossi”) (US Patent Application Publication No. 20190119642, published April 25, 2019; International Application WO2017201537, filed March 15, 2017; effective filing date March 15, 2016) in view of Pellin et. al. (hereinafter “Pellin”) (Nature Communications, 2019, 10(1), 1-15; and Supplementary Information, 2019, 10(1), 1-39).
The combined references of Rossi and Pellin is not the best reference for this rejection.
In view of the withdrawn rejection, Applicant’s arguments are rendered moot.
Maintained Objections/Rejections
Claim Rejections - 35 USC § 112(b)
The rejection of claims 1, 7 and 11 are maintained under 35 U.S.C. 112(b) as being indefinite for failing to particularly point out and distinctly claim the subject matter which applicant regards as the invention.
Claims 1, 7 and 11 are indefinite for the recitation of the term “have not been modified by fucosylation” such as recited in claim 1, line 7 because the meaning of the term is unclear. It is unclear whether the term refers to a complete absence of fucosylation in CD34+ HSPCs; whether the term refers to exo- (or ex vivo) fucosylation; and/or synthetic fucosylation (e.g., synthetic modification). It is known that that sLeX is a sialofocosylated terminal lactosaminyl glycan (e.g., it is fucosylated) as evidenced by Richichi (Abstract, lines 6-7); and it is known that sLeX can only be created by fucosylation of sialylated LacNAc, wherein the biosynthesis of sLeX critically pivots on fucose addition programmed by a(1,3)-fucosyltransferases as evidenced by Sackstein (US20210017562; paragraph [0012], lines 15-18), such that sLeX expression encompasses ‘fucosylation’ (and, thus, modification by fucosylation) and, thus, the metes and bounds of the claim cannot be determined.
Claim Rejections - 35 USC § 102
The rejection of claims 1, 7 and 11 is maintained under 35 U.S.C. 102(a1)/102(a2) as being anticipated by Karakantza et. al. (hereinafter “Karakantza”) (British Journal of Haematology, 1994, 86, 883-886).
Regarding claims 1, 7 and 11, Karakantza teaches an investigation into sialylated Lewis x (sLeX) antigen expression on CD34 positive (CD34+) haemopoietic progenitors in the bone marrow of eight healthy volunteers using monoclonal antibodies, wherein CD34+ bone marrow progenitors strongly expressed the sLeX antigen (interpreting bone marrow progenitors as HSPCs; CD34+; sLeX; contacting CD34+ HSPCs with a binding molecule; measuring the expression of sLeX; highly expressing CD34+ sLeX including highest 10-15%; bone marrow; and humans, claims 1, 7 and 11) (Abstract, Summary). Karakantza teaches that scattergrams were generated by combining right-angle light scatter with fluorescence and regions drawn around clear-cut positive populations (CD34+ or sLex+), wherein the frequencies of CD34+ and sLex+ populations in the entire nucleated populations were obtained by subtracting the percentage of cells in the regions of the negative controls from those in the regions stained with both anti-CD34 and anti-sLeX, such that a logical gate was then defined to quantitate cells satisfying both CD34+ and sLex+ regions (CD34+/sLeX+) as shown in Figure 1 (interpreted as sLeXhigh and expressing CD34+ sLeX including highest 10-15% sLeX expression level, claim 1) (pg. 883, col 2, third full paragraph; and pg. 884, Figure 1). Karakantza teaches a two-color fluorescence was also performed using anti-CD34 and anti-CD15 to confirm the specificity of anti-sLeX binding to CD34+ cells (Fig 2) (interpreted as contacting CD34+ HSPCs with a binding molecule; measuring the expression of sLeX; and interpreting CD34- to select for lineage negative, claims 1, 7, 8 and 11) (pg. 883, last full paragraph; and pg. 884, Figure 2).
Figures 1 and 2 are shown below:
PNG
media_image1.png
364
810
media_image1.png
Greyscale
PNG
media_image2.png
360
378
media_image2.png
Greyscale
PNG
media_image3.png
358
372
media_image3.png
Greyscale
PNG
media_image4.png
356
380
media_image4.png
Greyscale
Figure 1
PNG
media_image5.png
354
802
media_image5.png
Greyscale
PNG
media_image6.png
354
376
media_image6.png
Greyscale
PNG
media_image7.png
354
378
media_image7.png
Greyscale
PNG
media_image8.png
372
376
media_image8.png
Greyscale
Figure 2
Karakantza teaches that the results are summarized in Table 1, wherein the percentage of CD34+ cells in the mononuclear population of the bone marrows studied ranged from 0.49% to 1.66% (mean 1.03%), such that the percentage of double-stained CD34+/sLex+ cells in the mononuclear population ranged from 0.34% to 1.36% (mean 0.9%); and the percentage of CD34+ cells that were also sLeX+ ranged from 65% to 100% (mean 87%), where Table 1 is shown below:
PNG
media_image9.png
286
322
media_image9.png
Greyscale
(interpreted as sLeXhigh and expressing CD34+ sLeX including selecting for the highest 10-15% sLeX expression level, claim 1) (pg. 886, col 1, first full paragraph; and Table 1).
Karakantza meets all the limitations of the claims and, therefore, anticipates the claimed invention.
