DETAILED ACTION
Applicant’s amendment and Arguments/Remarks received on 02 February 2026 have been entered. Claims 1-2 and 4-15 were previously pending in the application. No claims have been cancelled, and no new claims have been added by Applicant. Claims 1-2 and 4-15 are currently pending in the application. Claims 1, 4, 7, 10, 12, 14, and 15 are independent claims.
Applicant’s election of the following species remains in effect in the instant application:
Sample: (a) a human acute myeloid leukemia (AML) sample,
Model system: (b) animal model,
Protein/gene/drug: (a) hIL-8,
Method of treating animal model with the hIL-8 or hIL-8 agonist (as elected in 3): (a) administering the hIL-8.
Claims 4-14 remain withdrawn from consideration as being directed to a nonelected species, there being no allowable generic or linking claim.
Claims 1-2 and 15 are currently pending and under examination in the instant application. An action on the merits follows.
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA . The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Information Disclosure Statement
The information disclosure statement filed 02 February 2026 has been considered by the Examiner. Examiner notes the filing of IDS Size Fee assertion, as required under 37 CFR 1.98, indicating that no IDS size fee is required under 37 CFR 1.17(v) at this time.
Claim Rejections - 35 USC § 112(b)
The rejection of amended and previously presented claims 1-2 and 15 under 35 U.S.C. 112(b) as failing to particularly point out and distinctly claim the subject matter which the inventor(s) regards as the invention for multiple issues of indefiniteness is withdrawn over amended and previously presented claims 1-2 and maintained over amended claim 15 in view of Applicant’s amendments clarifying the claims.
Applicant has amended independent claim 15 to overcome issues of indefiniteness arising from recitation of “determining whether or not the drug reduces growth or differentiation or subclonal complexity or increases apoptosis of the human AML, the human MDS, the human IL-8 dependent tumor, human preleukemia cells, or the human preleukemia clone or subclone xenograft” in lines 12-15 with respect to the antecedent basis for a) the human AML, b) the human MDS, c) the human IL-8 dependent tumor, d) human preleukemia cells, or e) the human preleukemia clone or subclone. Applicant’s claim now recites, “determining whether or not the drug reduces growth or differentiation or subclonal complexity or increases apoptosis of the human AML sample, the human MDS sample, the human IL-8 dependent tumor sample, human preleukemia cells sample, or the human preleukemia clone or subclone xenografted into the non-human animal model”, which is still indefinite because it is unclear what the reducing growth or differentiation or increasing apoptosis of the human AML sample (as elected) is relative to in that no control samples or conditions are recited within the claim.
As such, the metes and bounds of the claim still cannot be determined.
**The following new rejection is necessitated by amendments to the claims.
Amended and previously presented claims 1-2 are newly 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. Previously presented claim 2 is included in this rejection due to its dependence on independent claim 1.
Amended independent claim 1 newly recites, “wherein the human AML sample… has been xenotransplanted into a non-human animal model” in lines 8-11, which is indefinite because it is unclear whether the xenotransplantation of the human AML sample into a non-human animal model is an active step of the method and whether “has been xenotransplanted into a non-human animal model” is meant to be the means whereby the non-human xenograft animal model recited in lines 4 and 8 was generated or whether the xenotransplantation into a non-human animal model is creating an alternative xenograft animal model. Therefore, it is unclear whether the human AML sample is xenografted into the xenograft animal model recited in lines 4 and 8. If xenografted into an alternative non-human animal model, it is unclear whether the adding the hIL-8 to the human AML sample by administering exogenous hIL-8 to the non-human xenograft animal model is before or after the human AML sample is xenotransplanted into the non-human animal model.
As such, it is further unclear whether the enhancing growth of the human AML sample is enhancing growth of the human AML sample xenotransplanted in the xenograft animal model, whether the growth enhancement occurs within the xenograft animal model before or after the human AML sample is in the non-human animal model, or whether the growth enhancement occurs within the alternative non-human animal model following xenotransplantation of the human AML sample. Accordingly, it is also unclear what that growth enhancement is relative to under each of the various scenarios of engraftment described above.
As such, the metes and bounds of the claim cannot be determined.
