Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 08/05/2026 has been entered.
Application Status
Claims 1 and 9-24 are pending and examined on the merits herein.
Grounds of Rejection Withdrawn
Previous objection to claim 1 is withdrawn in view of claim amendment.
All previous rejections of claims 2-8 are rendered moot by claim cancellation.
Previous rejections of claims 1 and 9-24 under 35 U.S.C. 103 are withdrawn in view of claim amendments.
Claim Rejections - 35 USC § 103New Rejection Necessitated by Amendment
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 1, 10-12, 15-16, 19 and 24 are rejected under 35 U.S.C. 103 as being unpatentable over Latik (International Journal of Molecular Sciences. 2019; 20(21):5347; cited in OA 12/09/2025), Fransen ( Int. J. Cancer, 132: 1971-1976; cited in OA 05/05/2026), Wainwright (Front Immunol. 2013 May 15;4:116; cited in OA 05/05/2026), and Ma (J. Appl. Polym. Sci., 116: 1985-1993; PTO-892).
Regarding claims 1 and 10, Latik teaches that glioblastoma (GBM) is the most common primary central nervous system cancer and has an extremely expansive course where aggressive tumor growth correlates with short median overall survival (abstract). Latik further teaches that the interaction of the proteins programmed death-1 (PD-1) and programmed cell death ligand (PD-L1) creates an immunoregulatory axis promoting invasion of glioblastoma multiforme cells in the brain tissue and PD-L1 expression on glioblastoma surface promotes PD-1 receptor activation in microglia, resulting in the negative regulation of T cell responses (abstract). Latik further teaches that studies demonstrated that the expression of PD-L1 in glioma correlates with WHO grading and could be considered as a tumor biomarker and further that studies in preclinical GBM mouse models confirmed the safety and efficacy of monoclonal antibodies targeting the PD-1/PD-L1 axis including significant regression of tumor mass and longer animal survival time were observed (abstract). Latik further teaches that the CNS was believed to be an immune privileged organ based on the blood brain barrier (BBB) and lack of a typical lymphatic system but several studies have shown that the CNS has a specific connection with the deep cervical lymph nodes (page 2, para 2). Latik further teaches that the BBB is dysfunctional in patients with GBM and that the concomitant inflammation enhances the CNS interplay with the lymphatic system (page 2, para 3). Latik further teaches that monoclonal antibodies (mAbs) have produced a turning point in the immunotherapy of cancer that has been FDA approved in a number of cancers and are currently under investigation for treatment of GBM including nivolumab and pembrolizumab (section 8, page 7-8; Table 1). Latik further teaches that recent clinical studies on PD-1L/PD-1 inhibitors have presented effective responses, even though the trials do not confirm critical extension of OS, these inhibitors may confer different benefits if combined with standard therapies (summary).
Latik does not teach that the anti-PD-1 antibody is in a composition comprising a thermosensitive PCL-PEG-PCL hydrogel administered to the deep cervical draining lymph node.