Response to Arguments
Applicant’s arguments filed December 18, 2025 have been fully considered and are not found persuasive. Applicants essentially assert that: (a) the Office does not attempt to identify where Karakantza has disclosed each and every element as arranged in claim 1 (Applicant Remarks, pg. 22, last partial paragraph); (b) Karakantza does not teach selecting the highest 15% or 10% sLeX expressing cells (Applicant Remarks, pg. 23, first partial paragraph through pg. 24, first full paragraph); and (c) the pending Specification explains "[i]t has been surprisingly discovered that that high sLeX expression is characteristic of human HSCs, and, more specifically, that, among human CD34+CD38-HSCs, the marker combination consisting of CD90+, CD45RA-, and CD49f+ can altogether by supplanted by high sLeX expression." Specification, [0056], which is quantitatively different than anything disclosed in Karakantza (Applicant Remarks, pg.24, second full paragraph).
Regarding (a), Applicant’s assertion that the Office does not attempt to identify where Karakantza has disclosed each and every element as arranged in claim 1, is not found persuasive. The teachings of Karakantza and how they relate to the instant claims are clearly denoted in the Office Action mailed August 18, 2025.
Regarding (b), although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26USPQ2d 1057 (Fed. Cir. 1993). As noted in MPEP 2112.01(I),
where the claimed and prior art products are identical or substantially identical in structure or composition, or are produced by identical or substantially identical processes, a prima facie case of either anticipation or obviousness has been established. In re Best, 562 F.2d 1252, 1255, 195 USPQ 430, 433 (CCPA 1977). "When the PTO shows a sound basis for believing that the products of the applicant and the prior art are the same, the applicant has the burden of showing that they are not." In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990).
Applicant’s assertion that Karakantza does not teach selecting the highest 15% or 10% sLeX expressing cells, is not found persuasive. The Examiner respectfully notes that no specific method of ‘selecting’ is recited in instant claim 1. Regarding fucosylation, as noted in the 35 USC 112(b) rejection, it is unclear whether the limitation of ‘human HSPCs that have not been modified by fucosylation’ applies to cells that express sLeX (which is a sialofocosylated terminal lactosaminyl glycan). It is unclear how a CD34+ human HSPC that has not been modified by fucosylation, can bind/express sLeX, which is indicative of a cell modified by fucosylation. Additionally, instant claim 1 uses the term “comprising”, which is open-ended and does not exclude additional, unrecited elements or method steps, including sLeXhigh cells within an entire population of cells. Karakantza teaches:
Bone marrow samples were obtained and bone marrow mononuclear cells were isolated (interpreting bone marrow samples as heterogenous population of CD34+ HSPCs).
Scattergrams were generated, which show the frequencies of CD34+ and sLeX populations for the entire nucleated population, which were obtained after subtraction of the negative controls from those stained with both anti-cd34 and anti-sLeX; and quantitating cells satisfying both CD34+ and sLeX, followed by quantitating cells satisfying both CD34+ and sLeX regions. Figure 1 is an example of dot plot showing two-color fluorescence for quantitating the CD34+/sLeX cells using anti-CD34+ and anti-sLeX antibodies.
The percentage of CD34+ cells in the mononuclear population of the bone marrows studied ranged from 0.49% to 1.66% (mean 1.03%), such that the percentage of double-stained CD34+/sLex+ cells in the mononuclear population ranged from 0.34% to 1.36% (interpreted as selecting the highest 15% of the one or more cells).
Thus, Karakantza teaches selecting one or more CD34+ sLeXhigh cells that have the highest 15% expression level within the population of CD34+ HSPCs. The claims remain rejected.
Regarding (c), Applicant’s argument is unclear. It is not clear whether Applicant is asserting that the method of claim 1 provides surprising results, or whether Applicant is suggesting that some portion of claim 1 is not taught by Karakantza. The Examiner respectfully notes that instant claim 1 does not recite any particular method of selecting (e.g., graphing, plotting, binding, enriching, isolating, etc.). Moreover, instant claim 1 does not recite CD34+CD38- HSCs; a marker combination consisting of CD90+, CD45RA- and CD49f+; and/or supplanting the marker combination consisting of CD90+, CD45RA-, and CD49f+ with high sLeX expression. Thus, Applicant’s ‘surprising discovery’ does not read on the limitations as recited in instant claim 1. Applicant’s has not provided any evidence of improved properties that are reasonably commensurate in scope with the claimed invention
Claim Rejections - 35 USC § 103
The rejection of claims 1, 7 and 11 is maintained under 35 U.S.C. 103 as being unpatentable over Laine et. al. (hereinafter “Laine”) (US Patent Application No. 20120190058, published July 26, 2012; of record) in view of Miller et. al. (hereinafter “Miller”) (US Patent Application No. 2011091434, published April 21, 2011; of record) as evidenced by Carrascal et al. (hereinafter “Carrascal”) (BBA – General Subjects, 2018, 1862, 2069-2080; of record); and Murtadha et al. (hereinafter “Murtadha”) (bioRxiv, 2023, 1-32; of record) and Pang et al. (hereinafter “Pang”) (PNAS, 2011, 108(50), 20012-20017).