Claim Rejections - 35 USC § 112(a)
The rejection of amended and previously presented claims 1-2 and 15 under 35 U.S.C. 112(a) for while being enabling for:
A method of enhancing growth of a human acute myeloid leukemia (AML) sample in a non-human xenograft animal model, the method comprising adding human interleukin-8 (hIL-8) to the human AML sample by administering exogenous hIL-8 to the non-human xenograft animal model by injection, wherein the human AML sample has been xenotransplanted into the non-human animal model to produce the non-human xenograft animal model, wherein the non-human animal model is immunocompromised, and wherein hIL-8 is present in an amount effective to enhance growth of the human AML sample in the non-human xenograft animal model; and
A method for screening for drugs against human AML, the method comprising administering a drug to a non-human xenograft animal model produced by xenotransplanting a human AML sample into a non-human animal model and administering exogenous hIL-8 to the non-human animal model by injection, wherein the hIL-8 is present in an amount effective to enhance growth of the human AML sample in the non-human xenograft animal model, and determining whether or not the drug reduces growth or differentiation or subclonal complexity or increases apoptosis of the human AML sample xenografted in the non-human animal model, wherein the non-human animal model is immunocompromised;
does not reasonably provide enablement for:
A method of enhancing growth of a human acute myeloid leukemia (AML) sample in any non-human xenograft animal model, the method comprising adding human interleukin-8 (hIL-8) to the human AML sample by administering exogenous hIL-8 to any animal model by injection, wherein hIL-8 is present in an amount effective to enhance growth of the human AML sample in the non-human xenograft animal model; or
A method for screening for drugs against human AML, the method comprising administering a drug to any non-human xenograft animal model produced by xenotransplanting a human AML sample into any animal model and administering exogenous hIL-8 to the non-human animal model by injection, wherein the hIL-8 is present in an amount effective to enhance growth of the human AML sample in the non-human xenograft animal model, and determining whether or not the drug reduces growth or differentiation or subclonal complexity or increases apoptosis of the human AML xenograft in the animal;
is withdrawn in view of Applicant’s amendments to the claims in accordance with the identified enabled scope for the elected species.
Note that this scope of enablement rejection under 35 U.S.C. 112(a) is being withdrawn with respect to the elected species only. If at some point the nonelected species are rejoined for consideration, they will then be considered for issues of enablement and a new rejection may be applied at that time.
Claim Rejections - 35 USC § 103
The rejection of amended and previously presented claims 1-2 and 15 under 35 U.S.C. 103 as being unpatentable over Corrado et al. [2014, Cancer Letters, 348, 71-76]; in view of Hemmati et al. [2017, Frontiers in Oncology, 7, 265, 1-17]; Schinke et al. [2015, Blood, 125(20), 3144-3152]; and Bhatia et al. [2016, Expert Opinion on Drug Discovery, Vol. 11(11), 1081-1091], cited in a prior action, is maintained. Applicant's amendments to the claims and arguments have been fully considered but have not been found persuasive in overcoming the rejection for reasons of record as discussed in detail below.
Applicant amended the claims to address issues of indefiniteness and to align with the enabled scope for the elected species. However, the amendments do not alter the scope in such a way as to overcome a finding of obviousness under 35 U.S.C. 103 over the cited references of Corrado, Hemmati, Schinke, and Bhatia in that Corrado already teaches wherein the animal model is a NOD/SCID immunocompromised mouse model [column 4 ¶ 5].
Applicant argues that:
There is no reasonable expectation of success in combining the teaching of the cited art to arrive at the instant invention because CML and AML are distinct conditions with distinct pathophysiology, risk factors, and treatment strategies;
The studies Hemmati describes demonstrating that inhibition of IL-8 signaling inhibited leukemia progression and improved survival in an AML xenograft mouse model were obtained with a stable AML cell line, U937, which is known to efficiently xenotransplant into mice and has been used an alternative to using patient-derived cells, which have notoriously poor xenotransplantation efficiency;
The only data described by Hemmati on the effects of primary AML cells treatment with IL-8 was obtained in cell culture, and not in xenografts as required by claims 1 and 15;
The ordinarily skilled artisan would have to make several significant assumptions before attempting to use IL-8 treatment to improve xenotransplantation efficiency of primary AML cells in immunocompromised mice, including:
Assuming IL-8 signaling would have the same or comparable effect on CML and AML cells xenotransplanted in mice despite the fact that the nature of the two conditions is sufficiently different to display different and even opposing effects of certain cytokines,
Assuming that the prosurvival effect of IL-8 on stable AML cell lines that display an effective xenotransplantation even in its absence is equivalent to improved xenotransplantation of primary AML cells due to IL-8 signaling, and
Assuming that the prosurvival effects of IL-8 on primary AML cell in culture are equivalent to improving the ability of these cells to efficiently establish a xenotransplant in mice;
Bhatia flatly teaches away from administration of exogenous cytokines in mouse leukemia models in the course of pre-clinical drug testing by noting that the administration of exogenous cytokines is “not appropriate for longer readouts” and that injection of cytokines results in the production of non-physiological systemic concentrations; and
Applicant’s have demonstrated unexpected results, including the data in Figure 2 addressed in the prior action and the data presented in Figure 3, wherein the data in Figure 3 shows that xenotransplantation of primary AML cells into NSG mice pre-transplanted with hIL-8 transgenic and doxycycline-induced congenic bone marrow cells leads to a more than 10-fold increase of AML cell engraftment, which is 3-fold higher than the results observed with IL-8 stimulated CML cells in Corrado, which would be viewed by a skilled artisan as a major improvement over the presently available models in light of the well-known difficulty of establishing primary AML cell xenografts in mice.