Regarding claims 1, 11, and 24, Fransen teaches that tumor-draining LNs (TDLNs) have a dubious position as they can induce antitumor T-cell responses but are at the same time under the direct influence of the often immunity-dampening tumor microenvironment (page 1971). Fransen further teaches that the APCs in the tumor mass and TDLNs frequently display a certain level of maturation owing to the presence of endogenous danger signals from the growing tumor but still yield inadequate T cell priming without costimulation (page 1971). Fransen further teaches that Immune suppression within the tumor microenvironment and TDLNs is characterized by an unfavorable mixture of immunosuppressive cytokines, growth factors and various
immunosuppressive cell populations including Treg suppression of effector T cells (page 1972, col 1, para 2). Fransen further teaches that increased presence of Tregs in TDLNs compared to nondraining LNs has been well established in both animal
models and cancer patients and that Treg accumulation in tumor bearing animals can result from either proliferation of natural, thymic-differentiated Tregs or conversion of naive CD4þ T cells into Tregs (page 1973, col 1, para 3). Fransen further teaches that there are toxic side effects from systemic administration of immune activating targets (page 1972, col 2, para 2) and that one way of reducing side effects is to exclusively target the tumor lymphoid drainage area (page 1973, col 1, para 3). Fransen further teaches an important role for slow-release formulations in targeting immune-stimulating agents to the TDLNs, because they keep the tumor-draining area, or regional basin,
in a proinflammatory status for a prolonged period of time, allowing the T-cell response to fully develop and the immune suppression to remain blocked while keeping the concentration of an immune stimulatory agent remains high only locally and not systemically, thereby preventing undesirable side effects and unspecific overstimulation (page 1974, col 1, para 2). Fransen further teaches that the discovery of several new sustained release systems, such as hydrogels opens up possibilities for targeted treatments and further that the targeted approach for delivery of immunotherapy lends itself without difficulty for combined use with other cancer treatments, like adoptive T-cell transfers and chemotherapy which has been described to have immune-enhancing properties (page 1974, col 1, para 3). Fransen further teaches that the TDLNs are the key locations for important antitumor immunological processes, and therefore the quintessential targets for immune-modulating therapies in solid tumor-bearing subjects because both priming of tumor-specific T-cell responses and immune suppression occur in this area, local therapies designed to balance this equilibrium toward more effective
antitumor T-cell responses will be most efficient (page 1974, col 2, para 3).
Regarding claims 1 and 24, Wainwright teaches that one of the hallmark features of GBM is the accumulation of regulatory T cells which are associated with the promotion of pathological outcomes and immunotherapeutic failure (abstract). Wainwright further teaches that tumors recruit Tregs which is associated with an impaired immune response and further that elimination of the CD25+ Treg population in preclinical studies resulted in a CD8+ mediated tumor rejection in various models (Page 3, col 1, para 3). Wainwright further teaches that most Treg within the tumor in glioma are thymus derived, which travel through the cervical lymph node (Figure 1). Wainwright further teaches that targeting these Treg could be therapeutically beneficial with fewer side effects than systemic treatment in line with the dogma that Treg depletion is associated with more effective anti-glioma response and survival (Page 4, col 1, para 1). Wainwright further teaches that given the pathogenic role that Treg mediate in the context of malignant brain tumors, an obvious therapeutic direction is their selective depletion from both the tumor microenvironment and/or secondary lymphoid tissues, wherein GBM drains to the cervical draining lymph node (Fig 3). (page 7, col 1, para 4; Fig 3).
Regarding claims 11-12, 15-16, and 19, Wainwright teaches that Treg accumulation in brain tumors is dependent on the expression of IDO and that IDO is an attractive target for therapeutic consideration given its minimal expression in normal CNS-resident neurons and glia, versus its high expression in GBM (page 11, col 2, para 2). Wainwright further teaches that IDO promotes glioma genesis by increasing the recruitment of Treg to brain tumors (page 11, col 2, para 2) as well as numerous clinical studies targeting inhibition of IDO as adjuvant immunotherapy in GBM (Table 2). Wainwright further teaches that tenzolomide is a second generation DNA alkylating agent, methylates the O6 position of guanine causing double stranded DNA cross-linking (page 7, last para). Wainwright further teaches that although TMZ is well-tolerated and has an overall beneficial impact on patient survival and is the current standard of car for glioma patients (page 8).
