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
1. This application is a CON of 17/554,284 12/17/2021 PAT 12129262; 17/554,284 has PRO 63/127,853 12/18/2020.
2. Claims 1-25 are pending.
Claim Rejections - 35 USC § 112 (b)
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.
3. Claim 25 is 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. 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 25 recites the broad recitation additional therapeutic agent, and the claim also recites various classes of the agents and further specific examples of the classes which is the narrower statement of the range/limitation. 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.
Claim Rejections - 35 USC § 112 (a)
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.
4. Claims 1-25 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 enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention. There are many factors to be considered when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any necessary experimentation is "undue." These factors include, but are not limited to the following:
(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
In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988).
(A) The claims are drawn to a method of treating all auto-immune diseases, neurodegeneration, inflammatory diseases, and viral infections. “Neurodegenerative disorders (NDs) consist of a large number of disorders affecting the nervous system. It includes the heterogeneous group of disorders such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), and many more. The heterogeneous disorders are characterized by progressive and selective loss of neurons (Sheikh et al. 2013). In most cases, the loss of function of the affected neuronal type defines the major phenotype of the disease. The main cause of most NDs is still unknown and, therefore, there is no effective cure. NDs treatment depends on retardation or alleviation of symptoms (Jaiswal et al. 2012).” (Rai “The Role of PI3K/Akt and ERK in Neurodegenerative Disorders” Neurotoxicity Research (2019) 35:775–795). Examples of additional neurodegenerative diseases include: 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); Friedreich 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 (abetalipoproteinemia), 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. Prion diseases, notably Creutzfeldt-Jakob Disease (CJD), which occurs in both sporadic and familial forms; Gerstmann-Straussler-Scheinker Disease (GSS); and fatal familial insomnia. 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). 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. 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, Ovarioleukodystrophy 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, Infantile Refsum Disease, Niemann-Pick disease, Pelizaeus-Merzbacher disease, Sulfatide lipidosis, Amaurotic (familial) idiocy (Batten, Jansky-Bielschowsky, Kufs', Spielmeyer-Vogt Tay-Sachs, Gangliosidosis), Gaucher's disease, Hunter's disease, Mucopolysaccharidosis, Alpers' disease or gray-matter degeneration,, Infantile necrotizing encephalomyelopathy, Leigh's disease, Subacute necrotizing encephalopathy or encephalomyelopathy. 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. 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 produce abnormalities of posture, movement or speech, such as Striatonigral degeneration, and others produce 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.
There is no one cause of these diseases. Creutzfeldt-Jakob Disease (CJD), which occurs in both sporadic and familial forms; Gerstmann-Straussler-Scheinker Disease (GSS); and fatal familial insomnia are Prion diseases. So called tauopathy diseases 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). Down’s syndrome is genetic chromosomal abnormality. Dementia puglisitica is caused by repeated head trauma. Neurodegeneration can also arise from stroke, and from certain types of spinal cord injuries. These exhibit a very broad range of effects and origins. Many give distinctive and different patterns of effect. Frontotemporal dementias (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 produce abnormalities of posture, movement or speech, such as Striatonigral degeneration, and others produce progressive ataxias, such as OPCA. Some give an extremely broad range of effects. For example, corticobasal degeneration (CBD) can give apraxia, alien limb phenomenon, cortical sensory loss, aphasia, myoclonus, bradykinesia, rigidity, dystonia, tremor, memory impairment and/or personality/behavioral changes. Thus, the scope of neurodegeneration is broad.