However, this is not agreed.
In response to Applicant’s arguments against the references individually, it is noted that the test for obviousness is not whether the features of a secondary reference may be bodily incorporated into the structure of the primary reference; nor is it that the claimed invention must be expressly suggested in any one or all of the references. Rather, the test is what the combined teachings of the references would have suggested to those of ordinary skill in the art. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981). One cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). Further, the Examiner recognizes that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). In addition, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
Specifically, regarding Applicant’s arguments 1) and 4)a., although CML and AML are distinct conditions which each have distinct pathophysiology, risk factors, and treatment strategies with different and even opposing effects of certain cytokines, the present claims specifically relate to the effect of IL-8 on the growth of the cells such that IL-8 enhances the growth of a human AML sample in a non-human xenograft animal model. The claims do not address the diverse pathophysiology, risk factors, and treatment strategies of the disease nor the effects of “certain cytokines” other than IL-8 itself.
Corrado was relied on for teaching a method of enhancing growth of a human chronic myelogenous leukemia (CML) sample in a non-human xenograft animal model (e.g., a NOD/SCID mouse), the method comprising adding human interleukin-8 (hIL-8) to the sample by administering exogenous hIL-8 to the animal model by injection, wherein hIL-8 is present in an amount effective to enhance growth of the human CML sample in the non-human xenograft animal model [column 4 ¶ 5, column 8 ¶ 2, Figure 5].
Additionally, Hemmati was cited for teaching Hemmati that IL-8 plays an important role in hematologic malignancies, including both CML and AML [column 19 ¶ 1-2]. Hemmati further teaches that knockdown or pharmacologic inhibition of the IL-8 receptor CXCR2 with the inhibitor SB332235, thereby inhibiting IL-8 signaling, in AML cell lines and in MDS and AML patient samples led to G0/G1 cell cycle arrest, and also inhibited leukemia progression in a xenograft mouse model [column 19 ¶ 1-2]. Hemmati additionally teaches that AML cells cocultured with bone marrow stromal cells stimulates IL-8 production by the stroma, which in turn promotes the survival of AML cells [column 19 ¶ 2]. Hemmati further teaches that IL-8 secreted by the bone marrow microenvironment promotes survival of a CML cell line in a xenograft mouse model in vivo [column 19 ¶ 2].
Therefore, the combined teachings of Corrado and Hemmati demonstrate that IL-8 is a prosurvival chemokine for both CML and AML, despite the differences of the conditions. The skilled artisan is not required to assume that IL-8 signaling would have the same or comparable effect on CML and AML cells xenotransplanted in mice, but merely that IL-8 treatment of an AML cell xenograft would enhance growth of the AML sample in a non-human xenograft animal model. Given the teachings that IL-8 is pro-survival for both CML and AML, a skilled artisan would have a reasonable expectation that IL-8 administration to an AML cell xenograft would demonstrate at least some growth enhancement, as was seen for the CML cell xenograft of Corrado.
Regarding Applicant’s arguments 2) and 4)b., note that the claims as written require that the xenotransplanted sample be a human AML sample, but do not require that the sample be or comprise primary patient-derived cells. Further, the teachings of Hemmati that IL-8 signaling inhibited leukemia progression and improved survival in an AML xenograft mouse model would not be dismissed by the ordinarily skilled artisan as irrelevant to human AML samples merely because the xenografts used were able to grow well in the xenograft animal model in the absence of exogenous IL-8. The fact that the cell line xenograft is sensitive to IL-8 signaling inhibition would alternatively indicate a possible role for IL-8 in promoting the survival of the AML cell lines in the xenograft and would lead an ordinarily skilled artisan to consider that IL-8 expression in the cell lines may be a factor in their improved xenotransplantation efficiency.