Regarding claim 1, Ma teaches that that PCL-PEG-PCL thermosensitive hydrogels are biodegradable and injectable to allow controlled drug delivery for therapeutic proteins (abstract). Ma further teaches that PCL-PEG-PCL hydrogels showed the ability to control the release of incorporated BSA and HRP with conserved biological activity and further that the hydrogels were able to sustain at least 45 days by subcutaneous injection, which is very useful for its application as in situ gel-forming drug delivery systems (conclusion).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to treat GBM with an anti-PD-1 antibody as taught by Latik in a composition with a PCL-PEG-PCL gel as taught by Ma, administered to a draining lymph node as taught Fransen which is the deep cervical draining lymph node for GBM and also treated with chemotherapy as taught by Wainwright. The ordinary artisan would have been motivated to do so because Latik teaches that PD-1/ PD-L1 creates an immunoregulatory axis promoting invasion of glioblastoma multiforme cells in the brain tissue and negative regulation of T cell responses. Latik further teaches that preclinical mouse studies demonstrated safety and efficacy of PD-1 targeting antibodies as well as recent clinical studies on PD-1L/PD-1 inhibitors that have presented effective responses. Fransen teaches that the TDLNs are the key locations for important antitumor immunological processes, and therefore the quintessential targets for immune-modulating therapies in solid tumor-bearing subjects because both priming of tumor-specific T-cell responses and immune suppression occur in this area, and that local therapies designed to balance this equilibrium toward more effective antitumor T-cell responses will be most efficient. Fransen further teaches that the targeted approach for delivery of immunotherapy lends itself without difficulty for combined use with other cancer treatments, like chemotherapy which has been described to have immune-enhancing properties. Wainwright teaches that one of the hallmark features of GBM is the accumulation of regulatory T cells which are associated with the promotion of pathological outcomes and immunotherapeutic failure and that given the pathogenic role that Treg mediate in the context of malignant brain tumors, an obvious therapeutic direction is their selective depletion from both the tumor microenvironment and/or secondary lymphoid tissues. Ma teaches that the PCL-PEG-PCL hydrogel is thermoresponsive to body temperature and has demonstrated that this triblock polymer can be used to encapsulate protein therapeutics while retaining activity and also sustaining local release over an extended period of time. The ordinary artisan has a reasonable expectation of success to substitute PCL-PEG-PCL for Pluronic F-127 hydrogel in the method of treating a GBM with a composition of a hydrogel and an anti-PD-1 antibody administered to a draining lymph node to enhance efficacy, lower cost, lower toxic side effects, and increase patient comfort during treatment. Therefore the ordinary artisan has a reasonable expectation of success to administer a composition comprising a thermosensitive PCL-PEG-PCL hydrogel, an anti-PD-1 antibody (nivolumab) and chemotherapy to the deep cervical draining lymph node for a subject with GBM to enhance efficacy, lower cost, lower toxic side effects, and increase patient comfort in the treatment for this difficult to access tumor location.
Claim 9 is rejected under 35 U.S.C. 103 as being unpatentable over Latik (International Journal of Molecular Sciences. 2019; 20(21):5347; cited in OA 12/09/2025), Fransen ( Int. J. Cancer, 132: 1971-1976; cited in OA 05/05/2026), Wainwright (Front Immunol. 2013 May 15;4:116; cited in OA 05/05/2026), and Ma (J. Appl. Polym. Sci., 116: 1985-1993; PTO-892) as applied to claims 1, 10-12, 15-16, 19 and 24 above and further in view of Huynh (Polymer, 2009, 50(12): 2565-71; PTO-892).
The teachings of Latik, Fransen, Wainwright and Ma regarding claims 1 and 10-12, 15-16, 19 and 24 are detailed above.
Latik, Fransen, Wainwright and Ma do not teach wherein the hydrogel further comprises one or more pH sensitive moieties.