Regarding claims 1, 7 and 11, Laine teaches specific sialylated structures present on human stem cells and cell populations derived thereof; as well as, methods to control the status of stem cells by observing changes in sialylation of the cells; and control of potential contaminations of biological materials; and reagents and methods used in connection with the cells in order to avoid alterations of the cell glycosylation by contaminating materials; as well as, novel structures found from human stem cell and cord blood cell populations; and specific sialylated structures present on early human cells (interpreting cell populations including cord blood cell populations as a heterogenous population of lin- HSCPs; human stem cell and cord blood sialylated structures; lineage negative cells; from cord blood, claims 1 and 7) (Abstract; and paragraph [0033]). Lain teaches that Figure 11 shows (A) cultured in the presence of FBS by Neu5Gc-specific antibody, (B) after detergent extraction, (C) after sialidase treatment, decreased staining indicates that antibody binding was dependent on sialic acids such as Neu5Gc (interpreted as contacting the heterogenous population of lin- HSPCs with an antibody binding molecule for sLeX, claim 1) (paragraph [0026]). Laine teaches that NeuAca3Galb4 structures have been previously indicated to be present in human cord blood CD34 + hematopoietic cells by the use of a specific monoclonal antibody (Magnani, J., et al., U.S. Pat. No. 5,965,457) (interpreted as contacting with a binding molecule), wherein the invention claims all CD34+ cells and especially ones from cord blood and bone marrow (interpreting cord blood and bone marrow as a heterogenous population of lin- HSPCs as indicated in the as-filed Specification where the heterogenous population of lin- HSPCs is from bone marrow, umbilical cord blood, etc. at paragraph [0015]; CD34+ cells; interpreting a monoclonal antibody as a specific binding molecule; and human cord blood as comprising a heterogenous population of lineage negative HSPCs, claims 1, 3 and 7) (paragraph [0006]), where in human bone marrow, the HSC population is highly enriched within the Lin-CD34+CD38-CD90+CD45RA- population as evidenced by Pang (interpreted as a heterogenous population of lin- HSPCs) (pg. 20012, col 1, last partial paragraph). Laine teaches that the most preferred cells are early human blood cell populations including human cord blood cells and subpopulations thereof, which have been found useful in therapeutic cell transplantations, such that the present invention is specifically directed to multipotent cells capable of differentiating to non-hematopoietic cells and/or to hematopoietic cells including embryonal-type cells; as well as, cord blood and bone marrow from older individuals or adults, wherein the differentiation status includes solid tissue progenitor cells such as mesenchymal-stem cells (interpreted as heterogenous population of lin- HSCPs; cord blood, bone marrow, lin- cells; adult and embryonic cells, claims 1 and 7) (paragraphs [0034]; and [0047]). Laine teaches that the CD34 positive cell population is large and heterogenous (interpreted as CD34+; and heterogenous population, claims 1, 3, and 11) (paragraph [0081], lines 1-2). Laine teaches that the invention is directed to cell modification by sialyltransferases and fuscosyl-transferases, which can be used to produce important cell adhesion structures that are sialylated and fucosylated N-acetyl-lactosamines such as silalyl-Lewis x (sLeX) (interpreted as sLeX, claims 1 and 11) (paragraph [0284]). Laine teaches that purification of cells includes at least one of the steps including the use of controlled reagent, comprising: (1) washing cell material with controlled reagent; (2) when antibody-based processes are used, cell material is blocked with controlled Fc-receptor blocking reagent; (3) contacting cells with immobilized cell binder material such as magnetic beads and controlled gelatin material, which can contain N-glycolyl-neuraminic acid (interpreted as contacting the HSPCs with a binding molecule including antibodies, claim 1) (paragraphs [0246]-[0249]). Laine teaches that the invention describes reactions effectively modifying cord blood cells by fuscosyl-transferases to produce sialylated and fucosylated N-acetyl-lactosamines on cell surfaces such as sLeX and related structures, wherein the increased sialylated and/or fucosylated structures on cells surfaces are for targeting the cells including for selectin directed targeting of the cells (interpreted as sialylated Lewis X or sLeX; and selectin as a specific binding molecule, claims 1 and 11) (paragraph [0293]), where it is known that sialyl-Lewis-X is a primary ligand for E-selectin, regulating subsequent tumor cell extravasation into distant organs as evidenced by Carrascal (Abstract, Background). Laine teaches the effective specific sialylation methods for the specific cell populations were developed including sialylation methods for modification of human cord blood cells and subpopulations thereof and multipotent stem cell lines (interpreting cord blood cells as a heterogenous population of lin- HSPCs; and sLeX, claim 1) (paragraph [0302]). Laine teaches that the invention is further directed to testing methods for selecting optimal and/or most effective and/or -optimal for a specific cell material-binding reagents from reagents known to have suitable specificity allowing recognition of preferred structures according to the invention including antibodies such as monoclonal antibodies and lectin recognizing same or similar terminal monosaccharide residues structures including involving potential binding to preferred oligosaccharide or glycan sequences according to the invention (interpreted as selecting; and interpreting antibodies as binding molecules, claims 1 and 11) (paragraph [0332]). Laine teaches the positive selection of CD34+ cells (interpreted as selecting cells; and CD34+, claims 1 and 11) (paragraph [0366], lines 1 and 4). Laine teaches that the invention is directed to the selection of a cell population from the preferred cell population according to the present invention, when the cell population demonstrates increased amount of a 3-sialylation when compared with the baseline cell population, wherein specific subpopulations of native cord blood cells express increased amounts of a3-linked sialic acid (interpreted as selecting cells based on the level of sLeX expression including CD34+; selecting based on sLeX expression inherently including cells having the highest 15% sLeX expression level; sLeX+lin- HSPCs; and measuring the amount of sLeX present on individual cells, claim 1) (paragraphs [0296]; and [0298]). Laine teaches that the invention is specifically directed to selection of a cell population from the preferred cell population according to the