COMBINATION OF A CXCR7 ANTAGONIST WITH AN S1P1 RECEPTOR MODULATOR

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 . DETAILED ACTION Claims 1, 3-10, 12, 13, 15, 17, 18 and 22-24 are pending in the instant application. Election/Restrictions Applicant’s election with traverse of Group I, PNG media_image1.png 470 638 media_image1.png Greyscale , and the election of the species of the claimed pharmaceutical composition comprising (3S,4S)-1-Cyclopropylmethyl-4-{[5-(2,4-difluoro-phenyl)-isoxazole-3-carbonyl]-amino}-piperidine-3-carboxylic acid (1-pyrimidin-2-yl-cyclopropyl)-amide (the COMPOUND) and the S1P1 receptor modulator Fingolimod, PNG media_image2.png 276 156 media_image2.png Greyscale , in the reply filed on February 4, 2026 was acknowledged in the previous Office Action. The requirement was deemed proper and therefore made FINAL in the previous Office Action. Information Disclosure Statement The information disclosure statement (IDS) submitted on September 24, 2026 was filed after the mailing date of the non-final Office Action on May 13, 2026. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner. Rejections and objections made in the previous Office Action that do not appear below have been overcome by Applicant’s amendments to the specification and to the claims. Therefore, arguments pertaining to these rejections and objections will not be addressed. Rejoinder Claims 1 and 3 are directed to an allowable product. Pursuant to the procedures set forth in MPEP § 821.04(B), claims 4-10, 12, 13, 15, 17, 18 and 22-24, directed to the process of making or using an allowable product, previously withdrawn from consideration as a result of a restriction requirement, are hereby rejoined and fully examined for patentability under 37 CFR 1.104. Because all claims previously withdrawn from consideration under 37 CFR 1.142 have been rejoined, the restriction requirement as set forth in the Office action mailed on December 4, 2025 is hereby withdrawn. In view of the withdrawal of the restriction requirement as to the rejoined inventions, applicant(s) are advised that if any claim presented in a divisional application is anticipated by, or includes all the limitations of, a claim that is allowable in the present application, such claim may be subject to provisional statutory and/or nonstatutory double patenting rejections over the claims of the instant application. Once the restriction requirement is withdrawn, the provisions of 35 U.S.C. 121 are no longer applicable. See In re Ziegler, 443 F.2d 1211, 1215, 170 USPQ 129, 131-32 (CCPA 1971). See also MPEP § 804.01. As a result of the current amendments to the claims per the Amendment filed August 13, 2026 and the rejoinder of the method of use claims, the following objection and rejections now apply. Claim Objections Claim 12 is objected to because of the following informalities: in claim 12, an “and” should have been added after the phrase “below per day of fingolimod;” (the end of line 6 of the claim). Claim Rejections - 35 USC § 112 The following is a quotation of the first paragraph 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 the first paragraph of pre-AIA 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 4-10, 12, 13, 15, 17, 18 and 22-24 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 for treatment of a patient diagnosed with multiple sclerosis (MS), does not reasonably provide enablement for a method for the prevention, the prophylaxis or treatment of all autoimmune or inflammatory diseases or disorders, or a transplant rejection or all neurodegenerative diseases or disorders. 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. 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 in Liebel-Flarsheim Co. v. Medrad, Inc., 481 F.3d 1371, 82 USPQ2d 1113; 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). 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: (1) Breadth of claims. (a) Scope of the compounds. (b) Scope of the diseases covered. The scope of the prevention, the prophylaxis or treatment of all autoimmune or inflammatory diseases or disorders, or the prevention, the prophylaxis or treatment of all types of transplant rejections or the prevention, the prophylaxis or treatment of all neurodegenerative diseases or disorders. The “autoimmune diseases” are processes which can take place in virtually any part of the body. There is a vast range of forms that it can take. There are dozens of such diseases, which have fundamentally different mechanisms and different underlying causes. Known autoimmune disorders, or disorders generally considered to be autoimmune, include Polymyositis, Scleroderma, Osteosclerosis, Meniere's disease, Idiopathic neutropenia, Idiopathic thrombocytopenic purpura, Autoimmune hemolytic anemia, Premature ovarian failure, Idiopathic hypoparathyroidism, primary biliary cirrhosis, Pemphigus, multiple sclerosis, autoimmune uveitis, Addison's