DETAILED ACTION
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 4/14/2026 has been entered.
Claims 2, 5-8, 10, 14 and 50 are pending.
The instant application claims priority to provisional application 63/063,657 filed 8/10/2020 which claims priority to PCT/IB2021/057381 filed 8/10/2021.
Information Disclosure Statement
An IDS filed 4/14/2026 has been identified and the documents considered. The signed and initialed PTO Form 1449 has been mailed with this action. Initials indicate that the document has been considered even if the reference is lined through.
Applicants have asserted that a size fee is not due.
Response to Amendments
The amendments are sufficient to overcome the objections to the claims. The rejection under 35 USC 112, first paragraph. The art does not appear to teach prior to the filing date use of MPCs to deliver oncolytic virus.
Claim Objections
Claims 5 and 14 are objected to because of the following informalities: each of the promoters require an article prior to. Claim 14 requires an article prior to “oncolytic adenovirus”. Appropriate correction is required.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 5 and 8 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claims 5 and 8 recite the limitation "the oncolytic virus" in claim 1. There is insufficient antecedent basis for this limitation in the claim. Claim 1 refers to oncolytic herpes simplex virus and oncolytic adenovirus and the claims do not ascertain whether one or both are encompassed.
Claim Rejections - 35 USC § 112, first paragraph
The following is a quotation of the first paragraph of 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 2, 5-8, 10, 14 and 50 are rejected under 35 U.S.C. 112, first paragraph, because the specification, while being enabling for a oncolysis in a preclinical model, the method comprising administering a composition of culture expanded STRO-1+ mesenchymal lineage precursor or stem cells comprising an oncolytic virus to the cancer cells, does not reasonably provide enablement for any other embodiment. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the invention commensurate in scope with these claims. This rejection is maintained.
The test of enablement is whether one skilled in the art could make and use the claimed invention from the disclosures in the patent coupled with information known in the art without undue experimentation (United States v. Telectronics, Inc., 8 USPQ2d 1217 (Fed. Cir. 1988)). Whether undue experimentation is required is not based on a single factor but is rather a conclusion reached by weighing many factors (See Ex parte Forman, 230 USPQ 546 (Bd. Pat. App. & Inter, 1986) and In re Wands, 8USPQ2d 1400 (Fed. Cir. 1988); these factors include the following:
1) Nature of invention. The instant claims are drawn to an oncolytic viral approach combined with cell therapy approach to treat cancer.
2) Scope of the invention. The scope of the invention has been amended to limit the cancer to lung cancer, pancreatic cancer, colorectal cancer, liver cancer, cervical cancer, prostate cancer, breast cancer and melanoma. As well, the oncolytic virus is HSV or adenovirus. However, the scope has not been narrowed to methods that encompass methods of administration for cancer therapy that have a predictable amount of success as set forth below.
3) Number of working examples and guidance. The specification teaches that MLPSC or MPC are either mesenchymal progenitor or stem cells. These cells furthermore are characterized by
[0138] In an example, mesenchymal lineage precursor or stem cells are culture expanded. “Culture expanded” mesenchymal lineage precursor or stem cells media are distinguished from freshly isolated cells in that they have been cultured in cell culture medium and passaged (i.e. sub-cultured).
[0110] STRO-1+ cells are cells found in bone marrow, blood, dental pulp cells, adipose tissue, skin, spleen, pancreas, brain, kidney, liver, heart, retina, brain, hair follicles, intestine, lung, lymph node, thymus, bone, ligament, tendon, skeletal muscle, dermis, and periosteum; and are capable of differentiating into germ lines such as mesoderm and/or endoderm and/or ectoderm. Thus, STRO-1+ cells are capable of differentiating into a large number of cell types including, but not limited to, adipose, osseous, cartilaginous, elastic, muscular, and fibrous connective tissues. The specific lineage-commitment and differentiation pathway which these cells enter depends upon various influences from mechanical influences and/or endogenous bioactive factors, such as growth factors, cytokines, and/or local microenvironmental conditions established by host tissues.