Some autoimmune diseases include Acute Disseminated Encephalomyelitis (ADEM), Acute necrotizing hemorrhagic leukoencephalitis, Addison’s disease, Agammaglobulinemia, Alopecia areata, Amyloidosis, Ankylosing spondylitis, Anti-GBM/Anti-TBM nephritis, Antiphospholipid syndrome (APS), Autoimmune angioedema, Autoimmune aplastic anemia, Autoimmune dysautonomia, Autoimmune hepatitis, Autoimmune hyperlipidemia, Autoimmune immunodeficiency, Autoimmune inner ear disease (AIED), Autoimmune myocarditis, Autoimmune oophoritis, Autoimmune pancreatitis, Autoimmune retinopathy, Autoimmune thrombocytopenic purpura (ATP)Autoimmune thyroid disease Autoimmune urticariaAxonal & neuronal neuropathiesBalo disease Behcet’s disease, Bullous pemphigoid, Cardiomyopathy, Castleman disease, Celiac disease, Chagas disease, Chronic fatigue syndrome, Chronic inflammatory demyelinating polyneuropathy (CIDP), Chronic recurrent multifocal ostomyelitis (CRMO), Churg-Strauss syndrome, Cicatricial pemphigoid/benign mucosal pemphigoid, Crohn’s disease, Cogans syndrome, Cold agglutinin disease, Congenital heart block, Coxsackie myocarditis, CREST disease, Essential mixed cryoglobulinemia, Demyelinating neuropathies, Dermatitis herpetiformis, Dermatomyositis, Devic’s disease (neuromyelitis optica), Discoid lupus, Dressler’s syndrome, Endometriosis, Eosinophilic esophagitis, Eosinophilic fasciitis, Erythema nodosum, Experimental allergic encephalomyelitis, Evans syndrome, Fibromyalgia, Fibrosing alveolitis, Giant cell arteritis (temporal arteritis), Giant cell myocarditis, Glomerulonephritis, Goodpasture’s syndrome, Granulomatosis with Polyangiitis (GPA) (formerly called Wegener’s Granulomatosis), Graves’ disease, Guillain-Barre syndrome, Hashimoto’s encephalitis, Hashimoto’s thyroiditis, Hemolytic anemia, Henoch-Schonlein purpura, Herpes gestationis, HypogammaglobulinemiaIdiopathic thrombocytopenic purpura, (ITP)IgA nephropathy, IgG4-related sclerosing disease, Inclusion body myositis, Interstitial cystitis, Juvenile arthritis, Juvenile diabetes (Type 1 diabetes), Juvenile myositis, Kawasaki syndrome, Lambert-Eaton syndrome, Leukocytoclastic vasculitis, Lichen planus, Lichen sclerosus, Ligneous conjunctivitis, Linear IgA disease (LAD), Lupus (SLE), Lyme disease (chronic), Meniere’s disease, Microscopic polyangiitis, Mixed connective tissue disease (MCTD), Mooren’s ulcer, Mucha-Habermann disease, Multiple sclerosis, Myasthenia gravis, Myositis, Narcolepsy, Neuromyelitis optica (Devic’s), Neutropenia, Ocular cicatricial pemphigoid, Optic neuritis, Palindromic rheumatism, PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus), Paraneoplastic cerebellar degeneration, Paroxysmal nocturnal hemoglobinuria (PNH), Parry Romberg syndrome, Parsonnage-Turner syndrome, Pars planitis (peripheral uveitis), Pemphigus, Peripheral neuropathy, Perivenous encephalomyelitis, Pernicious anemia, POEMS syndrome, Polyarteritis nodosa, Type I, II, & III autoimmune polyglandular syndromes, Polymyalgia rheumatic, Polymyositis, Postmyocardial infarction syndrome, Postpericardiotomy syndrome, Progesterone dermatitis, Primary biliary cirrhosis, Primary sclerosing cholangitis, Psoriasis, Psoriatic arthritis, Idiopathic pulmonary fibrosis, Pyoderma gangrenosum, Pure red cell aplasia, Raynauds phenomenon, Reactive Arthritis, Reflex sympathetic dystrophy, Reiter’s syndrome, Relapsing polychondritis, Restless legs syndrome, Retroperitoneal fibrosis, Rheumatic fever, Rheumatoid arthritis, Sarcoidosis, Schmidt syndrome, Scleritis, Scleroderma, Sjogren’s syndrome, Sperm & testicular autoimmunity, Stiff person syndrome, Subacute bacterial endocarditis (SBE), Susac’s syndrome, Sympathetic ophthalmia, Takayasu’s arteritis, Temporal arteritis/Giant cell arteritis, Thrombocytopenic purpura (TTP), Tolosa-Hunt syndrome, Transverse myelitis, Type 1 diabetes, Ulcerative colitis, Undifferentiated connective tissue disease (UCTD), Uveitis, Vasculitis, Vesiculobullous dermatosis, Vitiligo, Wegener’s granulomatosis (now termed Granulomatosis with Polyangiitis (GPA).