disease, thyroiditis, atrophic gastritis, myasthenia gravis, hemolytic anemia, systemic lupus erythematosus, Wegener's granulomatosis, polyarteritisnodosa, erythema nodosum leprosum, Guillain-Barré syndrome (GBS), allergic encephalomyelitis, acute necrotizing hemorrhagic encephalopathy, idiopathic bilateral progressive sensorineural hearing loss (IPBSNHL), aplastic anemia, pure red cell anemia, polychondritis, scleroderma, Stevens-Johnson syndrome, idiopathic sprue, lichen planus, Crohn's disease, Graves ophthalmopathy, sarcoidosis, primary biliary cirrhosis, type I diabetes, autoimmune optic neuritis, uveitis posterior, or interstitial lung fibrosis, alopecia, Sjogren's Syndrome, Goodpasture Syndrome, inflammatory bowel disease, Essential Mixed Cryoglobulinemia, Bechet's Syndrome, Antiphospholipid Syndrome, Relapsing Polychondritis (systemic chondromalacia or von Meyenburg disease), Retroperitoneal Fibrosis, immune dysregulation, polyendocrinopathy, enteropathy, etc. Further, inflammation is a process which can take place in virtually any part of the body. There is a vast range of forms that it can take, causes for the problem, and biochemical pathways that mediate the inflammatory reaction. It is one of the most pervasive of all body processes. Inflammation is a very general term which encompasses a huge variety of specific processes. Inflammation is the reaction of vascularized tissue to local injury; it is the name given to the stereotyped ways tissues respond to noxious stimuli. These occur in two fundamentally different types. Acute inflammation is the response to recent or continuing injury. The principal features are dilatation and leaking of vessels, and recruitment of circulating neutrophils. Chronic inflammation or "late-phase inflammation" is a response to prolonged problems, orchestrated by T-helper lymphocytes. It may feature recruitment and activation of T- and B- lymphocytes, macrophages, eosinophils, and/or fibroblasts. The hallmark of chronic inflammation is infiltration of tissue with mononuclear inflammatory cells. Mechanistically, chronic inflammation encompasses a broad spectrum of immunologic processes, including antibody formation, antibody-dependent cell- mediated cytotoxicity, and cell-mediated immunity (delayed-type hypersensitivity). Granulomas are seen in certain chronic inflammation situations. They are clusters of macrophages which have stuck tightly together, typically to wall something off. Granulomas can form with foreign bodies such as aspirated food, toxocara, silicone injections, and splinters. Otitis media is an inflammation of the lining of the middle ear and is commonly caused by Streptococcus pneumoniae and Haemophilus influenzae. Its numerous forms include acute suppurative otitis media, chronic tubotympanic suppurative otitis media, chronic atticoantral suppurative otitis media, acute nonsuppurative otitis media, chronic serous otitis media, chronic mucoid otitis media, allergic seromucinous otitis media, exudative transudative otitis media, catarrhal serous otitis media, allergic otitis media and chronic purulent otitis media. Myringitis (sometimes included with otitis externa) is inflammation of the tympanic membrane. It comes in numerous forms. Acute myringitis can occur because of direct trauma to the tympanic membrane through penetration by a foreign body. Primary myringitis may also be caused by unsuccessful removal of a foreign body, typically an insect, or by self-cleaning of the ear. Acute bullous myringitis and acute hemorrhagic myringitis can both be the consequence of a bacterial or viral infection. Fungal myringitis can be the consequence of a fungal infection. Eczematous myringitis can occur in cases of dermal eczema of the tympanic membrane's epidermis. Myringitis granulosa occurs when the tympanic membrane is covered with granulation tissue, and can result in destroying the tympanic membrane. Idiopathic inflammatory medial meatal fibrotizing otitis is a disorder of the external auditory canal characterized by desquamation of the medial canal skin, chronic inflammation, and eventual canal stenosis. Otitis externa (also known as "Swimmer's ear") is an inflammation of the outer ear and ear canal. The chronic form may be secondary to eczema, whereas the acute form tends to be in response to a microbial infection. Perichondritis of auricle, cholesteatoma of external ear and keratosis obturans are generally included with this. Otitis interna (labyrinthitis) is an inflammation of the inner ear that typically results in severe vertigo and is generally thought to arise from a viral infection, from a viral inflammation. Treatment is generally with vestibular suppressants (suppression of symptoms), but antibiotics may be given in bacterial infection is suspected. The term “neurodegenerative disease” covers an immense array of largely unrelated diseases that have different modes of action and different