Accordingly, given the teachings that IL-8 signaling inhibition decreases leukemia progression for the cell line xenograft, a skilled artisan would be motivated to administer IL-8 to a human AML sample xenograft to promote survival of the xenotransplanted cells. An ordinarily skilled artisan would not be required to assume that the prosurvival effect of IL-8 on stable AML cell lines is equivalent to improved xenotransplantation of primary AML cells due to IL-8 signaling, merely that the prosurvival effects of IL-8 indicate a reasonable expectation that the administration if IL-8 may support enhanced growth of a human AML sample in a non-human xenograft animal model. The teachings of Hemmati that IL-8 signaling inhibition decreases leukemia progression provides a reasonable expectation for the ordinarily skilled artisan to expect some amount of enhanced growth of a human AML sample in a non-human xenograft animal model.
Regarding Applicant’s arguments 3) and 4)c., note that the claims as written do not require that the IL-8 administration cause a successful xenograft of primary human AML samples. The claims as written merely require that the IL-8 administration enhance the growth of any human AML sample in a non-human xenograft animal model.
Hemmati teaches:
“In a coculture study with AML patient samples, IL-8 was secreted by the bone marrow microenvironment as a result of hypoxia (O2 1% for 48 h) by AML cells more than by normal cells (122)… Abdul-Aziz et al. also demonstrated that AML cells cocultured with bone marrow stromal cells secrete macrophage inhibitory factor, which stimulates IL-8 production by the stroma, which in turn promotes the survival of AML cells (123). Furthermore, shRNA knockdown of IL-8 inhibited the prosurvival effects of the stroma on AML cells (123). Cordycepin, an adenosine analog, blocks mesenchymal stromal/stem cells from expressing VCAM-1 or IL-8 via impaired NF-κB signaling. The inhibitory effects of cordycepin in preclinical AML models support the importance of targeting the crosstalk between AML cells and the bone marrow niche in the treatment of AML. Combined with an adenosine deaminase inhibitor, cordycepin prolonged survival in U937 and K562 xenograft mouse models of AML (124). While IL-8 could be useful as a biomarker in multiple hematologic malignancies and could be a promising therapeutic target for MDS and AML, no clinical trials have been initiated targeting IL-8 or its downstream mediators.” [column 19 ¶ 2].
Given the extensive teachings of Hemmati on work down with IL-8 in cell culture, including conditions which recapitulate at least some of the effects of the in vivo microenvironment, such as co-culture with bone marrow stromal cells and hypoxia, wherein IL-8 is repeatedly shown to be a pro-survival factor for human AML samples, the ordinarily skilled artisan would have had a reasonable expectation of success that administration of exogenous IL-8 would enhance growth of a human AML sample, whether in culture or in a xenograft animal model. The ordinarily skilled artisan would not have to assume that the prosurvival effects of IL-8 on primary AML cell in culture are equivalent to improving the ability of these cells to efficiently establish a xenotransplant in mice, but merely have a reasonable expectation that IL-8 administration would enhance growth of a human AML sample in a non-human xenograft animal model.
Regarding Applicant’s argument 5), Bhatia was cited for teaching that the xenograft model is one of the most extensively accepted models for examining the response of therapy directly on human malignant cells, engrafted into immunocompromised animals [column 2 ¶ 2], and that xenograft models allow the selection of potential therapeutic compounds by initially testing them on human leukemic cell lines [column 2 ¶ 2- column 3 ¶ 1]. Bhatia further teaches that the more complex the emerging antileukemic therapy, the higher the need for complex disease models which closely recapitulate the human phenotype, with the aim to adapt murine models to the complexity of the human disease phenotype, including improving engraftment to allow the emergence of all leukemia subclones to better represent the tumor heterogeneity and cover more oncogenomic variations reported clinically [column 14 ¶ 3- column 15 ¶ 2]. Therefore, Bhatia provides the motivation to use a xenograft animal model to test potential therapeutic interventions as well as the motivation to improve the engraftment models. Bhatia was not cited for teaching the motivation and reasonable expectation of success for the administration of exogenous hIL-8 to enhance the growth of the human AML sample, which, as discussed above, was provided by the teachings of Hemmati.