While a full analysis of the treatment of all systemic inflammatory diseases is not possible partial list of inflammatory respiratory diseases of the lung (including those of the trachea) excluding those with a neurological basis includes: abnormal diffusion, abnormal perfusion, abnormal ventilation, accelerated silicosis, actinomycosis, acute air space pneumonia (acute bacterial pneumonia), acute bronchiolitis, acute congestion, acute infections of the lung, acute interstitial pneumonia, acute necrotizing viral pneumonia, acute organic dust toxic syndrome, acute pneumonia, acute radiation pneumonitis, acute rheumatic fever, acute silicosis, acute tracheobronchitis, adenocarcinoma, adenoid cystic carcinoma, adenosquamous carcinoma, adenovirus, adult respiratory distress syndrome (shock lung), agenesis, air embolism, allergic bronchopulmonary mycosis, allergic granulomatosis and angiitis (Churg-Strauss), allograft rejection, aluminum pneumoconiosis, alveolar microlithiasis, alveolar proteinosis, amebic lung abscess, amniotic fluid embolism, amyloidosis of the lung, anomalies of pulmonary vasculature, anomalous pulmonary venous return, apiration pneumonia, aplasia, asbestosis, asbestos-related diseases, aspergillosis, asthma, atelectasis, atriovenous fistulas, atypical mycobacterial infection, bacteremia, bacterial pneumonia, benign clear cell tumor, benign epitbelial tumors, benign fibrous mesothelioma, berylliosis, blastomycosis, bromchial atresia, bronchial asthma, bronchial carcinoid tumor, bronchial isomerism, bronchial obstruction, bronchial stenosis, bronchiectasis, bronchiolalveolar carcinoma, bronchiolitis, bronchiolitis obliterans-organizing pneumonia, bronchocentric granulomatosis, bronchogenic cyst, bronchopneumonia, bronchopulmonary dysplasia, bronchopulmonary sequestration, bullae, bullous emphysema, cancer, carcinoid tumors, carcinoma of the lung (bronchogenic carcinoma), central (bronchogenic) carcinoma, central cyanosis, centriacinar emphysema, cetrilobular emphysema, chest pain, Chlamydial pneumonia, chondroid hamartoma, chronic airflow obstruction, chronic bronchitis, chronic diffuse interstitial lung disease, chronic idiopathic pulmonary fibrosis, chronic lung abscess, chronic obstructive pulmonary diseases, chronic radiation pneumonitis, chronic silicosis, chylothorax, ciliary dyskinesia, coal worker's pneumoconiosis (anthracosis), coccidioidomycosis, collagen-vascular diseases, common cold, compensatory emphysema, congenital acinar dysplasia, congenital alveolar capillary dysplasia, congenital bronchobiliary fistula, congenital bronchoesophageal fistula, congenital cystic adenomatoid malformation, congenital pulmonary lymphangiectasis, congenital pulmonary overinflation (congenital emphysema), congestion, cough, cryptococcosis, cyanosis, cystic fibrosis, cysticercosis, cytomegalovirus, desquamative interstitial pneumonitis, destructive lung disease, diatomaceous earth pneumoconiosis, diffuse alveolar damage, diffuse pulmonary hemorrhage, diffuse septal amyloidosis, difuse panbronchiolitis, Dirofilaria immitis, diseases of the pleura, distal acinar (paraceptal) emphysema, drug-induced asthma, drug-induced diffuse alveolar damage, dyspnea, ectopic hormone syndromes, emphysema, empyemma, eosinophilic pneumonias, exercise-induced asthma, extralobar sequestration, extrinsic allergic asthma, fat emboli, focal dust emphysema, follicular bronchiolitis, follicular bronchitis, foreign-body embolism, Fuller's earth pneumoconiosis, functional resistance to arterial flow (vasoconstriction), fungal granulomas of the lung, fungal infections, Goodpasture's syndrome, graphite pneumoconiosis, gray hepatization, hamartomas, hard metal disease, hemoptysis, hemothorax, herniation of lung tissue, herpes simplex, heterotopic tissues, high-altitude pulmonary edema, histoplasmosis, horseshoe lung, humidifier fever, hyaline membrane disease, hydatid cysts, hydrothorax, hypersensitivity pneumonitis (extrinsic allergic alveolitis), hypoxic vascular remodeling, iatrogenic drug-, chemical-, or radiation-induced interstitial fibrosis, idiopathic interstitial pneumonia, idiopathic organizing pneumonia, idiopathic pulmonary fibrosis (fibrosing alveolitis, Hamman-Rich syndrome, acute interstitial pneumonia), idiopathic pulmonary hemosiderosis, immunologic interstitial fibrosis, immunologic interstitial pneumonitis, immunologic lung disease, infections