Huynh teaches that intelligent polymers and hydrogels responding to both temperature and pH changes have attracted increasing interest as they offer unique advantages compared with polymers that respond to only a single stimulus synthesis (intro, para 1). Huynh further teaches production of a copolymer by conjugation of PAE to both ends of a triblock parent polymer PCL-PEG-PCL to make a pentablock polymer that is pH and temperature sensitive (page 2565, col 2, para 1). Huynh further teaches that the PAE-PCL-PEG-PCL-PAE pentablock polymer exhibited many advantages including the possibility of ionic link formation involving the positive charges of PAE and the negative charges of drugs/proteins, that could be injected with no surgical procedure, no clogging during injection, straightforward drug loading to the polymer solution, no initial burst of release, and long sustained release (page 2565, col 2, para 1). Huynh further teaches that the pentablock polymer showed a shift in sol–gel transition compared to that of the polymer solution alone and that control of such a shift by pH and temperature near physiological values is important in practical applications (page 2565, col 2, para 2). Huynh further teaches that sol–gel transition window can be precisely tuned by varying PEG molecular weight, the hydrophobic/hydrophilic block ratio (PCL/PEG), the molecular weight of the pH-sensitive block (PAE), and the polymer concentration and that this novel material enlarges applications of injectable hydrogels as new templates for anionic drug, protein, and DNA delivery (conclusion).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to add pH sensitive moieties to the hydrogel as taught by Deng to the method of treating GBM with a composition of PCL-PEG-PCL hydrogel and anti-PD-1 antibody administered to a draining lymph node as taught by Latik, Fransen, Wainwright, and Ma. The ordinary artisan would have been motivated to do so because Huynh teaches many advantages to the addition of pH sensitive PAE to both ends of the parent polymer PCL-PEG-PCL including the possibility of ionic link formation involving the positive charges of PAE and the negative charges of drugs/proteins, injection with no surgical procedure, no clogging during injection, straightforward drug loading to the polymer solution, no initial burst of release, and long sustained release. Huynh further teaches that the sol–gel transition window can be precisely tuned by varying PEG molecular weight, the hydrophobic/hydrophilic block ratio (PCL/PEG), the molecular weight of the pH-sensitive block (PAE). The ordinary artisan has a reasonable expectation of success to add pH sensitive moieties to the hydrogel triblock polymer to better control solution to gel properties and improve sustained release in the method of treating a GBM with a composition of a hydrogel and an anti-PD-1 antibody administered to a deep draining lymph node to enhance efficacy.
Claims 13-14, 18, 20-21, and 23 are rejected under 35 U.S.C. 103 as being unpatentable over Latik (International Journal of Molecular Sciences. 2019; 20(21):5347; cited in OA 12/09/2025), Fransen ( Int. J. Cancer, 132: 1971-1976; cited in OA 05/05/2026), Wainwright (Front Immunol. 2013 May 15;4:116; cited in OA 05/05/2026), and Ma (J. Appl. Polym. Sci., 116: 1985-1993; PTO-892) as applied to claims 1, 10-12, 15-16, 19 and 24 above and further in view of Khasraw (Clinical Cancer Research 26.20 (2020): 5287-5296; cited in OA 12/09/2025).
The teachings of Latik, Fransen, Wainwright and Ma regarding claims 1 and 10-12, 15-16, 19 and 24 are detailed above.
Latik, Fransen, Wainwright and Ma do not teach the specific combination therapy in addition to the anti-PD-1 antibody and hydrogel composition.
Regarding claim 11, Khasraw teaches that glioblastoma (WHO grade IV glioma) is the most common malignant primary brain tumor in adults and while immunotherapy and especially immune checkpoint inhibitors and programmed cell death (PD)-1/PD-L1 inhibitors have transformed the landscape of cancer treatment and improved patient survival in a number of different cancer types, there is still no evidence that PD-1 blockade can lead to meaningful clinical benefit in glioblastoma (abstract). Khasraw further teaches that several phase I/II trials in recurrent and newly diagnosed glioblastoma are evaluating anti-PD-1 agents such as nivolumab, pembrolizumab, cemiplimab, or anti-PD-L1 antibodies including atezolizumab, avelumab, durvalumab, alone or in combination with other therapies (page 5287, col 2, para 3; Table 1), although phase II and phase III trials have yet to prove efficacy (table 2). Khasraw further teaches that although single agent PD-1 blockade has not yielded efficacious results there are a number of new strategies being considered including combination therapy and targeting therapy (page 5293, col 2, para 2) and that combination therapy with two or more therapeutic agents is a cornerstone of cancer therapy (page 529, col 2, para 3).