present invention, when the cell population demonstrates increased amount of a3-sialylation when compared with the baseline cell populations, wherein the quantitative composition means relative amounts of components of individual peaks measured as intensity of the peaks (interpreted as contacting the positively selected cord blood cells including CD34+ cells with a binding molecule; and measuring the amount of sLeX present; and selecting, claim 1) (paragraph [0414]). Laine teaches the quantitative composition means relative amounts of components of individual peaks are measured as intensity of the peaks; and the determination of the quantitative composition of glycomes isolated from animal proteins and quantitative comparisons of the compositions (interpreted as measuring the highest 10% and 15% of expression of sLex, claims 1 and 11) (paragraph [0414]). Laine teaches that the invention is directed to methods involving-binding to the preferred structures on early human cells including the use of a specific binding molecule, referred as "binder", which binds a marker structure on surface of a cell population, such as the use of a protein binding molecule such as a human mono-clonal antibody, lectin or glycan binding molecules (interpreted as contacting samples comprising early human cells (e.g., including CD34+) with a binding molecule (antibodies), claim 1) (paragraph [0323]-[0325]). Lain teaches the positive selection of CD34+/CD133+ from cord blood, wherein labeled cell suspension was passed through a column and the negative cell fraction collected (CD34- or CD133-), such that the column retained positive cells CD34+ or CD133+ (interpreted as selecting CD34+; and selecting for lineage negative cells, claims 1 and 8) (paragraphs [0365]-[0367]). Laine teaches the negative selection of Lin- cells to deplete lineage committed cells (interpreted as selecting for lineage negative cells, claims 1 and 8) (paragraph [0370]). Laine teaches the isolation and culture of bone marrow-derived stem cells and bone marrow-derived MSCs (interpreted as including CD34+, claim 1) (paragraph [0376], lines 1-2). Laine teaches sialylation to produce preferred structures according to the invention from the surfaces of preferred cells (interpreted as contacting CD34+ HSPC with a binding molecule for sLeX, claim 1) (paragraph [0304]). Laine teaches that when the labelled binding molecule is contacted with the cells according to the invention, the cells can be monitored, observed and/or sorted based on the presence of the label on the cell surface, wherein monitoring and observation can occur by regular methods for observing labels such as fluorescence measuring devices, microscopes, scintillation counters and other devices for measuring radioactivity (interpreted as measuring and selecting cells based on the level of sLeX expression including CD34+; inherently including cells having the highest 15% sLeX expression level; sLeX+lin- HSPCs; and measuring the amount of sLeX present on individual cells, claims 1 and 11) (paragraph [0334). Laine teaches that the inventors were able to find differences between cell populations with regard to expression of the sialylated structures (interpreted as sLeX expression, claim 1) (paragraph [0152]).
Laine does not specifically exemplify additional heterogenous populations of CD34+ human HSPCs (claim 7, in part).
Regarding claim 7 (in part), Miller teaches the identification of novel methods that enhance cell trafficking and engraftment to areas of need in a simple and clinically applicable manner (paragraph [0007]). Miller teaches that the cell population can comprise or consist essentially of a population of stem cells, both embryonic and adult and expanded cell populations including embryonic stem cells, cord blood stem cells, placental stem cells, bone marrow stem cells, amniotic fluid stem cells, hematopoietic stem cells, mesenchymal stem cells, neuronal stem cells, cardiomyocyte stem cells, circulating and immobilized peripheral blood stem cells, endothelial progenitor cells, monocyte-derived stem cells, muscle stem cells, germinal stem cells, adipose tissue derived stem cells, exfoliated teeth derived stem cells, hair follicle stem cells, dermal stem cells, parthenogenically-derived stem cells, reprogrammed stem cells such as induced pluripotent stem cells or somatic nuclear transfer and side population stem cells; and the stem cells can be hematopoietic, mesenchymal, neural or cardiomyocyte stems cells, wherein the hematopoietic stem cells can be defined and differentiated as CD38-, lin- or ALDH-bright cells (interpreted as CD38- cells, claim 4) (paragraph [0016]). Miller teaches that cell surface oligosaccharides are highly diversified in their structures and are associated with a variety of cell functions, such that in an inflammatory response, neutrophils or leukocytes bind to injured tissues where the adhesion process occurs; wherein this process has been found to be mediated by the tetra-saccharide sialyl Lewis X on neutrophiles or leukocytes and the receptor ELAM-1 (endothelial leukocyte adhesion molecule 1), a glycoprotein of the selectin family; and that several sialyl lewis analogues and mimetics have been analyzed (paragraph [0048], lines 3-12). Miller teaches the confirmation of fucosylated epitopes on the cells of interest as means of confirming maximal levels of fucosylation can be verified by Flow Cytometry utilizing agents and procedures well-known to someone skilled !n the art, wherein sialyl Lewis X is a fucosylation epitope found on both P and E-selectins, such that by incubation of the FT-treated cells with anti-sLeX mAb HECA 452 (IgM) followed by treatment with FITC-conjugated fragment to the IgM, the sLeX epitopes on the cell surface can be visualized using standard Flow Cytometry procedures (interpreted as contacting cells with a binding molecule; selecting for one or more of CD34+ sLexhigh cells; and interpreting maximal levels as sLeXhigh, claims 1 and 11) (paragraph [0050]). Miller teaches that the patient in need of treatment with a cell population suffers from a condition selected from the group consisting of: an acute leukemia, a chronic leukemia, a myelodysplastic syndrome, a stem cell disorder, a myeloproliferative disorder, a lymphoproliferative disorder, a phagocyte disorder, a histiocytic disorder, a lysosomal storage disease, a congenital immune system disorder, an inherited erythrocyte abnormality, an inherited platelet abnormality, a plasma cell disorder, a tumor and an autoimmune disease including peripheral arterial diseases, ischemic limb injury, diabetes, heart disease, liver disease, bone disease, muscular dystrophy, Alzheimer's disease, ALS, multiple sclerosis, Parkinson's disease, spinal cord injury, stroke, infertility and acute myelogenous Leukemia (AML) (paragraph [0063]; and Table 1), wherein it is