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 .
This office action is in response to an amendment filed 12/15/2025.
Claims 2, 5-8, 10, 14, 31 and 32 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 12/15/2025 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 as well as the rejections under 35 USC 112, second. As well, the art does not appear to teach prior to the filing date use of MPCs to deliver oncolytic virus.
Claim Objections
Claim 4 is grammatically incorrect. The claim states the promoter is a list of promoters but does not indicate that –the promoter is selected from one of—and –TRP1 promoter and Tyr promoter--. Appropriate correction is required.
Claims 31 and 32 are objected to under 37 CFR 1.75 as being a substantial duplicate of claim 2. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m). The claims simply recite an outcome that is apparently inherent in the method of claim 2. There are no additional steps, simply a desired outcome.
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, 31 and 32 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 a oncolytic approach combined with cell therapy approach to treating cancer.
2) Scope of the invention. The scope of the invention is extremely broad in that the oncolytic virus and cancer are any. This presents a broad group of potential targets as well as tools to treat. As well, the mode of administration is not provided which as set forth below abuts the obstacles hindering therapy with biomolecules.
3) Number of working examples and guidance. The specification teaches that MLPSC 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, PTENa, on 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 with RSV which virus 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 means 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.
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.
The art has found a bias of some viral types for specific tumors (see Table 2 in Zheng et al which demonstrates the specificity with which genes, virus, co-therapies and routes of administration are being tested). In general, aside from hematological cancers, cancers are affected in part by (Zheng, page 235, col 2),
The presence of an envelope is also an important factor when selecting an OV because the oncolytic properties of enveloped viruses are less efficient than those of naked viruses, and enveloped viruses are more likely to be cleared by host immunity. The size of the OV also determines its oncolytic properties. Smaller viruses are easier to infiltrate and are diffuse throughout the tumor, while larger viruses are better able to insert the therapeutic genes. Furthermore, tumor tropism, potential pathogenicity, immunogenicity, druggability, and viral stability are important factors to be considered in virus selection.22
Hence broadly claiming an oncolytic virus and a tumor type does not provide requisite compatibility for therapeutic potential. This is complicated by delivery obstacles. many tumors 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).
Finally, claims drawn to expression by the mlpsc of Ang1 and VEGF are not adequately described. It is not clear if the cells are selected or cultured to express certain amounts or if this is an inherent property. There are no steps or guidance in the disclosure to provide insight as to how the cells are known to express the recited amounts. The written description requirement for genus claims may be satisfied through sufficient description of a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant identifying characteristics, i.e. structure or other physical and/or chemical properties, by functional characteristics coupled with known or disclosed correlations between function and structure, or by a combination of such characteristics sufficient to show that the applicant was in possession of the claimed genus. To this end, the MPEP provides such guidance (emphasis added). If the application as filed does not disclose the complete structure (or acts of a process) of the claimed invention as a whole, determine whether the specification discloses other relevant identifying characteristics sufficient to describe the claimed invention in such full, clear, concise, and exact terms that a skilled artisan would recognize applicant was in possession of the claimed invention.
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 they have surprisingly found that MPC show a superior capacity to MSC to allow for replication and survival of a variety of diverse oncolytic virus. Example 7-8 and figure 13-14 and 26-31 show this comparison. Applicants provide a number of exhibits showing cancers treating by oncolytic virus.
As a first issue, the claims are not drawn to methods of promoting and survival of oncovirus but to methods of treating cancer. There are more considerations than just promotion and survival. The virus in the MPC are protected from degradation and most immune reactions in the cell and hence tolerate systemic administration. However, the ability to traverse the TME and target all cancers, even the slightly reduced list of cancers is not a given. The cell line and some animal model systems are able to show results as the issues of tropism, TME and organ location are not relevant. Wang provided as Exhibit A states this. (Page 02, col 1), ..”substantial challenges remain. These include extracellular matric (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.” This is not to say that the method will not work. However, my claiming the method broadly, applicants claims abut all the obstacles associated with cell and oncolytic therapy for cancer. The limitation to the list of lung cancer, pancreatic cancer, colorectal cancer, liver cancer, cervical cancer, prostate cancer, osteosarcoma, breast cancer and melanoma does not provide the connection between cell type for delivery/target organism and OV. Wang, exhibit A, discusses these issues invoking a need to enable the design of OV with selective infectivity and cytotoxicity toward specific tumor subpopulations thereby improving treatment precision and efficacy (page 7, col 1). As (page 6, col 1), “In clinical practice, patient responses to oncolytic virus (OV) therapy very significantly primarily due to the high heterogeneity of immune statis, tumor microenvironment, and tumor cell gene expression profiles.