origins. The term covers such diverse diseases/disorders as Alzheimer's Disease; Parkinson's Disease; ALS and variants such as forms of ALS-PDC; dementia of the frontal lobe type (DFT) and DFT with motor neuron disease (DFT-MND); Diffuse Lewy Body Disease; Cortical Lewy body disease; Hallervordon-Spatz disease; Senile dementia of the neurofibrillary tangle type (“tangle-only dementia”); progressive familiar myoclonic epilepsy; Corticodentatonigral degeneration; more than a dozen dementias collectively called "frontotemporal dementia” (FTD); Tourette's syndrome; multiple systems atrophy (MSA; once called Shy-Drager syndrome), which exists in two forms: MSA-P type or MSA-C type; Neurological syphilis; Neurosarcoidosis; Pure autonomic failure (Bradbury-Eggleston syndrome); Friedrich's ataxia and other spinocerebellar degenerations; Olivopontocerebellar atrophy (OPCA); spasmotic torticollis; Striatonigral degeneration; various types of torsion dystonia; certain spinal muscular atrophies, such as Werdnig-Hoffmann and Wohlfart-Kugelberg-Welander; Hereditary spastic paraplegia, Primary lateral sclerosis; peroneal muscular atrophy (Charcot-Marie-Tooth); Hypertrophic interstitial polyneuropathy (Dejerine-Sottas); ophthalmic disorders such as primary open-angle glaucoma (POAG) and retinitis pigmentosa; Leber's Disease; Wallerian degeneration, and Hypertrophic interstitial polyneuropathy. There is the neuroacanthocytosis family, a difficult to define group of genetic disorders which includes Bassen-Kornsweig disease (abetali-poproteinemia), Familial hypobetalipoproteinemia, Chorea-acanthocytosis (ChAc), McLeod syndrome (MLS), Huntington disease–like2 (HDL2) and Pantothenate kinase–associated neurodegeneration (PKAN), FHBL1, FHBL2, Familial acanthocytosis with paroxysmal exertion-induced dyskinesias and epilepsy (FAPED), and Anderson disease. There is a group of Prion diseases, notably Creutzfeldt-Jakob Disease (CJD), which occurs in both sporadic and familial forms; Gerstmann-Straussler-Scheinker Disease (GSS); and fatal familial insomnia. There is another group called the Taupathy diseases, which includes Pick's disease; cortical-basal ganglionic degeneration (CBGD or CBD); progressive supranuclear palsy (PSP); Parkinsonism-dementia complex (PDC), and the amyotrophic lateral sclerosis/Parkinsonism-dementia complex (ALS-PDC). Another group is the Polyglutamine diseases: Huntington's disease; spinal-bulbar muscular atrophy (Kennedy's disease or SBMA), Dentatorubral-Pallidoluysian Atrophy (DRPLA), Machado-Joseph disease (MJD, also called spinocerebellar ataxia type 3), and the other SCA diseases, viz SCA-1, SCA-2, SCA-6, and SCA-7. The leukodystrophies are a group of over 30 assorted genetic disorders that affect the central nervous system by disrupting the growth or maintenance of the myelin sheath. This category includes 18q-Syndrome, Acute disseminated encephalomyeolitis (ADEM), Acute Disseminated Leukoencephalitis, Acute Hemorrhagic Leukoencephalopathy, Adrenoleukodystrophy, Adrenomyeloneuropathy (AMN), Aicardi-Goutieres Syndrome, Alexander Disease, Adult-onset Autosomal Dominant Leukodystrophy (ADLD), Autosomal Dominant Diffure Leukoencephalopathy with neuroaxonal spheroids, Autosomal Dominant late-onset leukoencephalopathy, Childhood Ataxia with diffuse CNS Hypomyelination (CACH or Vanishing White Matter Disease), Canavan Disease, Cerebral Autosomal Dominant Arteriopathy with Subcortical Infacts (CADASIL) and Leukoencephalopathy, Cerebrtendinous Xanthomatosis (CTX), Craniometaphysical dysplasia with leukoencephalopathy, Extensive Cerebral White Matter abnormality without clinical symptoms, Familial adult-onset leukodystrophy manifesting as cerebellar ataxia and dementia, Familial leukodystrophy with adult onset dementia and abnormal glycolipid storage, Globoid Cell Leukodystrophy (Krabbe Disease), Hereditary adult onset leukodystrophy simulating chronic progressive multiple sclerosis, Lipomembranous osteodysplasia with leukodystrophy (Nasu Disease), Metachromatic Leukodystrophy, Megalencephalic leukodystrophy with subcortical cysts (MLC), Neuroaxonal leukoencephalopathy with axonal spheroids,Oculodetatoldigital Dysplasia with cerebral white matter abnormalities, Orthochromatic leukodystrophy with pigmented glia, Ovarioleuko-dystrophy Syndrome, Pelizaeus-Merzbacher Disease, Refsum Disease, Sjogren-Larsson Syndrome, Sudanophilic Leukodystrophy, Van der Knapp Syndrome, Vanishing White Matter Disease, X-linked Adrenoleukodystrophy (X-ALD), and the Zellweger Spectrum: Zellweger Syndrome, Neonatal Adrenoleukodystrophy, and Infantile Refsum Disease. The neuronal ceroid lipofuscinoses (NCLs) are the most common neurodegenerative disorders of childhood. These are generally characterized by loss of vision, seizures, motor dysfunction leading to spastic quadriplegia, cognitive loss, and early death. Juvenile Neuronal Ceroid Lipofuscinosis (JNCL), or Batten