As well, the specification teaches in vitro delivery of virus to MSC (mesenchymal stem cells) and an understanding of dose necessary. In the examples, HSV oncolytic virus expressing PTENa and loaded into MSC with no impact on cell viability.
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Their ability to target breast cancer was shown in vitro and co-culture with breast cancer cells lead to an increase in cell death of the breast cancer cells. When incubated with glioma cells, PTEa was increased and AKT phosphorylation reduced.
MPC cells experienced increased survival with HSV oncovirus. Increased infection and shedding of RSV was found in MPC over MSC were found. RSV had increased capability of infecting cancer cell lines.
In vivo use is prophesized.
4) State of the art. Cancer therapy using oncolytic viruses has been in progress for some time with impacts of poor delivery negatively affecting their use. Multiple means of overcoming these issues have been attempted. The instant invention relies upon cell carriers that are based in mesenchymal progenitor and stem cells. The instant claims recite as carriers culture expanded mesenchymal precursor cells (MPC). The art teaches that MPC are MSC precursor cells.
Mesenchymal stem cells are immature cells capable of self-renewing and differentiating into many cell types that belong to three germinal layers. Due to their inherent tumor tropism mesenchymal stem cells loaded with oncolytic virus can improve delivery of the therapeutic cargo to cancer sites. Shielding of oncolytic viral construct from antiviral host immune response makes these cells prospective delivery vehicles to even hard-to-reach metastatic neoplastic foci.
MSC are isolated from a variety of sources including bone marrow, adipose tissue, placenta, dental pulp, synovial membrane, peripheral blook and more. The markers used to identify the cells are of two types, sole markers and st3emness markers. STRO-1+ is a stemness marker (see Lv for review).
5) Unpredictability of the art. Applicants have presented their results as proof of potential through in vitro results. However, the ability to correlate in vitro activity to the complexity of human delivery is highly unpredictable (Chakraborty, abstract).
A wide variety of preclinical models exist to effectively study cancer and design more efficient treatments. However, a majority of cancer models cannot accurately recapitulate cancer as it exists in humans. Animal models physiologically differ from humans. In vitro models, such as organoids, allow construction with human-based components, but most fail to accurately mimic the overall tumor microenvironment (TME), which is composed of stromal and immune cells, as well as a complex extracellular matrix (ECM).
The limitations of the techniques are fatally flawed primarily for this, (conclusion, Chakraborty).
It has thus been established that CAFs and ECM components are key players in a cancerous environment and unmissable to effectively study cancer biology and tumor metastasis. These cellular and environmental stromal components have multifarious functions in the different stages of tumor growth and proliferation. However, they are often not modeled into in vitro setups used to study cancer in its separate stages of progression and as iterated earlier, despite a variety of such models, very few incorporate CAFs into their build and most utilize simplistic or nonrepresentative matrices and the results thus generated are inconclusive and inaccurate representations of what goes on in a cancer-laden tissue.
Even using cell carriers has shown lack of complete correlation (Hadrys, page 9, col 2).
Even though the preclinical studies are highly promising, effectiveness of oncolytic virotherapy remains suboptimal, with only a fraction of patients undergoing complete tumor regression (called “elite responders ”) but the majority still do not (Bell and McFadden, 2014). Effectiveness of virotherapy ultimately relies on eliminating factors that impede efficient virus delivery to the target sites, particularly for disseminated cancer burden (e.g., insufficient numbers of tumor-penetrating viral particles) (Marchini et al., 2016).
