DETAILED ACTION 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. This is the first action on the merits. Claims 1-6, 11-14 and 16-20 are pending and under consideration. Claim Objections Claim 1 is objected to because of the following informalities: the term “ e scluded ” should be replaced with “ excluded, ” see the definition of R 2 . Appropriate correction is required. Claim 2 is objected to because of the following informalities: the term “C1-C6” should be replaced with “C 1 -C 6. ” Appropriate correction is required. Claim 6 is objected to because of the following informalities: the term “deifid” should be replaced with “defined,” see step 7, page 9, line 2. 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. Claim s 6, 16, 17 and 19 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 pre-AIA the applicant regards as the invention. Regarding claim 6 , the phrase "such as" renders the claim indefinite because it is unclear whether the limitations following the phrase are part of the claimed invention , see step 4, page 8, line 6 ; and step 9, page 10, line 15 . See MPEP § 2173.05(d). In claim 6 , the phrase “double bond/hydrogenation” is vague and ambiguous. Regarding claim 19 , the phrase "such as" renders the claim indefinite because it is unclear whether the limitations following the phrase are part of the claimed invention, see page 13 and page 14. See MPEP § 2173.05(d). A broad range or limitation together with a narrow range or limitation that falls within the broad range or limitation (in the same claim) may be considered indefinite if the resulting claim does not clearly set forth the metes and bounds of the patent protection desired. See MPEP § 2173.05(c). In the present instance, claim 19 recites broad recitation s , and the claim also recites “including” which is the narrower statement of the range/limitation , see seven different times in said claim . The claim(s) are considered indefinite because there is a question or doubt as to whether the feature introduced by such narrower language is (a) merely exemplary of the remainder of the claim, and therefore not required, or (b) a required feature of the claims. With regards to claims 16 and 17 , the phrase "disease cause by and/or associated with dysregulated CDC7 kinase activity" is indefinite. There is no standard list of diseases which are CDC7 caused by or associated with dysregulation of CDC7 . On pages 19 and 20, the specification provides a list of diseases as preferable emodiments . What other diseases are contemplated? It is unclear what diseases and treatments Applicant is intending to encompass because there are so many different diseases. Note that the claim covers both an increase and a decrease in activity. In claim 18 , the term “disorder” is found, which lacks antecedent basis. The following is a quotation of 35 U.S.C. 112(a): (a) IN GENERAL.—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 or joint inventor of carrying out the invention. The following is a quotation of 35 U.S.C. 112 (pre-AIA), first paragraph: 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 16-20 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention. The instant specification does not adequately describe the nexus between the phrase “cause by and/or associated with dysregulated CDC7" and the claimed diseases/conditions . The phrase “cause by and/or associated with dysregulated CDC7" refer s to the ability of a compound to increase or decrease the function, or activity of, for example, CDC7 . Modulation, in its various forms, is intended to encompass inhibition, antagonism, partial antagonism, activation, agonism and/or partial agonism of the activity associated with CDC7 . CDC7 inhibitors are compounds that, e.g., bind to, partially or totally block stimulation, decrease, prevent, delay activation, inactivate, desensitize, or down regulate signal transduction. CDC7 activators are compounds that, e.g., bind to, stimulate, increase, open, activate, facilitate, enhance activation, sensitize or up regulate signal transduction. These modulations are sometimes opposite reactions to the same receptor. It is not seen where the instant specification adequately describes the nexus between the modulation of the glucocorticoid receptor and a useful treatment of a single disease or condition. The ability of a compound to modulate CDC7 can be demonstrated in an enzymatic assay or a cell-based assay. Claim s 16-20 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA), first paragraph, because the specification, while being enabling for a method of inhibiting CDC7 , does not reasonably provide enablement for a method of treating cancer , cell proliferation disorders, or immune-related disorders, generally. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims. The treatment of cancer, cell proliferation disorders, or immune-related disorders, generally cannot possibly be considered enabled. As a general rule, enablement must be commensurate with the scope of claim language. MPEP 2164.08 states, “The Federal Circuit has repeatedly held that “the specification must teach those skilled in the art how to make and use the full scope of the claimed invention without undue experimentation’.” In re Wright , 999 F.2d 1557, 1561, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993)” (emphasis added). The “make and use the full scope of the invention without undue experimentation” language was repeated in 2005 in Warner-Lambert Co. v. Teva Pharmaceuticals USA Inc. , 75 USPQ2d 1865, and Scripps Research Institute v. Nemerson , 78 USPQ2d 1019 asserts: “A lack of enablement for the full scope of a claim, however, is a legitimate rejection.” The principle was explicitly affirmed most recently in Auto. Tech. Int’l, Inc. v. BMW of N. Am., Inc. , 501 F.3d 1274, 84 USPQ2d 1108 (Fed. Cir. 2007), Monsanto Co. v. Syngenta Seeds, Inc. , 503 F.3d 1352, 84 U.S.P.Q.2d 1705 (Fed. Cir. 2007), and Sitrick v. Dreamworks, LLC , 516 F.3d 993, 85 USPQ2d 1826 (Fed. Cir. 2008). See also In re Cortright , 49 USPQ2d 1464, 1466 and Bristol-Myers Squibb Co. v. Rhone-Poulenc Rorer Inc. , 49 USPQ2d 1370. Pursuant to In re Wands , 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988), one considers the following factors to determine whether undue experimentation is required: (A) The breadth of the claims; (B) The nature of the invention; (C) The state of the prior art; (D) The level of one of ordinary skill; (E) The level of predictability in the art; (F) The amount of direction provided by the inventor; (G) The existence of working examples; and (H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure. Some experimentation is not fatal; the issue is whether the amount of experimentation is “undue”; see In re Vaeck , 20 USPQ2d 1438, 1444. The analysis is as follows: (A) Breadth of claims. (a) Scope of the compounds. The instant claims encompass millions of compounds with a substituted 3-amido-pyrrole scaffold with a variety of substituents at four different positions. (b) Scope of the diseases covered. The full scope is not known, see the 112(b) rejection above. Several of the umbrella terms will be further addressed here. Cancer is not a single disease, or cluster of closely related disorders. Cancer is embraced also by cell proliferative disorders. There are hundreds of cancers, which have in common only some loss of controlled cell growth. Cancers are highly heterogeneous at both the molecular and clinical level, something seen especially in, for example, the cancers of the breast, brain and salivary glands. They can occur in pretty much every part of the body. Here are some assorted categories: A. CNS cancers cover a very diverse range of cancers in many categories and subcategories. There are an immense range of neuroepithelial tumors. Gliomas, the most common subtype of primary brain tumors, most of which are aggressive, highly invasive, and neurologically destructive tumors are considered to be among the deadliest of human cancers. These are any cancers which show evidence (histological, immunohistochemical, ultrastructural) of glial differentiation. These fall mostly into five categories. There are the astrocytic tumors (astrocytomas): pilocytic astrocytoma (including juvenile pilocytic astrocytoma, JPA, and pediatric optic nerve glioma) diffuse astrocytomas (including fibrillary astrocytomas, protoplasmic astrocytomas and gemistocytic astrocytomas), anaplastic astrocytomas (including adult optic nerve glioma), Glioblastoma multiforme (GBM), gliosarcoma and giant cell glioblastoma, and pleomorphic xanthoastrocytoma. GBM exists in two forms, primary and secondary, which have very different clinical histories and different genetics, but GBM is considered to be one clinical entity. second, there are the oligodendroglial tumors (oligodendrogliomas): low grade oligodendroglioma and anaplastic oligodendroglioma. Third, there is oligoastrocytomas (“mixed glioma”), a type of tumor with both astrocytoma & oligodendroglioma features. The fourth type is the ependymomas, which are intracranial gliomas, including papillary ependymoma, myxopapillary ependymoma, tanycytic ependymoma, anaplastic ependymoma and subependymal giant-cell astrocytomas. A fifth type is the gangliogliomas (glioneuronal tumors or glioneurocytic tumors), which have both glial and neuronal components, and are extremely varied, based in part on what types of glial and what types of neuronal components are present. These include Papillary Glioneuronal Tumor (PGNT), a range of supratentorial gangliogliomas, assorted intramedullary spinal cord gangliogliomas, pineal ganglioglioma, hypothalamic ganglioglioma, cerebellar ganglioglioma, ganglioglioma of the right optic tract, rosetted glioneuronal tumor (“glioneurocytic tumor with neuropil rosettes”), composite pleomorphic xanthoastrocytoma (PXA)-ganglioglioma, desmoplastic ganglioglioma (both infantile (DIG) and non- infantile), angioganglioglioma, and others. There are also some glial tumors which do not comfortably fit into these five categories, notably