Regarding Bhatia’s teachings that the administration of exogenous cytokines is “not appropriate for longer readouts” and that injection of cytokines results in the production of non-physiological systemic concentrations [column 5 ¶ 2], note that while the cited references must be considered in their entirety, including portions that would lead away from the claimed invention, the entirety of the cited references includes all of the cited references and the teachings that would motivate an ordinarily skilled artisan to modify the base reference to arrive at the instant invention as claimed. Corrado teaches the administration of exogenous IL-8 to promote growth of a leukemia xenograft. As such, the administration of IL-8 is a limitation taught by the base reference which does not require additional teachings and motivation to modify. Further, Applicant has not claimed either longer readouts or physiological systemic concentrations of IL-8 within the non-human xenograft animal model. The claims merely require some amount of administration of hIL-8 present in an amount to effectuate any amount of enhanced growth of any human AML sample within the non-human xenograft animal model. Therefore, teachings by Bhatia that injection of exogenous human cytokines is not appropriate for longer readouts and often results in the production of non-physiological systemic concentrations is not a teaching away modifying the xenograft animal model of Corrado to arrive at the instant invention as claimed.
Regarding Applicant’s argument 6), as discussed in the prior action, the level of enhanced engraftment presented as unexpected results in the instant specification Figure 2 is comparable to the level of enhanced engraftment presented by Corrado for CML xenografts administered hIL-8, as seen in Figure 5. Accordingly, the increased engraftment presented in the instant specification is not unexpected based on the prior art.
Regarding Figure 3, note that the data presented in Figure 3, showing a 10-fold increase in engraftment over untreated controls, was obtained according to the following procedure:
“We have generated a new transgenic mouse model in which we inserted a doxycycline-inducible human IL-8 transgene into the immunocompromised NSG mouse strain. We then performed congenic transplantation of hIL-8-transgenic bone marrow cells into 8 parental NSG mice, followed by doxycycline-triggered induction of hIL-8 in 4 of the recipient mice. 4 uninduced mice served as a control. We then xenotransplanted 5x106 leukemic cells from an AML patient into these animals and determined AML cell engraftment in the bone marrow 4 months post- transplantation. AML cells are notoriously difficult to transplant and in most cases are not suitable for expansion and use in patient derived xenograft (PDX) models due to low engraftment (here: control showed very low engraftment of only 4% ion average). The transplanted recipients with induced hIL-8 showed strikingly higher engraftment of primary AML patient cells (average: 42.2%, 10.4-fold increase, p = 0.0106, N=8). These data demonstrate that human IL-8 is indeed critical for the engraftment and maintenance of human AML stem cells (AML-initiating cells) in vivo.” [0032].
It is also noted that any evidence of unexpected results must be commensurate in scope with the claimed invention, and that a greater, or greater than additive, effect is not necessarily sufficient to overcome a prima facie case of obviousness because such an effect can either be expected or unexpected MPEP 716.02 (a) and (d). Whether the unexpected results are the result of unexpectedly improved results or a property not taught by the prior art, the "objective evidence of nonobviousness must be commensurate in scope with the claims which the evidence is offered to support." In other words, the showing of unexpected results must be reviewed to see if the results occur over the entire claimed range. In re Clemens, 622 F.2d 1029, 1036, 206 USPQ 289, 296 (CCPA 1980).
Specifically, note that the data presented in Figure 3 was obtained by a method completely different from the methods claimed in instant claims 1 and 15. The mice were not administered exogenous hIL-8 by injection following transplantation, as required by the claims. Instead, the mice had a prior transplantation of bone marrow cells which express exogenous hIL-8 secondary to doxycycline induction, which doxycycline induction was performed prior to xenotransplantation of the human AML sample into the mice. Therefore, the results obtained from the prior and ongoing induced expression of the hIL-8 within the bone marrow of the mice is not expected to be comparable to the injection of exogenous hIL-8 into the mouse following xenotransplantation. Accordingly, the data presented in Figure 3 is not commensurate in scope with the claimed invention and is not convincing as support for unexpected results according to the instantly claimed invention.
Therefore, Applicant’s amendments and arguments do not overcome a fining of obviousness under 35 U.S.C. 103, and the rejection is maintained.
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 Dr. KATIE L PENNINGTON whose telephone number is (703)756-4622. The examiner can normally be reached M-Th 8:30 am - 5:30 pm, Friday 8:30 am - 12:30 pm CT.
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DR. KATIE L. PENNINGTON
Examiner
Art Unit 1634
/KATIE L PENNINGTON/Examiner, Art Unit 1634
Dr. A.M.S. Wehbé
/ANNE MARIE S WEHBE/Primary Examiner, Art Unit 1634
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