One of the primary complications for oncoviruses is how to deliver. Intravenous delivery enables widespread OV infection to all lesions and avoids the need for localization technicians, especially when tumors are physically inaccessible. However, Zheng, col 1, page 235,
In solid tumors, there is a range of hurdles that the OV must circumvent to reach the tumor site. First, physical barriers post a big challenge to delivery because viruses must get past the endothelial layer to reach the target cells.13 In addition, the abnormal lymphatic networks and vascular hyperpermeability inside tumors and the dense extracellular matrix (ECM) of solid tumors result in interstitial hypertension,14 which can impair viral infiltration. Furthermore, OVs can induce a strong innate immune response because of interactions between them and antigen-presenting cells (APCs), together with widespread antiviral immunity, preexisting circulating antibodies, and blood factors such as the coagulation factors FIX, FX, and complement protein C4BP. Subsequently, OVs are more likely to be cleared by the host’s immune system, and it is difficult to make sure whether sufficient numbers reach the tumor site.14,15
The subsequent localized hypoxia and low-pH microenvironment might inhibit tumor cell apoptosis, promote angiogenesis, upregulate tumor growth factors, and make tumor cells more resistant to standard therapeutic methods such as radiotherapy, cytotoxic drugs, and immunotherapy.18–20 Therefore, once OVs reach the tumor site, it is crucial for them to maintain their functions within the immunosuppressive TME, which plays a key role in the proliferation and survival of cancer cells.
This has led to development of systems to provide improved delivery (Roy and Bell, abstract),
The optimal route for clinical delivery of oncolytic viruses is thought to be systemic intravenous injection; however, the immune system is armed with several highly efficient mechanisms to remove pathogens from the circulatory system. To overcome the challenges faced in trying to delivery oncolytic viruses specifically to tumors via the bloodstream, carrier cells have been investigated to determine their suitability as delivery vehicles for systemic administration of oncolytic viruses. Cell carriers protect viruses from neutralization, one of the most limiting aspects of oncolytic virus interaction with the immune system. Cell carriers can also possess inherent tumor tropism, thus directing the delivery of the virus more specifically to a tumor
However, it is not clear that these cells can obviate the delivery issues that plague cancer therapy. It is extremely nascent and advances are necessary prior to execution of methods with cell carriers. As to MSC as carriers, (Hadrys et al, page 8-9).
Use of mesenchymal stem cells has been criticized by some investigators as limiting proliferative abilities of primary cells and increasing the risk of malignant transformation, as well as attenuating therapeutic responses. However, majority of preclinical studies indicate safety and efficacy of mesenchymal stem cells used as carriers of oncolytic viruses. In view of contradictory postulates, the debate continues.
Clinical studies have yielded sub-optimal and incomplete responses such that,
Even though the preclinical studies are highly promising, effectiveness of oncolytic virotherapy remains suboptimal, with only a fraction of patients undergoing complete tumor regression (called “elite responders ”) but the majority still do not (Bell and McFadden, 2014). Effectiveness of virotherapy ultimately relies on eliminating factors that impede efficient virus delivery to the target sites, particularly for disseminated cancer burden (e.g., insufficient numbers of tumor-penetrating viral particles) (Marchini et al., 2016).
And results have been variable (Shi et al, abstract),
The unpredictability as set forth above of oncolytic virus and cells as carriers is complicated by the breadth of the claimed cancers to be treated by any oncolytic virus is not supported by description in the specification or by potential in the art. Cancer is an etiologically diverse and complicated genus of conditions. Roy and Bell, page 53, col 1.
It is likely that different tumor types may require different cell carriers in order to achieve tumor specific delivery and thus preclinical testing of these strategies remains an important and informative exercise.