Regarding claims 13-14, 18, and 20-21, Khasraw teaches hypo fractionated stereotactic irradiation with nivolumab, ipilimumab, and bevacizumab in patients with recurrent high-grade gliomas (table 2).
Regarding claim 23, Khasraw teaches nivolumab with radiotherapy and bevacizumab for recurrent MGMT-methylated glioblastoma (table 2).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to add an additional therapeutic as taught by Khasraw to the method of treating GBM with a composition of PCL-PEG-PCL hydrogel and anti-PD-1 antibody administered to a draining lymph node as taught by Latik, Fransen, Wainwright, and Ma. The ordinary artisan would have been motivated to do so because Khasraw teaches that combination therapy with two or more therapeutic agents is a cornerstone of cancer therapy and that several phase I/II trials in recurrent and newly diagnosed glioblastoma are evaluating anti-PD-1 agents such as nivolumab, pembrolizumab, cemiplimab, alone or in combination with other therapies. The ordinary artisan has a reasonable expectation of success to add an additional therapeutic in the method of treating a GBM with a composition of a hydrogel and an anti-PD-1 antibody administered to a draining lymph node to enhance efficacy.
Claim 17 is rejected under 35 U.S.C. 103 as being unpatentable over Latik (International Journal of Molecular Sciences. 2019; 20(21):5347; cited in OA 12/09/2025), Fransen ( Int. J. Cancer, 132: 1971-1976; cited in OA 05/05/2026), Wainwright (Front Immunol. 2013 May 15;4:116; cited in OA 05/05/2026), and Ma (J. Appl. Polym. Sci., 116: 1985-1993; PTO-892) as applied to claims 1, 10-12, 15-16, 19, and 24 above and further in view of Maxwell (Oncoimmunology. 2018 Sep 6;7(12):e1500108; cited in OA 12/25/2025).
The teachings of Latik, Fransen, Wainwright and Ma regarding claims 1, 10-12, 15-16, 19, and 24 are detailed above.
Latik, Fransen, Wainwright and Ma do not teach that combination therapy in addition to the anti-PD-1 antibody comprises dexamethasone or prednisone.
Maxwell teaches that corticosteroids are widely used in the course of cancer management but can have negative effects on the anti-PD-1 treatment response, however corticosteroid treatment did not abrogate the benefits conferred by anti-PD-1 therapy in a mouse model of intracranial tumors (abstract). Maxwell further teaches that clinically, corticosteroids are routinely used in the management of cancer for fatigue, night sweats, appetite stimulation, antiemesis, and the reduction of side effects associated with certain chemotherapies (platinum-based agents and taxanes) and corticosteroids are especially important in the management of tumors residing in the central nervous system (CNS), since they can effectively palliate neurological deficits and reduce complications caused by cerebral edema through restoring the integrity of the blood-brain barrier (BBB) (introduction; para 2). Maxwell further teaches that cerebral edema is often potentiated by the additive pro-inflammatory effects of brain radiation plus immunotherapy, even when not given concurrently, thus necessitating the use of corticosteroids post-treatment (introduction; para 2). Maxwell further teaches that dexamethasone is the most potent synthetic corticosteroid and demonstrated that dexamethasone treatment disrupted the benefits of PD-1 blockade in mice bearing peripheral colon adenocarcinoma tumors, antitumor immunity and responses mediated by anti-PD-1 therapy remained intact for those bearing intracranial glioma tumors (introduction; para 3).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to use dexamethasone as the additional therapeutic as taught by Maxwell to the method of treating GBM with a composition of PCL-PEG-PCL, anti-PD-1 antibody and an additional therapeutic administered to a deep cervical draining lymph node as taught by Latik, Fransen, Wainwright, and Ma. The ordinary artisan would have been motivated to do so because Maxwell teaches that dexamethasone is the most potent synthetic corticosteroid and that corticosteroids are especially important in the management of tumors residing in the central nervous system (CNS), since they can effectively palliate neurological deficits and reduce complications caused by cerebral edema through restoring the integrity of the blood-brain barrier. Maxwell further teaches that cerebral edema is often potentiated by the additive pro-inflammatory effects of brain radiation plus immunotherapy, even when not given concurrently, thus necessitating the use of corticosteroids post-treatment. The ordinary artisan has a reasonable expectation of success to use dexamethasone as the additional therapeutic in the method of treating a GBM with a composition of a hydrogel and an anti-PD-1 antibody administered to a deep draining cervical lymph node to reduce complications and inflammation caused by immunotherapy in patients.