known that elimination of drug-resistant leukemia stem cells (LSCs) is a major challenge to cure acute myeloid leukemia, wherein it is known that when CD38 expression on CD34+CD38- LSC-enrich blasts become CD38- Bionic targets, which results in an immune-mediated killing of both CD38- and CD38+ AML blasts, which culminates in LSC depletion as evidenced by Murtadha (Abstract). Miller teaches enhancing homing and engraftment of a therapeutically-administered cell in a patient comprising selecting a patient in need of treatment with a cell population; providing cells that have been contacted with an agent that modifies at least one surface molecule on the cells; resulting in a population of modified cells; and providing or administering the population of modified cells to a patient in need thereof (paragraph [0042]). Laine teaches preferred lectins and binding proteins such as antibodies includes reagents specifically binding to non-human sialic acid (interpreted as specific binding molecules for sLeX, claim 1) (paragraph [0327]). Miller teaches that the FT-treated cells are incubated with anti-sLeX mAb HECA 452 (IgM), followed by treatment with FITC-conjugated fragment to the IgM; and the sLeX epitopes on the cell surface are visualized using standard flow cytometry procedures (interpreted as contacting HSPCs with a binding molecule for sLeX including anti-sLeX mAb; and using flow cytometry to measure an amount of sLeX on individual cells) (paragraph [0077]). Miller teaches an examination of serially collected blood samples in addition to an examination of cells obtained from the bone marrow (interpreted as encompassing a heterogenous population of lin- HSPCs) (paragraph [0078]). Miller teaches that stem cells obtained from one of a number of different sources are incubated ex vivo with fuscosyl-transferase + GDP-fucose at sufficient concentrations and for a sufficient period of time to result in maximal formation of fucosylated product, such as sialyl Lewis X, on the cell surface, such that following treatment, the cell preparation is washed or directly injected into the patient (interpreted as contacting, measuring and selecting one or more sLeXhigh cells based on the level of sLeX expression; and having the highest 15% expression level within the HSPCs, claim 1) (paragraph [0080]). Miller teaches that the fluorescence intensity of samples was evaluated by FACSANTO as shown in Figure 1 (interpreted as measuring by fluorescence intensity and selecting, claim 1) (Figure 1).
It is prima facie obvious to combine prior art elements according to known methods to yield predictable results; the court held that, "…a conclusion that a claim would have been obvious is that all the claimed elements were known in the prior art and one skilled in the art could have combined the elements as claimed by known methods with no change in their respective functions, and the combination would have yielded nothing more than predictable results to one of ordinary skill in the art. KSR International Co. v. Teleflex Inc., 550 U.S. ___, ___, 82 USPQ2d 1385, 1395 (2007); Sakraida v. AG Pro, Inc., 425 U.S. 273, 282, 189 USPQ 449, 453 (1976); Anderson’s-Black Rock, Inc. v. Pavement Salvage Co., 396 U.S. 57, 62-63, 163 USPQ 673, 675 (1969); Great Atlantic & P. Tea Co. v. Supermarket Equipment Corp., 340 U.S. 147, 152, 87 USPQ 303, 306 (1950)”. Therefore, in view of the benefits of inhibiting a disease by administering a cell population to a patient, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify the method of altering cells such as hematopoietic stem/progenitor cells from cord blood cells, bone marrow cells and early human blood cells including CD34+ as disclosed by Laine to include producing a population of modified cells using an agent that modifies at least one surface molecule on the cells including CD38- cells as taught by Miller with a reasonable expectation of success in the cell-surface modification of CD34+ and CD38- cells; in increasing cell modification by sialyltransferases; in depleting structures from a biological material using a sialidase treatment to control the specificity of an antibody; and/or in enhancing homing and engraftment of a therapeutically-administered cell in a patient comprising, wherein the population of modified cells can be provided or administered to a patient in need thereof.
Thus, in view of the foregoing, the claimed invention, as a whole, would have been obvious to one of ordinary skill in the art at the time the invention was made. Therefore, the claims are properly rejected under 35 USC §103(a) as obvious over the art.
Response to Arguments
Applicant’s arguments filed December 16, 2025 have been fully considered and are not found persuasive. Applicants essentially assert that: (a) nowhere in the office action is there an explanation of the difference or differences in the claims (e.g., claim 1) over Laine (Applicant Remarks, pg. 30, last full paragraph); (b) Laine does not measure an amount of sLeX expressed on individual cells within a heterogenous population of CD34+ human HSPCs that have not been modified by fucosylation. Nor does Laine select for HSCs by selecting for one or more of CD34+ sLeXhigh cells based on the level of sLeX expression of the CD34+ human HSPCs that have not been modified by fucosylation (Applicant Remarks, pg. 31, first full paragraph); (c) Laine's suggestion to modify cells enzymatically defeats the entire purpose of the pending claims; i.e., selecting for the cells that naturally express high level of sLex to select for HSCs (Applicant Remarks, pg. 31, last partial paragraph; and pg. 32, first partial paragraph); (d) MS cannot measure glycoproteins on individual cells. Thus, it would be impossible to measure the highest 10% or 15% of expression of sLeX according to claim 1 using Laine's method (Applicant Remarks, pg. 34, first full paragraph); (e) The claims recite selecting for the highest 15% sLeX expressing cells. The claims do not recite selecting all sLeX expressing cells, which would be necessary to "inherently" select for the highest 15% (Applicant Remarks, pg. 35, first partial paragraph; and pgs. 36-37); (f) a POSITA would understand that Laine's para. [0327] discloses lectins and binding proteins such as antibodies that includes reagents specifically binding to non-human sialic acid (Applicant Remarks, pg. 35, last full paragraph); (g) Miller does not disclose or suggest using native levels of sLex to identify and/or isolate subpopulations of HSPCs; for example, Miller does not disclose that human HSCs have high sLeX expression or disclose the sLeX expression on these cells is a marker of hematopoietic "sternness" (Applicant Remarks, pg. 39, first full paragraph); and (h) the claims recite selecting unmodified cells using sLeX expression (Applicant Remarks, pg. 40, first full paragraph through pg. 43).