causing chronic granulomatous inflammation, infections causing chronic suppurative inflammation, infections of the air passages, infiltrative lung disease, inflammatory lesions, inflammatory pseudotumors, influenza, interstitial diseases of uncertain etiology, interstitial lung disease, interstitial pneumonitis in connective tissue diseases, intralobar sequestration of the lung (congenital), intrinsic (nonallergic) asthma, invasive pulmonary aspergillosis, kaolin pneumoconiosis, Kartagner's syndrome, Klebsiella pneumonia, Langerhans' cell histiocytosis (histiocytosis X), large cell undifferentiated carcinoma, larval migration of Ascaris lumbricoides, larval migration of Strongyloides stercoralis, left pulmonary artery "sling", Legionella pneumonia, lipid pneumonia, lobar pneumonia, localized emphysema, long-standing bronchial obstruction, lung abscess, lung collapse, lung fluke, lung transplantation implantation response, lymphangiomyomatosis, lymphocytic interstitial pneumonitis (pseudolymphoma, lymphoma, lymphomatoid granulomatosis, malignant mesothelioma, massive pulmonary hemorrhage in the newborn, measles, meconium aspiration syndrome, mesenchymal cystic hamartomas, mesenchymal tumors, mesothelioma, metal-induced lung diseases, metastatic calcification, metastatic neoplasms, metastatic ossification, mica pneumoconiosis, mixed dust fibrosis, mixed epithelial-mesenchymal tumors, mixed type neoplasms, mucoepidermoid tumor, mucoviscidosis, mycoplasma pneumoniae, necrotizing bacterial pneumonia, necrotizing sarcoid granulomatosis, neonatal respiratory distress syndrome, neoplasms of the pleura, neuromuscular syndromes, nocardiosis, nondestructive lung disease, North American blastomycosis, occupational asthma, organic dust disease, panacinar emphysema, Pancoast's syndrome, paracoccidioidomycosis, parainfluenza, paraneoplastic syndromes, paraseptal emphysema (paracicatricial), parasilicosis syndromes, parasitic infections of the lung, peripheral cyanosis, peripheral lung carcinoma, persistent pulmonary hypertension of the newborn, pleural diseases, pleural effusion, pleural plaques, pneumococcal pneumonia, pneumoconioses (inorganic dust diseases), Pneumocystis carinii pneumonia, pneumocystosis, pneumonitis, pneumothorax, precapillary pulmonary hypertension, primary (childhood) tuberculosis, primary (idiopathic) pulmonary hypertension, primary mesothelial neoplasms, primary pulmonary hypertensions, progressive massive fibrosis, psittacosis, pulmonary actinomycosis, pulmonary air-leak syndromes, pulmonary alveolar proteinosis, pulmonary arteriovenous malformation, pulmonary blastoma, pulmonary capillary hemangiomatosis, pulmonary carcinosarcoma, pulmonary edema, pulmonary embolism, pulmonary eosinophilia, pulmonary fibrosis, pulmonary hypertension, pulmonary hypoplasia, pulmonary infarction, pulmonary infiltration and eosinophilia, pulmonary interstitial air (pulmonary interstitial emphysema), pulmonary lesions, pulmonary nocardiosis, pulmonary parenchymal anomalies, pulmonary thromboembolism, pulmonary tuberculosis, pulmonary vascular disorders, pulmonary vasculitides, pulmonary veno-occlusive disease, pyothorax, radiation pneumonitis, recurrent pulmonary emboli, red hepatization, respiration failure, respiratory syncytial virus, Reye's syndrome, rheumatoid lung disease, Rickettsial pneumonia, rupture of pulmonary arteries, sarcoidosis, scar cancer, scimitar syndrome, scleroderma, sclerosing hemangioma, secondary (adult) tuberculosis, secondary bacterial pneumonia, secondary pleural neoplasms, secondary pulmonary hypertension, senile emphysema, siderosis, silicate pneumoconiosis asbestosis, silicatosis, silicosis, simple nodular silicosis, Sjogren's syndrome, small airway lesions, small cell carcinoma, small cell undifferentiated (oat cell) carcinoma, spontaneous pneumothorax, sporotrichosis, sputum production, squamous (epidermoid) carcinoma, stannosis, staphlococcal pneumonia, suppuration (abscess formation), systemic lupus erythematosus, talcosis, tension pneumothorax, tracheal agenesis, tracheal stenosis, tracheobronchial amyloidosis, tracheobronchomegaly, tracheoesophageal fistula, transient tachypnea of the newborn (neonatal wet lung), tungsten carbide pneumoconiosis, usual interstitial pneumonia, usual interstitial pneumonitis, varicella, viral pneumonia, visceral pleural thickening, Wegener's granulomatosis, and whooping cough.