Wang provided as Exhibit A states this. (Page 02, col 1), ..”substantial challenges remain. These include extracellular matrix (ECM barriers limiting viral penetration, highly immunosuppressive tumor microenvironments, difficulties in accurately evaluating treatment response (e.g., >40% false positive in PET-CT), and systemic delivery inefficiency.” Applicants have developed a carrier cell. Such a development does not obfuscate the complications associated with OV use in cancer therapy. These are as set forth above, difficulty in reaching the tumor site due to organ localization as well as TME. Tang (exhibit D, page 2199, col 1)¸
Previously, the primary method of delivery for OVs drugs was intratumoral administration, which maximized the distribution of OVs within the tumor [23]. However, this approach has several drawbacks: (i) OVs cannot be successfully injected into tumors due to the dense and high-pressure nature of tumor tissue; (ii) Intratumoral injection is often inappropriate for patients with malignancies in deep organs; (iii) Compliance with intratumoral administration is poor, especially for those requiring continuous administration [141-143].
As well, given the use of systemic administration localization of the cell to the tumor is not a demonstrated possibility (Tang et a, exhibit D, page 2199, col 1-2),
Compared with intratumoral injection, intravenous administration appears to be a better method for clinical application of OVs. Intravenous injection offers two significant advantages: it is highly convenient and feasible, and it possesses strong anti-metastasis and anti-recurrence capabilities [144]. Despite these advantages, the actual outcomes of intravenous OV administration have been unsatisfactory. The primary challenges of systemic delivery are as follows: (1) Pre-existing and rapidly formed neutralizing antibodies in the systemic circulation significantly impede the delivery and reduce the therapeutic effect of OVs. (2) The concentration of OVs retained in the tumor area after systemic administration is lower than that achieved by intratumoral injection, and the risk of systemic side effects is higher [145].
The use as a general cancer therapy is complicated as most cancers are multifaceted etiological (see Tang (Exhibit D), page 2191, col 2). Tang provides promising results in use of cell delivery with reference to MSC amongst other developments. A review of the references i.e. reference 150, Reale et al, teaches MSC cells may potential delivery agents. However,
Despite the potential of MSCs, there are many good reasons to also consider other carrier cell candidates. As MSCs have immunosuppressive properties, they may actually be counterproductive to the anti-tumor immune response, which the OV therapy aims to achieve. MSCs were also shown to have pharmacokinetic challenges, accumulating mainly in the lungs of experimental animals following intravenous injection, probably due to their dimensions. These problems resulted in some research groups trying to use MSCs for intratumoral delivery, which can make sense in some particular instances but mostly seems to contradict the rationale for the use of carrier cells.
The use of these cells do not address concerns iterated in the art while for the virus are also relevant for cell carriers (Yang et al, Exhibit F, page 6475),
Systemic delivery, on the other hand, is prone to immune clearance, underscoring the urgent need for improved delivery technologies to enhance bioavailability. Additionally, further research is required to determine the optimal timing for oncolytic virus therapy across different PC stages and to identify synergistic strategies with other treatments.
These delivery obstacles are real for many tumors as they cannot be targeted due to restrictions of TME, immune rejection and evasive locations. Hence, not every virus is able to treat every cancer. While progress is noted in the field of oncolytic therapy, the direction of oncolytic virus for therapy progress is still fairly nascent with incomplete understanding of the mechanism (see page 10, col 1 of Chen et al).
6) Undue experimentation. The claims have been evaluated in light of the art at the time of filing and found not to be commensurate in scope with the specification. MPEP 2164.05 teaches, “However, the examiner should carefully compare the steps, materials, and conditions used in the experiments of the declaration with those disclosed in the application to make sure that they are commensurate in scope; i.e., that the experiments used the guidance in the specification as filed and what was well known to one of skill in the art. Such a showing also must be commensurate with the scope of the claimed invention, i.e., must bear a reasonable correlation to the scope of the claimed invention. The invention recites use of a broad group of targets, oncolytic virus and therapies. Given the unpredictability of the art, the poorly developed state of the art with regard to predicting the ability to treat any cancer with any oncolytic virus with MLPSC, the lack of adequate working examples and the lack of guidance provided by applicants, the skilled artisan would have to have conducted undue, unpredictable experimentation to practice the claimed invention.”