astroblastoma, gliomatosis cerebri, and chordoid glioma, which is found solely in the hypothalamus and anterior third ventricle. Other neuroepithelial tumors include astrocytic tumors (e.g. astrocytomas) oligodendroglial tumors, ependymal cell tumors (e.g. myxopapillary ependymoma), mixed gliomas (e.g. mixed oligoastrocytoma and ependymo-astrocytomas) tumors of the choroid plexus(choroid plexus papilloma, choroid plexus carcinoma), assorted neuronal and neuroblastic tumors (e.g. gangliocytoma, central neurocytoma, dysembryoplastic neuroepithelial tumor, esthesioneuroblastoma, olfactory neuroblastoma, olfactory neuroepithelioma, and neuroblastomas of the adrenal gland), pineal parenchyma tumors (e.g. pineocytoma, pineoblastoma, and pineal parenchymal tumor of intermediate differentiation), embryonal tumors (e.g. medulloepithelioma, neuroblastoma, ependymoblastoma, atypical teratoid/rhabdoid tumor, desmoplastic medulloblastoma, large cell medulloblastoma, medullomyoblastoma, and melanotic medulloblastoma) and others such as polar spongioblastoma and gliomatosis cerebri. A second Division is tumors of the meninges. this includes tumors of the meningothelial cells, including meningiomas (meningothelial, fibrous (fibroblastic), transitional (mixed), psammomatous, angiomatous, microcystic, secretory, lymphoplasmacyte-rich, metaplastic, clear cell, chordoid, atypical, papillary, rhabdoid, anaplastic meningioma) and the non- meningioma tumors of the meningothelial cells (malignant fibrous histiocytoma, leiomyoma, leiomyosarcoma, rhabdomyoma, rhabdomyosarcoma, chondroma, chondrosarcoma, osteoma, osteosarcoma, osteochondroma, haemangioma, epithelioid haemangioendothelioma, haemangiopericytoma, angiosarcoma, kaposi sarcoma). There are also mesenchymal, non-meningothelial tumors (liposarcoma, (intracranial) solitary fibrous tumor, and fibrosarcoma) as well as primary melanocytic lesions (diffuse melanocytosis, melanocytoma, malignant melanoma, and meningeal melanomatosis). A third division are the tumors of cranial and spinal nerves. This includes cellular schwannomas, plexiform schwannomas and the melanotic schwannomas (e.g. psammomatous melanotic schwannoma, neuro-axial melanotic schwannoma, dorsal dumb-bell melanotic schwannoma). There is also Perineurioma (Intraneural and Soft tissue) and malignant peripheral nerve sheath tumor (MPNST), including Epithelioid, MPNST with divergent mesenchymal differentiation, and MPNST with epithelial differentiation. A fourth division are germ cell tumors, including germinoma, embryonal carcinoma, yolk sac tumor, choriocarcinoma, and teratoma (mature teratoma, immature teratoma, and teratoma with malignant transformation). A fifth division are the tumors of the sellar Region, viz. pituitary adenoma, pituitary carcinoma, granular cell myoblastoma and craniopharyngiomas (adamantinomatous and papillary). Yet another division are local extensions from regional tumors, including paraganglioma, chodroma, chordoma, and chondrosarcoma. There are also Primitive Neuroectodermal Tumors (PNETs) including medulloblastomas, medulloepitheliomas, ependymoblastomas and polar spongioblastomas. There are Vascular brain Tumors e.g. the hemangioblastomas, there is CNS Lymphoma (which can be primary or secondary) and Meningeal Carcinomatosis. There are lymphoma and haemopoietic neoplasms including malignant lymphomas (which can be primary or secondary), plasmacytoma, and granulocytic sarcoma. And there are many, many others. B. Leukemia is any malignant neoplasm of the blood-forming tissues. Leukemia can arise from many different sources. These include viruses such as EBV, which causes Burkitt's lymphoma, and HTLV-1, linked to certain T cell leukemias. Others are linked to genetic disorders, such as Fanconi's anemia, which is a familial disorder, and Down's Syndrome. Other leukemias are caused by exposure to carcinogens such as benzene, and some are actually caused by treatment with other neoplastic agents. Still other leukemias arise from ionizing radiation, and many are idiopathic. Leukemias also differ greatly in the morphology, degree of differentiation, body location (e.g. bone marrow, lymphoid organs, etc.) There are dozens of leukemias. There are B-Cell Neoplasms such as B-cell prolymphocytic leukemia and Hairy cell leukemia (HCL, a chronic Lymphoid leukemia). There are T-Cell Neoplasms such as T-cell prolymphocytic leukemia, aggressive NK cell leukemia, adult T cell leukemia/lymphoma (ATLL), and T-cell granular Lymphocytic leukemia. There are different kinds of acute myeloid leukemias (undifferentiated AML, acute myeloblastic, acute myelomonocytic leukemia, acute monocytic leukemias, acute monoblastic, acute megakaryoblastic ( AmegL) , acute promyelocytic leukemia (APL), and erythroleukemia). There is also lymphoblastic leukemia, hypocellular acute myeloid leukemia, Ph-/BCR- myeloid leukemia, and acute basophilic leukemia. Chromic leukemias include chronic lymphocytic leukemia (CLL, which exists in a B-cell and a T-cell type), prolymphocytic