Exhibit B, Perez teaches potential of OV for colorectal cancer but cautions that “several challenges hinder the widespread clinical application of Ovs in CRC.” Perez teaches that improvements are necessary in immune suppression and tumor selectivity. None of the OV proposed for CRC were shown to be able to “treat” cancer in humans. While this does not dissuade application of the instant invention, it demonstrates that blanketly claiming any OV and any of lung cancer, pancreatic cancer, colorectal cancer, liver cancer, cervical cancer, prostate cancer, osteosarcoma, breast cancer and melanoma by systemic administration of MPC cells that are from any source is simply complicated by too many unpredictable aspects. This is highlighted by Yang, Exhibit C which states on page 2, “While there is much potential for OV therapy, there are some important considerations to be made when utilizing viruses for therapeutic purposes. Ovs should utilize the inherent abilities of the infectious agent to attach cancer”. The OV and the ability to treat brain cancer is simply proposed with the conclusion of
Each virus, and the strategies that aim to leverage its immunostimulatory consequences, has the following three purposes: to increase tumor specificity/sparing of healthy tissue, tumor cytotoxicity, or attenuation/safety profiling. On the whole, current pre- clinical findings seem to have explored the possibilities of the first two goals, while clinical trials have primarily demonstrated tolerable safety profiles of this treatment modality, with future proposed trials to better dissect efficacy and outcomes. However, much still remains unknown
The application of the OV in brain cancer is shown and taught as well to result from direct administration into the brain. The blood brain barrier being such that passage any other way has not been shown to be effective in target delivery.
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.
The teachings of Hua et al (Exhibit G) punctuates the issues raised above as to ability to target cancer generally. This reference is only dedicated to liver cancer and even there see page 2, col 1),
The effectiveness of OVT against HCC can vary due to several factors, such as changes in receptor expression, host immune response, TME, and genetic alterations (14).
The reference in general supports the nascent state of the art for therapy (page 10),
The landscape of OVs in cancer treatment shows promising strides, but their application in liver cancer treatment faces a significant gap between preclinical promise and clinical validation. Although basic science studies offer encouraging insights, the lack of robust clinical evidence leaves a critical void in understanding their effectiveness in treating liver cancer.
To truly harness the potential of OVs in liver cancer treatment, extensive clinical investigation is imperative.
.
Some promise for urological cancers with a variety of viruses are also reported by Taguchi et al (exhibit H)(. However, these results rely on intratumoral administration of the virus. Hence, it is unclear how systemic administration of any OV using the MPC will function. This is confirmed by the teachings of Wedenkind (exhibit I). Wedenkind teaches that the therapeutic efficacy has been limited with use of OV (page 77).
The activity of these viruses is impacted not only by the susceptibility of tumor cells to infection but also by the tumor microenvironment (TME) and by tumor immunogenicity.
As to osteosarcoma, Wedenkind highlights that it is a nascent art with little information (page 86),
The future of oncolytic virotherapy for osteosarcoma has numerous possibilities. As there has been limited data in regard to the use of oncolytic virotherapy for osteosarcoma, there is much that needs be learned.
Finally, Dashel et al (exhibit) teach that the
Another major issue is the complex interaction between the host, tumor, and pathogen which can have a drastic impact on outcomes. It is clear that some tumors are exquisitely sensitive to viral replication and others are not. Similarly, it is likely that some tumors are very sensitive to immune therapy while others are not, and there is likely to be significant overlap between the viral-sensitive and the immune therapy-sensitive tumors.
Hence, the arguments do not allow one to accept that the breadth of the claims are enabled.
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
THIS ACTION IS MADE FINAL. 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.
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/MARIA MARVICH/Primary Examiner, Art Unit 1634