Regarding (a), Applicant’s assertion that nowhere in the office action is there an explanation of the difference or differences in the claims (e.g., claim 1) over Laine, is not found persuasive. There are no differences between the limitations recited in instant claim 1 and the teachings of the combined references of Laine and Miller. Additionally, the Examiner has clearly indicated what portions of Laine and/or Miller read on the limitations recited in instant claim 1. The combined references of Lain and Miller teach all of the limitations of the claims.
Regarding (b), please see the Examiner’s response in the Office Action mailed August 18, 2025; as well as, the discussion supra regarding the Examiner’s response to Applicant’s arguments. Applicant’s assertion that Laine does not measure an amount of sLeX expressed on individual cells within a heterogenous population of CD34+ human HSPCs; or select for HSCs by selecting for one or more of CD34+ sLeXhigh cells based on the level of sLeX expression of the CD34+ human HSPCs, is not found persuasive. Regarding fucosylation, as noted in the 35 USC 112(b) rejection, it is unclear whether the limitation of ‘human HSPCs that have not been modified by fucosylation’ applies to a complete absence of fucosylation including natural fucosylation by sLeX; whether the term refers to exo- or ex vivo fucosylation; or whether the term refers to something else.
Additionally, instant claim 1 does not recite any specific method of contacting, any specific method of measuring, any specific amount of sLeX expression, and/or any specific method of selecting. For example, a measurement of all cells expressing sLeX inherently includes the highest 15% expression level among the total cells measured. Moreover -
Laine teaches:
Sialyltransferases can be used to produce important cell adhesion structures such as sLex; and the selection of a cell population including increases in a3-sialyation (paragraphs [0284]; and [0295]).
Analyzing human stem cells and cord blood cell populations including the sialylic analysis (sLeX) of cord blood cells including contacting cells with binding material; and reactions modifying cord blood cells by fucosylatransferases in order to produce sialylated and fucosylated N-acetyl-lactosamines on cell surfaces, preferably sLeX (interpreting cord blood to including CD34+ cells; and contacting CD34+ HSPC with a specific binding molecule for sLeX, claim 1).
The invention is directed to methods involving-binding to the preferred structures on early human cells including the use of a specific binding molecule, referred as "binder", which binds a marker structure on surface of a cell population, such as the use of a protein binding molecule such as a human monoclonal antibody, lectin or glycan binding molecules (interpreted as contacting samples comprising early human cord blood cells, encompassing CD34+ cells, with a binding molecule such as an antibody, claim 1).
The inventors were able to find differences between cell populations with regard to expression of the sialylated structures (interpreted as including sLeX expression, claim 1) (paragraph [0152]).
The quantitative composition means the relative amounts of components (here sialylated structures) of individual peaks measured as intensity of the peaks (interpreted as contacting the positively selected cord blood cells including CD34+ cells with a binding molecule; and measuring the amount of sLeX present including the highest 15% and highest 10%; and selecting the highest 15% via individual peak intensity, claim 1) (paragraph [0414]).
Miller teaches:
Sialyl LewisX is a fucosylat10n ep1tope found on both P and E-selectins. By incubation of the FT-treated cells with anti-sLeX mAb HECA 452 (IgM) followed by treatment with FITC-conjugated fragment to the IgM, the sLeX epitopes on the cell surface can be visualized using standard Flow Cytometry procedures (paragraph [0050]).
The combined references of Laine and Miller teach all of the limitations of the claims. Thus, the claims remain rejected.
Regarding (c), please see the discussion supra regarding the Examiner’s response to Applicant’s arguments. Applicant’s assertion that Laine's suggestion to modify cells enzymatically defeats the entire purpose of the pending claims; i.e., selecting for the cells that naturally express high level of sLex to select for HSCs, is not found persuasive. The Examiner notes that instant claim 1 does not recite “selecting for the cells that naturally express high level of sLex to select for HSCs.” Thus, the claims remain rejected.
Regarding (d), please see the discussion supra regarding the Examiner’s response to Applicant’s arguments. Applicant’s assertion that MS cannot measure glycoproteins on individual cells. Thus, it would be impossible to measure the highest 10% or 15% of expression of sLeX according to claim 1 using Laine's method, is not found persuasive. Instant claim 1 does not recite “measuring the sLeX expression in individual cells.” Instead, instant claim 1 recites:
“selecting for one or more CD34+ sLeXhigh cells based on the level of sLeX expression of CD34+ human HSPCs that have not been modified by fucosylation of (2)”
Thus, the claims remain rejected.
Regarding (e), please see the discussion supra regarding the Examiner’s response to Applicant’s arguments. Applicant’s assertion that the claims recite selecting for the highest 15% sLeX expressing cells. The claims do not recite selecting all sLeX expressing cells, which would be necessary to "inherently" select for the highest 15%, is not found persuasive. As noted supra, instant claim 1 recites the term “comprising,” which is open-ended and does not exclude additional, unrecited elements or method steps, including measuring and selecting all cells including those having the highest and lowest levels of expression of sLeX. Thus, the claims remain rejected.