leukemia (PLL), large granular lymphocytic leukemia (LGLL, which goes under several other names as well), chronic myelogenous leukemia (CML), chronic myelomonocytic leukemia (CMML), chronic neutrophilic leukemia, chronic eosinophilic leukemia (CEL), and many others. These are just two categories of cancer which were elaborated. Others are: C. Carcinomas of the Liver, D. Lung and pleural cancer, E. Thyroid cancer, F. Cancer of the skin cells, G. Colorectal cancers, H. Renal carcinomas, I. Prostate Cancer, J. Penile carcinoma, K. The carcinomas of the extrahepatic bile ducts, L. Breast cancers, M. Ovarian cancers, N. Testicular cancers, O. Paratesticular cancers, P. Cancers of the vulva, Q. Vaginal cancers, R. Uterus cancers, S. Stomach cancers, T. Cancers of the esophagus, U. Cancers of the spleen, V. Salivary gland carcinomas, W. Cancers of the heart, X. Odontogenic tumors, Y. Cancers of the oral cavity and oropharynx, Z. Cancers of the lymph glands, AA. Cancers of the adrenal glands, AB. Cancers of the eye, AC. Cervical cancers, AD. Gestational Trophoblastic Neoplasias (cancer of the placenta), AE. Cancers of the throat, AF. Cancers of the thymus, AG. Fallopian Tube Cancer, AH. Bladder cancers, and AI. Cancers of the gallbladders. (B) The nature of the invention and predictability in the art: With specific reference to cancer, Ex parte Kranz , 19 USPQ2d 1216, 1219 notes the “general unpredictability of the field [of] …anti-cancer treatment.” In re Application of Hozumi et al. , 226 USPQ 353 notes the “fact that the art of cancer chemotherapy is highly unpredictable”. More generally, the invention is directed toward medicine and is therefore physiological in nature. It is well established that “the scope of enablement varies inversely with the degree of unpredictability of the factors involved,” and physiological activity is generally considered to be an unpredictable factor. See In re Fisher , 427 F.2d 833, 839, 166 USPQ 18, 24 (CCPA 1970). (C) Direction or Guidance: That provided is very limited. The dosage range information, found on page 21 of the s pecification gives about 10 to about 1000 mg per dose, from 1 to 5 times daily , which is broad. Moreover, this is generic, the same for the many disorders covered by the specification. Thus, there is no specific direction or guidance regarding a regimen or dosage effective specifically for any and all the disease or disorders embraced by the scope . (D) State of the Prior Art: The claimed compounds are substituted 3-amido-pyrroles . So far as the examiner is aware substituted 3-amido-pyrroles have not been successfully used as anticancer agents , generally . (E) Working Examples: The invention is drawn to a method of treating a disease caused by and/or associated with dysregulated CDC 7 kinase activity . There are no in vivo working examples in the Specification drawn to this utility to support the use of the claimed compounds to treat any and all diseases embraced by the scope . On pages 23-27 of the s pecification , there are several in vitro assays are presented , which provide data for the inhibition of CDC7 and an aldehyde oxidase test . (F) Skill of those in the art: Taken as a whole, the skill level in oncology must be considered as low. Many mechanisms have been proposed over the decades as methods of treating the assorted cancers generally. Cytotoxic agents could be applied directly to the tumor cells, directly killing them. Immunotherapy involves stimulating the patient's immune system to attack the cancer cells, either by immunization of the patient, in which case the patient's own immune system is trained to recognize tumor cells as targets, or by the administration of therapeutic antibodies as drugs, so the patient's immune system is recruited to destroy tumor cells by the therapeutic antibodies. Another approach would be to increase the amount or activity of the body’s tumor suppressor genes, e.g. p53, PTEN, APC and CD95, which can for example activate DNA repair proteins, suppress the Akt/PKB signaling pathway, or initiate apoptosis of cancer cells. The angiogenesis inhibitor strategy was based on cutting off the blood supply that growing tumors need by shutting off the growth of new blood vessels by, for example, suppressing proliferation of endothelial cells or inducing apoptosis of endothelial cells. There is also the cancer stem cell paradigm, which hypothesizes that cancer could be treated generally, either by targeting the cancer stem cells themselves, or by targeting the epithelial-to-mesenchymal transition which supposedly generates the cancer stem cells. Many of these approaches --- and there have been others as well --- have produced anti-cancer drugs. However, despite high hopes for success, and a plausible theory why these should work for cancers generally, none of these approaches have ever produced a drug which come anywhere near such a goal. Specifically, t he prior art knows that there never has been a compound capable of treating cancers generally. “The cancer therapy art