Some virus-related conditions are Alphavirus infection, Amur virus, Andes virus, Asymmetric periflexural exanthem of childhood, Arthropod-borne viral fevers and viral haemorrhagic fevers, Argentine hemorrhagic fever, Astrovirus, Avian nephritis virus, Avian orthoreovirus, Avian Reovirus, B virus infection, Bas-Congo virus, Bat-borne virus, Blueberry shock virus, Borna disease, Bovine adenovirus, Bovine coronavirus, Bovine ephemeral fever, Bovine herpesvirus 4, Bovine parvovirus, Bovine virus diarrhea, Brazilian hemorrhagic fever, Bulbul coronavirus HKU11, Bwamba Fever, Boston exanthem disease, Bovine papular stomatitis, Bowenoid papulosis, Buffalopox, Butcher's wart, Carrizal virus, Cat flu, Catacamas virus, Chandipura virus, Channel catfish virus, Chicken anaemia virus, Choclo virus, Common cold, Cricket paralysis virus, Cytomegalovirus, Chikungunya fever, Condylomata acuminate, Congenital rubella syndrome, Cowpox, Cytomegalovirus-associated diseases, Derzsy's disease, Dobrava-Belgrade virus, Downie bodies, Dengue (Break-bone fever), Disseminated herpes zoster, Ebola, El Moro Canyon virus, Elephant endotheliotropic herpesvirus, Enterovirus-associated diseases, Epstein–Barr virus-associated diseases, Farmyard pox, Feline leukemia virus, Fifth disease, Generalized vaccinia, Gianotti–Crosti syndrome (Infantile papular acrodermatitis, Papular acrodermatitis of childhood, Papulovesicular acrolocated syndrome) Giant condyloma acuminatum (Buschke–Löwenstein tumor, Giant condyloma of Buschke–Löwenstein tumor), Gou virus, Hand-foot-and-mouth disease, Hantavirus infections, Heck's disease (Focal epithelial hyperplasia), Hepatitis B, Hepatitis C, Herpangina, Herpes gladiatorum (Scrum pox), Herpes simplex, Herpes zoster oticus (Ramsay–Hunt syndrome), Herpetic keratoconjunctivitis, Herpetic sycosis, Herpetic whitlow, HIV infection, Human monkeypox, Human T-lymphotropic virus 1 infection, Human tanapox, Hantaan River virus, HCoV-EMC/2012, Henipavirus, Hepatitis D, Hepatitis E, Immune reconstitution inflammatory syndrome (Immune recovery syndrome), Infectious mononucleosis (Glandular fever), Imjin virus, Infectious pancreatic necrosis, Isla Vista virus, Inflammatory skin lesions following zoster infection (Isotopic response), Intrauterine herpes simplex, Kaposi sarcoma, Khabarovsk virus, Koi herpes virus, Kunjin virus, Lassa fever, Lipschütz ulcer (Ulcus vulvae acutum), Lábrea fever, Leucosis, Liebermeister's rule, Limestone Canyon virus, Lloviu cuevavirus, Lloviu virus, Lujo virus, Measles (Rubeola, Morbilli), Magboi virus, Marburg marburgvirus, Marburg virus, Marburg virus disease, Marburgvirus, Mayaro virus disease, Melaka virus, Menangle virus, Middle East respiratory syndrome coronavirus, Miniopterus Bat coronavirus 1, Miniopterus Bat coronavirus HKU8, Monkeypox, Monongahela virus, Muju virus, Myxomatosis, Milker's nodule, Modified varicella-like syndrome, Molluscum contagiosum, Mumps, Myrmecia, Neonatal herpes simplex, Ophthalmic zoster, Orf (Contagious pustular dermatosis, Ecthyma contagiosum, Infectious labial dermatitis, Sheep pox), Orf-induced immunobullous disease, Orolabial herpes (Herpes labialis), Oropouche fever, Papillomavirus-associated diseases, Pigmented wart, Postherpetic neuralgia (Zoster-associated pain), Post-vaccination follicular eruption, Parvovirus B19, Phytoreovirus, Pipistrellus bat coronavirus HKU5, Psittacine beak and feather disease, Pogosta disease, Porcine adenovirus, Prospect Hill virus, Progressive vaccinia (Vaccinia gangrenosum, Vaccinia necrosum) Pseudocowpox, Recurrent respiratory papillomatosis (Laryngeal papillomatosis), Qalyub virus, Rift Valley fever, Roseola infantum (Exanthem subitum, Exanthema