disease is the most common of these. Different forms arise from different genes: CLN1 most commonly causes infantile onset, but also Late Infantile- and Juvenile-Onset, as well as adult-onset. There is also late infantile (CLN2), juvenile-onset disease (CLN3), and late-infantile forms (CLN5). CLN8 underlies a form of progressive myoclonic epilepsy. The adult Kufs disease appears to be associated with CLN4. There are forms of late infantile NCL that are associated with CLN7 and CLN8, and another forms associate with NCL6. Of the 9 identified so far (CLN1-9), only 6 have their gene even identified. Neurodegeneration can arise from the attack of known or unknown viruses on the brain. For example, HIV-associated dementia (HAD) arises from HIV-1; some strains of influenza A can cause apoptotic neurodegeneration; West Nile virus can cause neurodegeneration, possibly as a result of cytotoxic lymphocytes. Neurodegeneration can also arise from stroke, and from certain types of spinal cord injuries. These exhibit a very broad range of effects and origins. For example, some give no dementia and affect only vision, such as POAG. Some give progressive dementia without other prominent neurological signs, such as Alzheimer's Disease, whereas other dementias do have such signs, such as Diffuse Lewy Body Disease. Many give distinctive and different patterns of effect. For example, FTDs, which have bilateral atrophy of the frontal and anterior temporal lobes, produce progressive nonfluent aphasia and semantic dementia, but, in contrast to e.g. Alzheimer's Disease, visuospatial skills and day-to-day memorizing is largely unaffected. Some give muscular wasting without sensory changes, e.g. ALS, and some do have the sensory changes such as Werdnig-Hoffmann. Some affect only vision such as retinitis pigmentosa, while others affect both vision and cognitive functions, such as Posterior cortical atrophy (PCA). Some are abnormalities of posture, movement or speech, such as Striatonigral degeneration, and other are progressive ataxias, such as OPCA. Some give an extremely broad range of effects. For example, CBD can give apraxia, alien limb phenomenon, cortical sensory loss, aphasia, myoclonus, bradykinesia, rigidity, dystonia, tremor, memory impairment and/or personality/behavioral changes. The toxic protein, for those diseases that involve one, also varies. In some cases, it is tau, i.e. in Alzheimer's Disease and other taupathies, and some are so linked to tau only sometimes (FTD). Alzheimer's Disease also involves β-amyloid. For Parkinson's disease it is α-synuclein. Prion disease involves PrPSc as its toxic protein, which involves missense. The polyglutamine diseases involve polyglutamine containing proteins. For Huntington's disease, it is huntingtin, for SBMA it is an androgen receptor, for DRPLA it is atrophin, for SCA-1 it is Ataxin-1, for SCA-2 it is Ataxin-2, for SCA-3 it is Ataxin-3, for SCA-6 it is a calcium channel protein, and for SCA-7 it is Ataxin-7. The nature of the protein deposits, when these occur, varies as well. In Alzheimer's Disease, there are extracellular plaques from β-amyloid and neurofibrillary tangles (from tau). In Parkinson’s disease, it is Lewy bodies and in ALS it is Bunina bodies. Taupathy produces cytoplasmic tangles, and Polyglutamine disease produce neuropil aggregates, intranuclear inclusions and cytoplasmic tangles. Prion disease produces prion plaque. And note that the disease form is not necessarily related to the protein deposits. For example, Alzheimer's Disease and Pick's disease both give progressive dementia without other prominent neurological signs. But, the characteristic Alzheimer's neurofibrillary tangles are not seen in Pick's Disease, which has straight fibrils, as opposed to the paired helical filaments of Alzheimer's Disease. Pick's Disease gives lobal atrophy, not seen in Alzheimer's Disease. The disease genes vary considerably as well. In Alzheimer's Disease, there is toxic gain of function with APP and loss of function of Presenilin 1 and presenilin 2. With Parkinson’s disease, there is toxic gain of function with α-synuclein, and loss of function of Parkin and UCHL1. In the Polyglutamine diseases, there is toxic gain of function with 9 different genes with CAG repeat expansion. In Prion disease, there is toxic gain of function with PRNP. In ALS, there is toxic gain of function with SOD1. FTDP-17 arises from mutations at chromosome 17, Huntington's Disease from chromosome 4, and the neurodegenerative disorder that people with Down's syndrome develop later in life is presumably connected in some way to chromosome 21. Certain forms of Retinitis pigmentosa have been linked to deficiency in production of the kinase CERKL. As can be seen from the above, unlike in some areas of medicine, there is no representative, or “typical” neurodegenerative disease/disorder. Some affect the mind, some affect movement, some affect both, and some effect neither. Alzheimer's Disease is the most common neurodegenerative disorder. However, its etiology involves both tau protein and β-amyloid. Such a statement is not true for any other important neurodegenerative disorder, and indeed the vast majority of neurodegenerative disorders involve neither one of those. (2) The nature of the invention and predictability in the art: 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). (3) Direction or Guidance: That provided is very limited. The dosage range information is disclosed on pages 16-17 of the instant specification. 