Response to Arguments
Applicants argue that
However, the results cited are not commensurate with the claims. There are issues of cancer/oncolytic virus/mode of administration as broadly claimed. The references provided only support the position of the rejection that the breadth is simply too large to encompass an adequate number of enabled combinations. The references are reviewed below. The major issues are that the results are not sufficient for two specific reasons. The virus shown provide features not contemplated nor claimed in the instant application wherein the later filing date means some inventive aspects must be considered.. These virus includes for example Hu and Zhao. Other issues that arise are that the results do not provide requisite evidence that obstacles noted in humans have been overcome. They are results showing proof of principle in mouse models or cell culture. While clinical results are not required, in this case where clinical data is clear that delivery and target specificity is not predictable with oncolytic virus and the art is clear (some reviews provided above) that mice models do not provide correlative data on these results due to difference between humans and mice, some indication that the obstacles duly noted in all the references have been overcome is necessary.
Hu et al (2025) teaches construction of OH2, an HSV2 oncolytic virus comprising deletions of ICP47 and ICP34.5 genes. The reference states notably post filing (page 2).
“Given limited clinical exploration of HSV-2 based virotherapy, OH2 represents a novel and potentially superior addition to the field.”
The impact of this virus was demonstrated on mice models. Zhao distinctly from the instant claims comprised a heterologous gene encoding an oncolytic product. This deviates from the system claimed and like Hu demonstrated efficacy only in mice. Zhao notes only 3 successful oncolytic virus to date as effective. And even then,
These marketed OV drugs bring a good prospect and important motivation for the development of OVs. However, the tumour-killing effect of OVs is still insufficient in current research, thus the modification of OVs and delivery of novel tumour suppressor to improve their safety and antitumor effect is a major trend for future research.
It further states, that the results demonstrate a prospect for their oncolytic virus.
Zhou et al were not directed to therapeutic effects of oHSV. It is a study on cell culture and mice to understand cancer associated fibroblast immunosuppression.
In conclusion, our study provided new theoretical insights into the application of OVs in cancer immunotherapy and laid the foundation for developing more refined therapeutic strategies.
Taylor discusses the state of oncolytic adenovirus in treating pancreatic cancer. The promise again is noted but the obstacles impede use.
Firstly, viral selectivity is reduced when there is widespread distribution of primary cellular receptors as systemic toxicity limits the viral dose that may be tolerated. The route of administration poses another challenge, as the commonly used intratumoural administration is relatively invasive and less suitable to target distant metastases than the intravenous route. This method itself poses the theoretical significant risk of liver tropism, which could cause considerable adverse effects and reduce the availability of adenovirus in the circulation.
A positive note of Garcia-Carbonero is made in this reference wherein intravenous administration was made possible but by design. The virus differs from that of the instant claims by encoding a foreign gene to aid in this process as well as use of nab-paclitaxel and gemcitabine.
VCN- 01 is a new oncolytic replication- competent adeno virus designed to overcome these challenges.6 VCN- 01 derives from ICOVIR- 157 and ICOVIR- 15K,8 which replicate only in cells with a dysfunctional RB1 pathway. VCN- 01 has been genetically engineered with two essential modifications giving advantage over its parental viruses. First, it incorporates an RGKD integrin motif in the fiber shaft, an effective method for liver detargeting and tumor retargeting. In addition, VCN- 01 expresses a soluble form of human recombinant hyaluronidase (PH20), which enables the virus to degrade the extracellular matrix, disrupt the tumor stroma, thus enhancing the intratumoral spreading of the virus.9
Zhang et al teach proof of principle for oHSV2 on colon cancer and Sato with oAd.
(Sato) In this study, we provide a proof of concept for the generating cancer stem-cell specific oncolytic adenovirus and its enhanced therapeutic effect. To this end, we focused on the CD133 as a target molecule for colon cancer stem cells and showed that a potent CD133-targeting OAd derived from the high-throughput Ad library screening has selective cytocidal effect. The resultant CD133-targeting OAd was effectively killed cancer stem cell-like colon cancer cells in a variety of in vitro assays and showed anti-tumor effect in xenograft models as well. Our novel therapeutic modality of targeting CD133+ cells will have a potential to prevent metastases and relapses of CRC.