subitum, Sixth disease), Roseola vaccinia, Rubella (German measles), Rabbit haemorrhagic disease, Ravn virus, Reston virus, Reticuloendotheliosis virus, Rhinolophus Bat coronavirus HKU2, Roseolovirus, Ross River fever, Ross River virus, Rotaviral enteritis, Rousettus bat coronavirus HKU9, Sandfly fever (Pappataci fever, Phlebotomus fever), Sealpox, Saaremaa virus, Sangassou virus, Scotophilus Bat coronavirus 512, Serang virus, Shope papilloma virus, Simian foamy virus, Sin Nombre virus, Soochong virus, Sudan ebolavirus, Sudan virus, Swine vesicular disease, Taï Forest ebolavirus, Taï Forest virus, Tanganya virus, Thottapalayam virus, Topografov virus, Tremovirus, Tropical spastic paraparesis, Tula virus, Turkey coronavirus, Turkey viral hepatitis, Turkeypox virus, Tylonycteris bat coronavirus HKU4, Varicella (Chickenpox) (Shingles), Variola major (Smallpox), Verruca plana (Flat warts), Verruca plantaris (Plantar wart), Verruca vulgaris (Wart), Verrucae palmares et plantares, Viral-associated trichodysplasia (Ciclosporin-induced folliculodystrophy), Viral plant pathogens and diseases, Varicella zoster virus, Venezuelan hemorrhagic fever, Veterinary virology, Viral arthritis (poultry), Viral gastroenteritis, Viral hemorrhagic fever, Viral hemorrhagic septicemia, Viral systemic diseases, Wasting syndrome, West Nile virus infection, Woodchuck hepatitis virus, Yellow fever, Zaire ebolavirus, Zika fever and various Zoonotic viral diseases. Thus, the scope is broad.
(B) This is a method of treating diseases with compounds.
(D) One of ordinary skill is a medical doctor.
(C) (E) The existence of a "silver bullet" for all these diseases is contrary to our present understanding of pharmacology and medicine. The causes of these neurodegenerative diseases are diverse as discussed above. Protein fragments are to blame in prion diseases like Creutzfeldt-Jakob disease. Viral infections are involved in some forms of neurodegeneration. Alzheimer's Disease involves tau and -amyloid proteins, although its exact cause is unknown. “However, while the development of these plaques and tangles has been implicated in the pathology of AD, it is uncertain whether they are a cause or an effect. Currently, there are no approved treatments to halt or slow the progression of AD, though medications are available to treat the cognitive symptoms of the disease and potential new agents are currently under clinical trial.” [Emphasis added.] University of Cambridge John van Geest Centre for Brain Repair School of Clinical Medicine “Alzheimer’s disease and tauopathy” Online “http://www.brc.cam.ac.uk/research/alzheimers-disease-and-tauopathy/” accessed September 10, 2015. According to Tomohiro Chiba "Emerging Therapeutic Strategies in Alzheimer's Disease" Intech 2013, 181-225, Table 1 on page 196 shows that none of the disease modifying therapies work. This leads Chiba to the conclusion: "Disease-modifying therapy for AD is not yet available despite vast efforts on drug development and plenty of candidate drugs. As shown in Table 1, failure rate of phase II and III clinical trials for AD are extremely high, meaning not only that current in vitro or pre-clinical models of AD can hardly predict the clinical efficacy but also that drugs, which showed only a mild effect in phase II studies, would eventually fail in phase III studies." No data has been presented for treating AD. Amyotrophic lateral sclerosis (ALS) has no clear cause. For Parkinson's disease -synuclein is involved. 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. In Friedreich ataxia, the problem is frataxin deficiency, which affects sensory neurons in the dorsal root ganglion responsible for position sense.