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 treating the various diseases embraced by the instant claims. (4) State of the Prior Art: (5) Working Examples: (6) Skill of those in the art: The skill level is quite low in this art. There are huge differences in origins of these disorders, even with what little is known. Chronic wasting disease (CWD), Creutzfeldt-Jakob Disease (CJD), Bovine spongiform encephalopathy (BSE) and other transmissible spongiform encephalopathies are caused by an infectious agent (a prion, a type of misfolded protein). Others arise from viruses, known and unknown. So far as can be determined, this is not so for Huntington's disease. Even among the hereditary disorders, the origins are clearly different, since different genes are involved. For example, in Batten’s disease, a genetic loss of CLN3P enzymatic activity leads to intracellular proteolipid accumulation and thence to neuronal loss. Many, e.g., neurosarcoidosis, are of unknown origin. The majority of these have no treatment at all, and of those that do, none or virtually none have been treated with agents such as are disclosed in this application. As an important example, ALS is an untreatable disease. Spinal Muscular Atrophy (SMA), which apparently kills more infants than any other genetic disease, arises when the SMN gene is deleted or mutationally inactivated, is untreatable. CWD and other transmissible spongiform encephalopathies are untreatable. The NCLs are all untreatable. Pretty much none of the leukodystrophies are considered to have a well established pharmaceutical treatment; some are amenable to bone marrow transplantation, gene therapy or hormone replacement. The dominant polyglutamine expansion diseases, which include spinocerebellar ataxia type 1 (SCA1) and Huntington disease, are untreatable. Retinitis pigmentosa (RP), the most common hereditary cause of adult blindness, has no form of pharmacological treatment which has been established as effective, although for some people, vitamin A may slightly retard the progression of the disease. The great diversity of diseases falling within the “neurodegenerative disorder” category means that it is contrary to medical understanding that any agent (let alone a genus of so many compounds) could be generally effective against such diseases. The intractability of these disorders is clear evidence that the skill level in this art is low relative to the difficulty of the task. Further, what little success there has been does not point in the direction of the mode of action in this application. Thus, what very few treatments that the massive research effort on Alzheimer's Disease has produced are means of providing Acetylcholinesterase inhibition, (Aricept®, Cognex®, Exelon®, and Reminyl®), or voltage-dependent NMDA-antagonists (Memantine), properties that the claimed compounds are not disclosed to have. POAG is treated with beta-blockers and other IOP lowering drugs. Such drugs are not used for any other form of neurodegenerative disorder. (7) The quantity of experimentation needed: Especially in view of points 1-3 and 6, this 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 justified here. 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, 8, 10 and 18 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. Regarding claims 5, 8, 10 and 18, the phrases “including”, “especially” and “such as” render the claims indefinite because it is unclear whether the limitations following the phrases are part of the claimed invention. See MPEP § 2173.05(d). Allowable Subject Matter Claims 1 and 3 are allowed over the prior art of record. Conclusion Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a). A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action. Telephone Inquiry Any inquiry concerning this communication or earlier communications from the examiner should be directed to: Laura L. Stockton (571) 272-0710. The examiner can normally be reached on Monday-Friday from 8:30 am to 6 pm, Eastern Standard Time. 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 acting supervisor, James Alstrum-Acevedo can be reached on 571/272-5548. 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. /LAURA L STOCKTON/ Primary Examiner, Art Unit 1626 Work Group 1620 Technology Center 1600 October 12, 2026 Book XXVII, page 89