remains highly unpredictable, and no example exists for efficacy of a single product against tumors generally.” (< http://www.uspto.gov/web/offices/pac/dapp/1pecba.htm#7 > ENABLEMENT DECISION TREE, Example F, situation 1). A similar statement appears at In re Application of Hozumi et al. , 226 USPQ 353: “In spite of the vast expenditure of human and capital resources in recent years, no one drug has been found which is effective in treating all types of cancer. Cancer is not a simple disease, nor is it even a single disease, but a complex of a multitude of different entities, each behaving in a different way”. There are compounds that treat a modest range of cancers, but no one has ever been able to figure out how to get a compound to be effective against cancer generally, or even a majority of cancers. The attempts to find compounds to treat the various cancers arguably constitute the single most massive enterprise in all of pharmacology. This has not resulted in finding any treatment for tumors generally. Indeed, the existence of such a "silver bullet" is contrary to our present understanding in oncology. This is because it is now understood that there is no “master switch” for cancers generally; cancers arise from a bewildering variety of differing mechanisms. Even the most broadly effective antitumor agents are only effective against a small fraction of the vast number of different cancers known. This is true in part because cancers arise from a wide variety of sources, primarily a wide variety of failures of the body's cell growth regulatory mechanisms, but also such external factors such as viruses (an estimated at least 20% are of viral origin e.g. Human papillomavirus, EBV, Hepatitis B and C, HHV-8, HTLV-1 and other retroviruses, and quite possibly Merkel cell polyomavirus, and there is some evidence that CMV is a causative agent in glioblastoma), exposure to chemicals such as tobacco tars, excess alcohol consumption (which causes hepatic cirrhosis, an important cause of HCC), ionizing radiation, and unknown environment factors. Accordingly, there is substantive “reason for one skilled in the art to question the objective truth of the statement of utility or its scope” ( In re Langer , 183 USPQ 288, 297). Similarly, In re Novak , 134 USPQ 335, 337-338, says “unless one with ordinary skill in the art would accept those allegations as obviously valid and correct, it is proper for the examiner to ask for evidence which substantiates them.” There is no such evidence in this case. Likewise, In re Cortright , 49 USPQ2d 1464, states: “Moreover, we have not been shown that one of ordinary skill would necessarily conclude from the information expressly disclosed by the written description that the active ingredient” does what the specification surmises that it does. That is exactly the case here. Even if applicants’ assertion that cancer in general could be treated with these compounds were plausible--- which it is not ---, that would not suffice, as was stated in Rasmusson v. SmithKline Beecham Corp. , 75 USPQ2d 1297, 1301: “If mere plausibility were the test for enablement under section 112, applicants could obtain patent rights to “inventions” consisting of little more than respectable guesses as to the likelihood of their success.” Different types of cancers affect different organs and have different methods of growth and harm to the body, and different vulnerabilities. The skill thus depends on the particular cancer involved. There are some cancers where the chemotherapy skill level is high and there are multiple successful chemotherapeutic treatments. The mechanism in these situations, however, is not necessarily the same as is alleged for these compounds. One skilled in the art knows that chemotherapy of brain tumors is especially difficult. This is because 1) the blood-brain barrier, which is often intact in parts or all of a brain tumor, will block out many drugs, as it is the purpose of the blood-brain barrier to protect the brain from alien chemicals, and 2) CNS tumors are characterized by marked heterogeneity, which greatly decreases vulnerability to chemotherapy. As a result, many categories of CNS tumors simply have no chemotherapy available. These include, generally, hemangioblastomas, meningiomas, craniopharyngiomas, acoustic neuromas, pituitary adenomas, optic nerve gliomas, glomus jugulare tumors and chordomas, to name just some. With regard to gliomas, GBM is considered untreatable; no effective agents have emerged for the treatment of GBM, despite 20 years of enrolling patients in clinical trials. It is radiation and surgery which are used for low grade gliomas (e.g. pilocytic astrocytoma and diffuse astrocytomas), as no drug has been found effective. There is no drug treatment established as effective for optic nerve gliomas or gangliogliomas. Indeed, very few gliomas of any type are treated with pharmaceuticals; it is one of the categories of cancer that is the least responsive to drugs. Cartilage tumors do not respond to