Claim 22 is rejected under 35 U.S.C. 103 as being unpatentable over Latik (International Journal of Molecular Sciences. 2019; 20(21):5347; cited in OA 12/09/2025), Fransen ( Int. J. Cancer, 132: 1971-1976; cited in OA 05/05/2026), Wainwright (Front Immunol. 2013 May 15;4:116; cited in OA 05/05/2026), Ma (J. Appl. Polym. Sci., 116: 1985-1993; PTO-892), and Khasraw (Clinical Cancer Research 26.20 (2020): 5287-5296; cited in OA 12/09/2025) as applied to claims 1, 10-16, 18-21, and 23-24 above and further in view of Polivka (Anticancer Res. 2017 Jan;37(1):21-33; cited in OA 12/09/2025).
The teachings of Latik, Fransen, Wainwright, Ma, and Khasraw regarding claims 1, 10-16, 18-21, and 23-24 are detailed above.
Latik, Fransen, Wainwright, Ma, and Khasraw do not teach combination therapy in addition to the anti-PD-1 antibody comprises cediranib.
Polivka teaches that the major role in tumor angiogenesis is played by vascular growth factors, especially vascular endothelial growth factor (VEGF) and excessive microvascular proliferation as well as VEGF overexpression were identified in tumor tissues from patients with GBM (page 24, col 1, para 1). Polivka further teaches the VEGFR tyrosine kinase inhibitor cediranib showed activity in an early phase II clinical trial as a monotherapy in patients with recurrent GBM but showed no PFS benefit as a monotherapy (page 24, col 2, para 2).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to use dexamethasone as the additional therapeutic as taught by Maxwell to the method of treating GBM with a composition of PCL-PEG-PCL hydrogel, an anti-PD-1 antibody and an additional therapeutic administered to the deep cervical draining lymph node as taught by Latik, Fransen, Wainwright, Ma, and Khasraw. The ordinary artisan would have been motivated to do so because Polivka teaches that the major role in tumor angiogenesis is played by vascular growth factors, especially vascular endothelial growth factor (VEGF) and excessive microvascular proliferation as well as VEGF overexpression were identified in tumor tissues from patients with GBM and that the VEGFR tyrosine kinase inhibitor cediranib showed activity in an early phase II clinical trial as a monotherapy in patients with recurrent GBM. The ordinary artisan has a reasonable expectation of success to use cediranib as the additional therapeutic in the method of treating a GBM with a composition of a hydrogel and an anti-PD-1 antibody administered to a draining lymph node to reduce tumor angiogenesis.
Response to Arguments
Applicant’s arguments with respect to claim(s) 1 and 9-24 have been considered but are moot because the new ground of rejection does not rely on any reference applied in the prior rejection of record for any teaching or matter specifically challenged in the argument.
Conclusion
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/AMBER K FAUST/Examiner, Art Unit 1643
/JULIE WU/Supervisory Patent Examiner, Art Unit 1643