Autoimmune diseases present similar challenges and have distinct etiologies. Multiple sclerosis is poorly understood and treatment is difficult. “Despite decades of research on MS pathogenesis, and significant achievements within recent years, the etiology of MS still remains unknown. It is generally accepted that MS is a complex autoimmune disease, but this assumption still has to be proved, and this theory has yet to be formally established” (pg. 1013) Georg Pilz, “Modern multiple sclerosis treatment – what is approved, what is on the horizon” Drug Discovery Today December 2008, Volume 13, Numbers 23/24 1013-1025. Major modalities of therapy include Glucocorticosteroids, Interferon, Glatiramer acetate, Natalizumab, and Mitoxantrone. Among the new compounds being tested for efficacy in MS, described in Pils, none are BTK inhibitors.
The claims are drawn to treating all inflammatory diseases, which are numerous and of different etiologies. Sepsis is a systemic inflammatory disease. According to Poli-de-Figueiredo “EXPERIMENTAL MODELS OF SEPSIS AND THEIR CLINICAL RELEVANCE” SHOCK, Vol. 30, Supplement 1, pp. 53-59, 2008:
Sepsis remains a major cause of morbidity and mortality worldwide despite developments in monitoring devices, diagnostic tools, and new therapeutic options (1, 2). It is a clinical syndrome resulting from a complex interaction between host and infectious agents, characterized by a systemic activation of multiple inflammatory pathways, including cytokine network and coagulation (3). The main cause of death is multiple organ failure, which is the final pathway for sepsis-induced systemic and regional hemodynamic changes, widespread microcirculatory disturbances, and cellular alterations, leading to an uncoupling between blood flow and metabolic requirements (4, 5).
Extensive clinical and animal research, with substantial expenses, have been undertaken to address the pathophysiology and treatment of severe sepsis and septic shock (6, 7). In contrast to many preclinical studies, most clinical trials of promising new treatment strategies for sepsis have failed to demonstrate efficacy (8, 9).
“There have been well over 100 clinical trials that utilized various biological response modifiers acting to suppress and/ or block the SIRS response [11,12], the majority of these having been enthusiastically successful in reducing mortality in murine models of abdominal sepsis.” [Gentile “HMGB1 as a therapeutic target for sepsis: it’s all in the timing!” Expert Opinion on Therapeutic Targets, 2014, 18:3, 243-245] In fact no drugs are effective. See Marshall “Why have clinical trials in sepsis failed?” Trends in Molecular Medicine, April 2014, Vol. 20, No. 4 195-203. “More than 100 randomized clinical trials have tested the hypothesis that modulating the septic response to infection can improve survival. With one short-lived exception, none of these has resulted in new treatments. The current challenge for sepsis research lies in a failure of concept and reluctance to abandon a demonstrably ineffectual research model.” “It can be conservatively estimated that upwards of $10 billion has been spent with the objective of developing effective adjuvant treatments to meet this unmet need. Yet, with the failure of a recent confirmatory trial of APC [31], no such treatments are currently available, and the prospect that this will change seems remote.” Animal models of sepsis are available however they are poor: Garrido "Experimental models of sepsis and septic shock: an overview" Acta Cirúrgica Brasileira - Vol 19 (2) 2004 82-88. The specification has no models of sepsis.
There is no basic causal link between the diseases listed and any known pharmacology. The only data in the specification is related to the inhibition of CDK4 and CDK6 enzymes on pages 160 ff., data in cell based assays for cancer treatment in adenocarcinoma cells. After reviewing the specification and the literature the compounds might find use as cancer drugs, (see Lukasik “ Cyclin-Dependent Kinases (CDK) and Their Role in Diseases Development–Review” Int. J. Mol. Sci. 2021, 22, 2935)
“6.3. CDK4/6
Numerous cancers have been found to be particularly sensitive to CDK4/6 inhibition.