chemotherapy, nor, generally, do cancerous teratomas. Of the thyroid cancers, only one (anaplastic thyroid cancer) can be treated with anticancer agents. The other are treated with radioactivity, surgery, or thyroid suppression hormones. Lymphomas of the stomach are not commonly treated with anti-cancer agents per se, but instead, surgery or radiation and antibiotic therapy (e.g. amoxicillin, metronidazole, bismuth, omeprazole) are the primary treatments. Neuroendocrine tumors of the cervix generally do not respond to chemotherapy. A number of sarcomas, including alveolar soft part sarcoma (ASPS), retroperitoneal sarcoma, most liposarcomas, and the assorted chondrosarcomas, are generally considered not to respond to chemotherapy; no chemotherapeutic agent has been established as effective. Aggressive NK cell leukemia is considered to be untreatable with pharmaceuticals. Myxoma of the heart ( atrial myxoma) is the most common primary cardiac tumor and has no chemotherapy; excision is the only treatment. Chemotherapy of spleen tumors is rarely even attempted, and no drug has been established as effective for any primary or secondary splenic tumor types. Many cerebral metastases, such as those from non-small-cell lung cancer and melanoma, are not chemosensitive and will not respond to chemotherapy. Hepatocellular Carcinoma (HCC or hepatoma) is, in humans, possibly the most prevalent solid tumor and in certain parts of the world is the most common cancer; it has long been understood as a chemotherapy-resistant tumor, with only very recently, some success seen with the Tyrosine protein kinase inhibitor Sorafenib . Metastatic esophageal cancer, and malignant melanoma of the esophagus do not respond to chemotherapy. It is important to note that tumors can need to be treated quite differently even though they are tumors of the same organ. For example, the drugs used most often to treat Wilms tumor, the most common malignant tumor of the kidneys in children, are actinomycin D and vincristine. Such drugs are never used with clear cell renal carcinoma, which is treated, although without much success, with Immunotherapy using the cytokines interleukin-2 and interferon-alpha. However, such immunotherapy has never been established as effective in non-clear cell RCC forms such as papillary renal cell carcinoma. Despite strenuous efforts over a period of decades, no chemotherapeutic agent has ever been found effective against this cancer. Cancers of the stomach can be lymphomas, GISTs, carcinoid tumors, carcinomas, or soft tissue sarcomas, and for a single agent to be effective against all or even most of these categories would be contrary to what is known in oncology. (G) The quantity of experimentation needed: Given the fact that, historically, the development of new cancers drugs has been difficult and time consuming, and especially in view of factors A and D and F, the quantity of experimentation needed is expected to be great. MPEP 2164.01(a) states, “A conclusion of lack of enablement means that, based on the evidence regarding each of the above factors, the specification, at the time the application was filed, would not have taught one skilled in the art how to make and/or use the full scope of the claimed invention without undue experimentation. In re Wright , 999 F.2d 1557,1562, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993).” That conclusion is clearly justified here. In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status. Claim Rejections - 35 USC § 103 The following is a quotation of 35 U.S.C. 103(a) which forms the basis for all obviousness rejections set forth in this Office action: (a) A patent may not be obtained though the invention is not identically disclosed or described as set forth in section 102 of this title, if the differences between the subject matter sought to be patented and the prior art are such that the subject matter as a whole would have been obvious at the time the invention was made to a person having ordinary skill in the art to which said subject matter pertains. Patentability shall not be negatived by the manner in which the invention was made. The factual inquiries set forth in Graham v. John Deere Co. , 383 U.S. 1, 148 USPQ 459 (1966), that are applied for establishing a background for determining obviousness under 35 U.S.C. 103(a) 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. This application currently names joint inventors. In considering patentability of the claims under 35 U.S.C. 103(a), the examiner presumes that the subject matter of the various claims was commonly owned at the time any inventions covered therein were made absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and invention dates of each claim that was not commonly owned at the time a later invention was made in order for the examiner to consider the applicability of 35 U.S.C. 103(c) and potential 35 U.S.C. 102(e), (f) or (g) prior art under 35 U.S.C. 103(a). Claim s 1-6, 11-14 and 16-20 are rejected under AIA 35 U.S.C. 103(a) as being unpatentable