These are in contrast to applicants statement that successful treatment has been demonstrated.
Wang similarly provides in vitro and mouse model therapy with HSV G47D for hepatocellular carcinoma (HCC) with only a thought of future clinical applications (see page 7). Yoon encoded AFP in the virus and demonstrated in mice that HCC, page 10.
In summary, systemic administration of the oncolytic Ad, replicating under the control of tumor microenvironment- and HCC-targeting AFP promoter, can induce a potent inhibition of tumor growth, with a good safety profile, rendering it a promising candidate for the treatment of primary tumors and distant metastases in patients with late stages of cancer.
Similar sentiments were provided by Kagabu which demonstrated in mice T-01 related to G47 wherein in a cervical mouse model effective tumor killing was identified. Kagabu concludes,
These results demonstrate that oncolytic HSV should be considered for further development as a therapeutic agent for cervical cancer.
Ghahaat provides a review of oncolytic virus in the treatment of HPV and their mechanisms but does not demonstrate specific virus and their targets that can be considered successful models for the genus as claimed. Yang and Vannini detail pre-clinical work with oncolytic HSV and adenovirus for prostate cancer. Yang on page 16 summarizes it thus-
However, issues that limit its utility in cancer therapy still need to be considered. For example, oncolytic adenoviruses have complex biological characteristics, including host specificity and virus-host interaction; These bio- logical characteristics remain not be fully understood in humans. Moreover, the inherent immunogenicity of oncolytic adenovirus can easily cause local tissue inflammation and possible overt immune response of the whole body.
Nabi, Xiao and Hu et al provide strategies for treatment of breast cancer and melanoma. Nabi et al teach a virus called VC2 which is a HSV oncolytic virus and oHSV1.1 and oHSV1.2. Hu et al teach that the provided for oncolytic adenovirus (ZD55) is different from other virus even Onyx-015, a well-known and used virus. First, it has an antitumor gene and an intact E3and it is an ad5 homozygote. Secondly, it was delivered using PEG/Lipids/Ca-P to overcome,
In addition, the greatest limitation of oncolytic virotherapy is that the vast majority of oncolytic viruses cannot be administered systemically (e.g., intra- venous injection and intraperitoneal injection), but must be administered intratumorally Hence, oncolytic viruses are difficult to be used to treat the vast majority of tumors in clinic.
Each of these references were based on mouse studies and as Nabi summarizes on page 10 ,
VC2 OVT produces durable immune response the prevent efficient metastasis to distant organs showing promise for further investigations in animal and ultimately human studies.
Future studies are needed to address the T cell anti-tumor mechanisms. Further manipulation of VC2 can be done to improve the efficacy by incorporating foreign genes that help attract and mature dendritic cells in the TME as well as others that can reduce immune suppressor cell populations. VC2 has the capacity to incorporate multiple genes toward this purpose.
Again proof of principle for the mechanism of action but no demonstrable ability for such a large genu so of oncolytic HSV and adenovirus to trat such a large genus of tumors wherein the virus/tumor/mode of administration is typically very related.
Secondly, applicants argue that the invention by administering the virus in MPC address immunoneutralization and homing. As well, the virus replicates higher in MPC than in MSC. It is unclear where data is to the ability of the MPC to home to tumors and to avoid immunoneutralization. The MPC are not limited to autologous and it is unclear if allogeneic cells will avoid immune responses from the host. The specification proposes means to do so but does not demonstrate such,
[0194] In one aspect, the mesenchymal lineage precursor or stem cells defined herein are treated in order to modify their cell-surface glycans. Modification of glycans on cell surface proteins such as CD44 has been shown to create E-selectin ligands which can bind to the E-selectin molecules expressed in vivo on microvessels at sites of inflammation. In this way, modification of cell-surface glycans on mesenchymal lineage precursor or stem cells improves homing of the mesenchymal lineage precursor or stem cells to sites of tissue damage in vivo.