Regarding (f), please see the discussion supra regarding the Examiner’s response to Applicant’s arguments. MPEP 2123(I) states:
“The use of patents as references is not limited to what the patentees describe as their own inventions or to the problems with which they are concerned. They are part of the literature of the art, relevant for all they contain.” In re Heck, 699 F.2d 1331, 1332-33, 216 USPQ 1038, 1039 (Fed. Cir. 1983) (quoting In re Lemelson, 397 F.2d 1006, 1009, 158 USPQ 275, 277 (CCPA 1968)).
A reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill in the art, including nonpreferred embodiments. Merck & Co. v.Biocraft Labs., Inc. 874 F.2d 804, 10 USPQ2d 1843 (Fed. Cir. 1989), cert. denied, 493 U.S. 975 (1989). See also Upsher-Smith Labs. v. Pamlab, LLC, 412 F.3d 1319, 1323, 75 USPQ2d 1213, 1215 (Fed. Cir. 2005) (reference disclosing optional inclusion of a particular component teaches compositions that both do and do not contain that component); Celeritas Technologies Ltd. v. Rockwell International Corp., 150 F.3d 1354, 1361, 47 USPQ2d 1516, 1522-23 (Fed. Cir. 1998) (The court held that the prior art anticipated the claims even though it taught away from the claimed invention. “The fact that a modem with a single carrier data signal is shown to be less than optimal does not vitiate the fact that it is disclosed.”).
Applicant’s assertion that the Examiner's assertion/interpretation is incorrect. A POSITA would understand that Laine's para. [0327] discloses lectins and binding proteins such as antibodies that includes reagents specifically binding to non-human sialic acid, is not found persuasive. The combined references of Laine and Miller clearly teach human HSPCs. As noted supra, the references are relevant for all they teach; and that a reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill in the art. For example -
Laine teaches:
The invention describes specific sialylated structures present on human stem cells and cell populations derived therefrom (interpreted as human HSPCs, claim 1) (Abstract).
The present invention is directed to novel glycan structures found from human stem cell and cord blood cell populations. The invention is specifically directed to specific sialylated structures present on early human cells (interpreted as human HSPCs) (paragraph [0033]).
The inventors of the present invention were able to analyze, in human stem cell and cord blood cell populations, the presence of both NeuAca.3 and NeuAca.6 structures and even NeuGca.3/6, and larger sialylated structures, including also information about the glycan core structures by which the glycans are linked to the cell (paragraph [0007]).
Specific sialyltransferases according to the invention, especially recombinant human sialyltransferases controlled with regard to glycosylation, are preferred for the process described in the present invention (interpreted as human) (paragraph [0012]).
Figure.1- MALDI-TOF mass spectrometric detection of sialylated N-glycans that are indicative of N-glycolylneuraminic acid (Neu5Gc). A Human embryonic stem cell line, B. mesenchymal stem cell line from bone marrow (interpreted as human) (paragraph [0016]; and Figure 1).
Miller teaches:
For P-selectin binding cells can be incubated with anti-CD34+-PE and with P-selectin isolated from human platelets, wherein P-selectin binding can be detected with FITC-labeled S12, a non-blocking mAb to human P-selectin (interpreted as human cells) (paragraph [0071]).
FT-treated cells are incubated with anti-sLeX mAb HECA 452 (IgM), followed by treatment with FITC-conjugated fragment to the IgM; and the sLeX epitopes on the cell surface are visualized using standard flow cytometry procedures (interpreted as contacting HSPCs with a binding molecule for sLeX including anti-sLeX mAb; and using flow cytometry to measure an amount of sLeX on individual cells) (paragraph [0077]).
The combined references of Laine and Miller clearly teach human HSPCs. Thus, the claims remain rejected.
Regarding (g), Applicant’s assertion that Miller does not disclose or suggest using native levels of sLex to identify and/or isolate subpopulations of HSPCs; for example, Miller does not disclose that human HSCs have high sLeX expression or disclose the sLeX expression on these cells is a marker of hematopoietic "sternness," is not found persuasive. Instant claim 1 does not recite using native levels of sLeX to identify and/or isolate subpopulations of HSPCs and/or that human HSCs have high sLeX expression or that the sLeX expression on these cells is a marker of hematopoietic "stemness." The combined references teach all of the limitations of the claims. Thus, the claims remain rejected.
Regarding (h), Applicant’s assertion that the claims recite selecting unmodified cells using sLeX expression, is not found persuasive. Instant claim 1 does not recite selecting unmodified cells using sLeX expression. Thus, the claims remain rejected.
New Objections/Rejections
Claim Rejections - 35 USC § 102
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 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.
(2) Claims 1, 7 and 11 are rejected under 35 U.S.C. 102(a1)/102(a2) as being anticipated by Sackstein et. al. (hereinafter “Sackstein”) (US Patent Application Publication 20200281985, published September 10, 2020) as evidenced by Wognum, Bert (hereinafter “Wognum”) (StemCell Technologies, 2024, 1-12). This is a new rejection necessitated by amendment of the claims in the response filed 12-18-2025.