over Brasca et al. (WO 2014019908 , cited on the IDS ) . The present application claims compounds of formula (I), compositions and kits thereof, a method of making compounds of formula (I), an in vitro method for inhibiting CDC 7 kinase activity and a method of treating a disease, e.g. cancer, comprising administering the compounds of formula (I) , see below, and , e.g., more specifically compound 9 in claim 5 . The ‘908 reference teaches the following species: , see page 96, compound 189 . The claims exclude this compound by proviso in the definition of R 2 . The only difference between the claimed compound 9 and compound 123 is the substitution on the phenyl ring at the 2 -position of the pyrrole ring, 5-chloro-2-methyl versus Applicant’s 2-chloro-4-methyl . These compounds are positional isomers and are considered equivalent. The MPEP 2144.09 states “Compounds which are position isomers (compounds having the same radicals in physically different positions on the same nucleus) or homologs (compounds differing regularly by the successive addition of the same chemical group, e.g., by -CH2- groups) are generally of sufficiently close structural similarity that there is a presumed expectation that such compounds possess similar properties. In re Wilder , 563 F.2d 457, 195 USPQ 426 (CCPA 1977). See also compound 5 in claim 5 (bottom left) compared to compound 206 on page 96 (bottom right) : compared to . The only difference s are 1) substitution o f the trifluoromethyl group o n the phenyl ring at the 2 -position of the pyrrole ring, the 5 -position versus Applicant’s 4-position; and 2) the ring at the 5 -position of the pyrrole ring , 6-aminopyrimidinyl versus Applicant’s pyrrolo[2,3-b]pyridinyl. The ‘908 reference teaches the equivalency of the following rings at this position , which embraces both rings : . Moreover, there is a guidepost with the pyrrolo[2,3-b]pyridinyl in the ‘908 reference, see compound 189 above. The synthesis of the compounds is taught on pages 13-22 and 103-109 of the ‘908 reference. An in vitro assay and composition or product is taught on page 110. A method of treating cancer is also taught on pages 10-110. Thus, the claims are rendered obvious by Brasca et al. Claims 1-6, 11-14 and 16-20 are rejected under AIA 35 U.S.C. 103(a) as being unpatentable over Vanotti et al. (WO 2007110344) in view of Brasca et al. (WO 2014019908). The present application claims compounds of formula (I), compositions and kits thereof, a method of making compounds of formula (I), an in vitro method for inhibiting CDC 7 kinase activity and a method of treating a disease, e.g. cancer, comprising administering the compounds of formula (I) , see below, and, e.g., more specifically compound 42 in claim 5 . The ‘344 reference teaches the following species: , see page 109. The only difference between the claimed compound 42 and compound F26 is the substitution on the p yrimidine ring at the 5-position of the pyrrole ring, 2-amino versus Applicant’s 6-amino . These compounds are positional isomers and are considered equivalent. The MPEP 2144.09 states “Compounds which are position isomers (compounds having the same radicals in physically different positions on the same nucleus) or homologs (compounds differing regularly by the successive addition of the same chemical group, e.g., by -CH2- groups) are generally of sufficiently close structural similarity that there is a presumed expectation that such compounds possess similar properties. In re Wilder , 563 F.2d 457, 195 USPQ 426 (CCPA 1977). Moreover, the Brasca reference teaches the 6-aminopyrimidine at this position on the pyrrole ring. An in vitro assay is taught on pages 27-30 and the composition or product is taught on pages 30-32. A method of treating cancer is also taught on page 126. Vanotti does not teach the presently claimed synthesis. This is remedied with the Brasca reference. The synthesis of the compounds is taught on pages 13-22 and 103-109 of the Brasca reference. Thus, the claims are rendered obvious by Vanotti et al. in view of Brasca et al. Double Patenting 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. A nonstatutory double patenting rejection is appropriate where the claims at issue are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg , 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); 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) or 1.321(d) may be used to overcome an actual or provisional rejection based on a nonstatutory double patenting ground provided the reference application or patent either is shown to be commonly owned with this application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b). The USPTO internet Web site contains terminal disclaimer forms which may be used. Please visit http://www.uspto.gov/forms/. The filing date of the application will determine what form should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to http://www.uspto.gov/patents/process/file/efs/guidance/eTD-info-I.jsp. Claims 1-6, 11-14 and 16-20 are rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claim s 1-5 of U.S. Patent No. 9688661 (this is the US 371 application for the WO 2014019908 reference) . Although the conflicting claims are not identical, they are not patentably distinct from each other because the present application claims compounds of formula (I), compositions and kits thereof, a method of making compounds of formula (I), an in vitro method for inhibiting CDC 7 kinase activity and a method of treating a disease, e.g. cancer, comprising administering the compounds of formula (I) , see below, and more specifically compound 9 in claim 5 , see also the 103 rejection above and compound 189 in the ‘661 patent, claim 2 . The claims in the ‘661 patent are drawn to compounds of formula (I) and compound 189 in claim 2 is embraced by the genus of claim 1. The same compound is used for the 103 rejection above and therefore, the same rationale is equally applicable here. Claims 1-6, 11-14 and 16-20 are rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 1- 2 of U.S. Patent No. 10071986 (this is a divisional of the US 371 application for the WO 2014019908 reference) . Although the conflicting claims are not identical, they are not patentably distinct from each other because the present application claims compounds of formula (I), compositions and kits thereof, a method of making compounds of formula (I), an in vitro method for inhibiting CDC 7 kinase activity and a method of treating a disease, e.g. cancer, comprising administering the compounds of formula (I) , and more specifically compound 9 in claim 5, see the 103 rejection above and compound 189 in the ‘ 986 patent . The claims in the ‘ 986 patent are drawn to a process of synthesizing the compounds of formula (I) , wherein the claims are a subgenus of the present claims. The s ynthesis is similar to the present claim 6 where the same argument may be applied for positional isomers that is used for the 103 rejection above . T herefore, the same rationale is equally applicable here. Moreover, there is no patentable distinction between compounds and method of making said compounds. Claims 1-6, 11-14 and 16-20 are rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 1- 16 of U.S. Patent No. 10479778 (this is a divisional of the US 371 application for the WO 2014019908 reference) . Although the conflicting claims are not identical, they are not patentably distinct from each other because the present application claims compounds of formula (I), compositions and kits thereof, a method of making compounds of formula (I), an in vitro method for inhibiting CDC 7 kinase activity and a method of treating a disease, e.g. cancer, comprising administering the compounds of formula (I) , and more specifically compound 5 in claim 5, see the 103 rejection above and compound 206 in the ‘ 778 patent, claim 4 . The claims in the ‘ 778 patent are also drawn to compounds of formula (I), compositions and kits thereof, a method of making compounds of formula (I), an in vitro method for inhibiting CDC 7 kinase activity and a method of treating a disease, e.g. cancer, comprising administering the compounds of formula (I) . The synthesis is similar to the present claim 6 , where the same argument may be applied that is used for the 103 rejection above . T herefore, the same rationale is equally applicable here. Claims 1-6, 11-14 and 16-20 are rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 1- 4 of U.S. Patent No. 10479779 (this is a divisional of the US 371 application for the WO 2014019908 reference) . Although the conflicting claims are not identical, they are not patentably distinct from each other because the present application claims compounds of formula (I), compositions and kits thereof, a method of making compounds of formula (I), an in vitro method for inhibiting CDC 7 kinase activity and a method of treating a disease, e.g. cancer, comprising administering the compounds of formula (I) , and more specifically compound s 5 and 9 in claim 5, see the 103 rejection above . The claims in the ‘779 patent are drawn to a method of treating, e.g. solid tumors, comprising administering a compound of formula (I), which are positional isomers and a subgenus of the present claims. T he same argument may be applied that is used for the 103 rejection above and therefore, the same rationale is equally applicable here. Conclusion Any inquiry concerning this communication or earlier communications from the examiner should be directed to FILLIN "Examiner name" \* MERGEFORMAT SUSANNA MOORE whose telephone number is FILLIN "Phone number" \* MERGEFORMAT (571)272-9046 . The examiner can normally be reached FILLIN "Work Schedule?" \* MERGEFORMAT Monday - Friday, 10:00 am to 7:00 pm . Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Jeffrey Murray can be reached on FILLIN "SPE Phone?" \* MERGEFORMAT 571-272-9023 . The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300. Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000. /SUSANNA MOORE/ Primary Examiner, Art Unit 1624