This is the Achilles heel of cancer therapy, reaching the tumor through the TME and avoiding clearance. Peng which is post-filing reviews these issues (see especially figure 1). Peng reviews the development of cell carriers and this reference demonstrates that homing is not native but must be the result of engineering (page 1115, col 1). It also cautions that immune responses are to be considered. The conclusion is Despite the theoretical advantages of cell-based therapies, practical application in clinical settings is constrained by significant limitations (page 1116,. Col 1).
While the results presented in the art do not necessarily preclude Applicant's hypothesis, they certainly fail demonstrate that by any mode of administration the broad genus of cancers can be treated by the still large group of virus. Consequently, the prior art (and post-filing art) when combined with the lack of any disclosed direct experimental test of Applicant's hypothesis, shows that one of skill in the art at the time the invention was made would have had no basis to reasonably predict or conclude the claimed invention would succeed. There is no evidence that the specification offers a solution to the problem set forth in the specification.
Double Patenting
A rejection based on double patenting of the "same invention" type finds its support in the language of 35 U.S.C. 101 which states that "whoever invents or discovers any new and useful process ... may obtain a patent therefor ..." (Emphasis added). Thus, the term "same invention," in this context, means an invention drawn to identical subject matter. See Miller v. Eagle Mfg. Co., 151 U.S. 186 (1894); In re Ockert, 245 F.2d 467, 114 USPQ 330 (CCPA 1957); and In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970).
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the "right to exclude" granted by a patent and to prevent possible harassment by multiple assignees. See In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970);and, In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) may be used to overcome an actual or provisional rejection based on a nonstatutory double patenting ground provided the conflicting application or patent is shown to be commonly owned with this application. See 37 CFR 1.130(b).
Effective January 1, 1994, a registered attorney or agent of record may sign a terminal disclaimer. A terminal disclaimer signed by the assignee must fully comply with 37 CFR 3.73(b).
Claims 2, 5-7, 8, 10, 13 and 35-37 are provisionally rejected under the judicially created doctrine of obviousness-type double patenting as being unpatentable over claims 1, 39-42, 45, 47 and 48 of copending Application No. 17/633,063.This rejection is maintained.
An obviousness-type double patenting rejection is appropriate where the conflicting claims are not identical, but an examined application claim is not patentably distinct from the reference claims because the examined claim is either anticipated by, or would have been obvious over, the reference claims. Although the conflicting claims are not identical, they are not patentably distinct from each other because the cited claims of the instant invention are generic to all that is recited in claims 1, 39-42, 45, 47 and 48 of copending Application No. 17/633,063. That is, the cited claims of copending Application No. 17/633,063 anticipate and fall entirely within the scope of the rejected claims of the instant application. Specifically, of copending Application No. 17/633,063 is drawn to compositions and methods overlapping that of the instant claims. Both sets of claims recite a population of STR-1+ mesenchymal cells that comprise an oncolytic virus to treat cancer.
Additionally, if a patent resulting from the instant claims was issued and transferred to an assignee different from the assignee holding copending Application No. 17/633,063, then two different assignees would hold a patent to the claimed invention of copending Application No. 17/633,063, and thus improperly there would be possible harassment by multiple assignees.
This is a provisional obviousness-type double patenting rejection because the conflicting claims have not in fact been patented.
Conclusion
The following reference provided teachings of MPC as carriers for oAd but did not teach one of the cancers to which the claims were limited- Komarova et al, Mesenchymal progenitor cells as cellular vehicles for delivery of oncolytic adenoviruses, Mol Cancer Ther 2006, pages 755-766
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/MARIA MARVICH/Primary Examiner, Art Unit 1634
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