These genomic or transcriptional aberrations that activate CDK4/6 may lead to alterations
in cell cycle machinery genes. For example, amplifications of CDK4 have been manifested in liposarcoma and glioblastoma, and CDK6 have been demonstrated in upper gastrointestinal cancers and neuroendocrine carcinoma of the prostate [211]. “ [Page 12]
Cancer however is not a claimed disease. CDK4/6 is also involved in “Autosomal recessive primary microcephaly (MCPH), also known as Microcephalia vera, is a rare congenital disorder.”, however it is loss of function so an inhibitor could not treat this disease. “Since CDK6 loss-of-function mutation causes microcephaly and cyclin D2 gain-of function mutation results in megalencephaly there should not be a surprise that these two proteins form a heterodimer to obtain an active protein kinase.” This does not appear to be a claimed disease either.
Lukasic discusses the role of CDKs in other disorders besides cancer on page 13 ff. in section 8. “ Role of CDKs in Other Disorders”. CDK4/6 are not mentioned as having utility in diseases besides cancer. Beyond Lukasic, Liang “The Therapeutic Potential of CDK4/6 Inhibitors, Novel Cancer Drugs, in Kidney Diseases” Int. J. Mol. Sci. 2023, 24, 13558 discusses CDK4/6 inhibitors in chronic kidney disease. The results are not clear, “However, there is limited research on the application of CDK4/6 inhibitors for the treatment of PKD” “There is limited information regarding the role of CDK4/6 inhibitors in the development of nephritis, with the underlying mechanisms still unclear. Therefore, a more thorough examination is needed to carefully evaluate the benefits and drawbacks of CDK4/6 inhibitors for the treatment of nephritis.” This however is not representative of all inflammatory conditions, discussed above and does not appear to have been contemplated in the specification since this evidence is post-filing and no mention of kidney disease is made. The sole mention of the claimed diseases is on page 31 of the specification at page [0615]: “Different disease conditions associated with CDK have been reported. CDK has been implicated, for example, auto-immune diseases, neurodegeneration (such as Parkinson's disease, Alzheimer's disease and ischaemia), inflammatory diseases, viral infections and cancer such as, for example…” These assertions are not supported by the specification or known CDK4/6 pharmacology.
A compound that would treat all known and unknown viral infections is contrary to our present understanding of pharmacology and medicine. See Muller and Kräusslich in “Antiviral Strategies” Handbook of Experimental Pharmacology Volume 189 Chapter 1, pages 1-24, “Viruses are obligatory intracellular parasites, whose replication depends on functions of the host cell. This defining feature has a number of consequences for the development and application of antiviral drugs. The intracellular replication and the appropriation of cellular pathways for purposes of the pathogen makes it difficult to define virus-specific targets for therapeutic intervention, and inhibition strategies have to be highly specific to prevent cell toxicity.” Pg. 2; “Another fundamental difference between viruses and other pathogens which affects the development of anti-infectives concerns the fact that viruses strongly rely on host cell pathways for many of their replication steps and thus do not present many pathogen-specific targets for pharmaceutical intervention. There are no structural or metabolic features common to many viruses, which fundamentally differ from the features of the mammalian cell – comparable with, for example, the bacterial cell wall, the 70S ribosome, or the distinct metabolic pathways of parasitic pathogens. Therefore, a broad-spectrum antiviral is difficult to conceive and selection of an effective drug for antiviral treatment usually requires that the identity of the pathogen has been precisely determined by diagnostic procedures. Current genome-wide screening approaches probing, for example, the relevance of all kinases of the human genome for replication of specific viruses (see Sect. 5.3 herein) may eventually define common requirements for larger groups of viruses and thus pave the way for broader acting antivirals targeting host cell factors. Accordingly, antiviral drugs are available against only a limited number of viruses..” ibid., page 9. The specification has no data for treating viral infections and there is no known link between inhibiting CDK4/6 and treating viral disease.
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.
5. Claims 1-25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 23 of U.S. Patent No. 12,129,262. Although the claims at issue are not identical, they are not patentably distinct from each other because the applicant received a patent to the following claim:
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It would be impossible to practice the claimed method, administering a compound to various patients, without infringing the patent claims since administering the compound would inherently have the patent claim activity. Claim 1 compound scope is identical to claim 1 compound scope.
Conclusion
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/DAVID K O'DELL/ Primary Examiner, Art Unit 1621
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