Regarding claims 1 and 11, Sackstein teaches that a variety of methods can be utilized to prepare the population of cells for administration to the subject including, where the population is prepared by: (i) contacting the cell or a population of cells with glycosyltransferase together with appropriate donor nucleotide sugar; (ii) glycan engineering can be used to sialofucosylate CD44 to enforce the expression of Hematopoietic Cell E-selectin Ligand (HCELL), by glycosyltransferase-enforced expression of fucose residues (fucosylation), sialic acid residues (sialylation), or both (sialofucosylation); (iii) non-enzymatic methods can be used to covalently or non-covalently bind E-selectin and/or L-selectin ligands to cell surfaces, such as sLex (sialyl-Lewisx), glycomimetics and/or peptidomimetics of sLex glycans, sLea (sialyl Lewisa), glycomimetics and/or peptidomimetics of sLea glycans, and other moieties that bind E-selectin; and/or (iv) L-selectin can be non-covalently bound to cell surfaces using biotin-streptavidin pairs or covalently bound to the cell surfaces; whether covalent or non-covalent, the binding can be direct or via a linker such as, for example, phage display particles or antibodies that bind E-selectin and/or L-selectin can be covalently or non-covalently bound to the cell surface, in each case mediating adherence of treated cells to E-selectin and/or L-selectin (paragraph [0018]). Sackstein teaches that in cases where cells undergo glycan engineering to enforce sLex expression or undergo decoration with sLex structures (e.g., via avidin-streptavidin techniques), measurement of increased sLex expression on treated cells can be performed by fluorescence staining with mAb HECA452 or any other mAb which recognizes sLex determinants, followed by flow cytometry to detect cell fluorescence intensity, wherein the predetermined fluorescence threshold of the modified cell population is determined by first analyzing a sample of native (untreated) cells, such that increases in sLex of treated cells is defined as increase percentage of marker positive cells (e.g., HECA452-reactive cells) of greater than 10% compared to native population of cells and/or by a 10% increase in mean channel fluorescence intensity over that of the baseline (untreated) cell population (interpreted as contacting cells with a binding molecule for sLeX; interpreting fluorescence as measuring an amount of sLeX expressed; and interpreting FACS and increasing sLeX expression >10% to include selecting cells having the highest 10% or 15% sLeX expression level, claim 1and 11) (paragraph [0021], lines 1-15). Sackstein teaches that both heterogenous and homogenous cell populations are contemplated for use with the methods and compositions described (interpreted as a heterogeneous population of cells, claims 1 and 11) (paragraph [0141], lines 1-3). Sackstein teaches that any type of cell can modified and used in the treatment methods described herein; and for animal use it is preferable that the cell is of animal origin, while for human use it is preferably that the cell is a human cell, wherein the cell can be a primary cell, e.g., a primary hepatocyte, a primary neuronal cell, a primary myoblast, a primary mesenchymal stem cell, primary progenitor cell, or it can be a cell of an established cell line or of a culture expanded cell, wherein the cell can be of any cell type including, but not limited to embryonic stem cells, adult stem cells, induced pluripotent stem cells, blood progenitor cells, tissue progenitor cells, epithelial, endothelial, neuronal, adipose, cardiac, skeletal muscle, fibroblast, immune cells (e.g., dendritic cells, monocytes, macrophages, leukocytes, etc.), etc. (interpreted as human cells including human HSPCs, claims 1 and 11) (paragraph [0139], lines 1-22). Sackstein teaches that the cell can be a cell line, a stem cell (e.g., a mesenchymal stem cell, a hematopoietic stem cell, a tissue stem/progenitor cell (for example, a neural stem cell, gastrointestinal stem cell, myocyte stem cell, cardiomyocyte progenitor/stem cell, endothelial progenitor cell, or pulmonary stem cell), an umbilical cord stem cell, or an embryonic stem cell, or a primary cell isolated from any tissue including, but not limited to brain, liver, lung, gut, stomach, fat, muscle, testes, uterus, ovary, skin, spleen, endocrine organ and bone, and the like (interpreted as human cells including HSPCs, claim 1) (paragraph [0139], lines 31-40), wherein it is known that CD34+ is the most important marker of primitive human hematopoietic cells, wherein CD34+ is expressed in nucleated human bone marrow cells, cord blood cells, and in normal peripheral blood cells as evidenced by Wognum (pg. 5, col 2; first full paragraph). Sackstein teaches a method of enhancing cell delivery into a target tissue of a subject and/or enhancing tissue colonization in the target tissue of the subject, the method comprising: administering to the subject a population of cells that express an
E- selectin ligand and/or an L-selectin ligand, the population expressing the E-selectin ligand and/or
L-selectin ligand at a level that exceeds the level of expression of a native population of the cells (interpreted as selecting cells with the highest 10-15% sLeX expression, claims 1 and 11) (paragraph [0143]).
Regarding claim 7, Sackstein teaches that the cell can be a cell line, a stem cell (e.g., a mesenchymal stem cell, a hematopoietic stem cell, a tissue stem/progenitor cell (for example, a neural stem cell, gastrointestinal stem cell, myocyte stem cell, cardiomyocyte progenitor/stem cell, endothelial progenitor cell, or pulmonary stem cell), an umbilical cord stem cell, or an embryonic stem cell, or a primary cell isolated from any tissue including, but not limited to brain, liver, lung, gut, stomach, fat, muscle, testes, uterus, ovary, skin, spleen, endocrine organ and bone, and the like (interpreted as HSPC from bone marrow, umbilical cord blood, etc., claim 7) (paragraph [0139], lines 31-40).
Sackstein meets all the limitations of the claims and, therefore, anticipates the claimed invention.
Conclusion
Claims 1, 3, 4, 7, 8 and 11 are rejected.
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 AMY M BUNKER whose telephone number is (313) 446-4833. The examiner can normally be reached on Monday-Friday (6am-2:30pm).
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, Heather Calamita can be reached on (571) 272-2876. 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.
/AMY M BUNKER/Primary Examiner, Art Unit 1684