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 .
Claims 12, 20, 22-26, 28, 45, 47 and 50-62 are pending in this application.
Election/Restrictions
Applicant’s election without traverse of Group I in the reply filed on February 4, 2026 is acknowledged.
Claims 28, 53, 56 and 60-62 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on February 4, 2026.
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 47, 55 and 58 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AlA), 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.
In evaluating the enablement question, several factors are to be considered. In re Wands, 8 USPQ2d 1400 (Fed. Cir. 1988); Ex parte Forman, 230 USPQ 546. The factors include: 1) The nature of the invention, 2) the state of the prior art, 3) the predictability or lack thereof in the art, 4) the amount of direction or guidance present, 5) the presence or absence of working examples, 6) the breadth of the claims, and 7) the quantity of experimentation needed.
The nature of the instant invention has claims, which embrace substituted 1,2,6a,6b,7,8,8a,8b,11a,12,12a,12b-dodecahydro-4H-naphtho[2’,1’:4,5]indeno[1,2-d][1,3]dioxol-4-one compounds.
HOW TO USE: Claims 47, 55 and 58 are drawn to the method of treating or preventing an autoimmune or inflammatory condition, which is associated with glucocorticoid receptor agonist and modulator activity. Any evidence presented must be commensurate in scope with the claims and must clearly demonstrate the effectiveness of the claimed compounds. 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 scope of claims 47, 55 and 58 includes diseases and/or conditions not even known at this time, which may be associated with glucocorticoid receptor agonist and modulator activity. While the treatment of asthma, COPD, rheumatoid arthritis and inflammatory bowel disease has been
linked with glucocorticoid receptor agonist the art does not recognize use of such inhibitors as broad-based drugs for treating all disorders instantly embraced. “Inflammatory conditions” or “autoimmune conditions” cannot be deemed enabled. The notion that a compound could be effective against inflammatory conditions or autoimmune conditions in general is contrary to our current understanding of how pharmacologicals work. All attempts to find a pharmaceutical to treat inflammatory conditions, autoimmune conditions, etc. generally have thus failed.
For a compound or genus to be effective against inflammatory condition or autoimmune condition, generally is contrary to medical science.
Let’s begin with Inflammatory diseases:
Inflammation is a process that 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. There is no common mechanism by which all, or even most, inflammations arise. Mediators include bradykinin, serotonin, C3a, C5a, histamine, leukotrienes, cytokines, and many, many others. Accordingly, treatments for inflammation are normally tailored to the particular type of inflammation present, as there is no, and there can be no “magic bullet” against inflammation generally.
The scope of inflammation includes chronic inflammation caused by infiltration of tissue with mononuclear inflammatory cells. Granulomas are seen in certain chronic inflammation situations. They are clusters of macrophages that 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. Cystitis is an inflammation of the bladder, usually caused by bacteria. Blepharitis is a chronic inflammation of the eyelids that is caused by a staphylococcus. Dacryocystitis is inflammation of the tear sac, and usually occurs after a long-term obstruction of the nasolacrimal duct and is caused by staphylococci or streptococci. Preseptal cellulitis is inflammation of the tissues around the eye, and Orbital cellulitis is an inflammatory process involving the layer of tissue that separates the eye itself from the eyelid. These life-threatening infections usually arise from staphylococcus. Hence, these types of inflammations are treated with antibiotics.
Cholecystitis is gallbladder inflammation usually caused by a gallstone that cannot pass through the cystic duct. In those cases, it normally cannot be treated by pharmaceuticals but instead the gallbladder is removed. Cholecystitis without the formation of gallstones, called acalculous cholecystitis, is caused by bacteria such as Salmonella, Staphylococcus, Streptococcus (as part of scarlet fever), and leptospirosis, and thus may be treatable by treating the underlying infectious agent. Acute inflammation of the gall bladder can also arise from typhoid; treatment is with antibiotics.
In gout, joint inflammation is caused by the formation of monosodium urate monohydrate (MSU) crystals within the joint space. Acute attacks of gout are treated with colchicine (to inhibit of MSU-induced chemotactic factor release by PMNs) and after the acute phase with allopurinol to control the blood levels of uric acid. Pseudogout, sometimes referred to as calcium pyrophosphate disease (CPPD), is inflammation caused by calcium pyrophosphate (CPP) crystals. It is treated with nonsteroidal anti-inflammatory drugs, corticosteroids, and colchicine.
Sinusitis is the inflammation of the mucosal lining of one or more sinuses. It commonly accompanies upper respiratory viral infections and, in most cases, requires no treatment.
Pharyngitis (tonsillitis) is an inflammatory illness of the mucous membranes and underlying structures of the throat (nasopharynx, uvula, and soft palate). The illness can be caused by bacteria, viruses, mycoplasmas, fungi, and parasites, and uncertain causes, especially Streptococcus pyogenes, adenoviruses, influenza viruses, parainfluenza viruses, Epstein-Barr virus, enteroviruses, and Mycoplasma pneumoniae. Similarly, Osteomyelitis is the inflammation of bones, generally caused by bacteria (most commonly Staphylococcus Aureus). Fungi or viruses can cause the disease. Dacryoadenitis, an inflammation of the tear gland, can arise from infectious mononucleosis, mumps, gonorrhea, or influenza. Conjunctivitis (pink eye) is inflammation of the conjunctiva and can be caused by many microorganisms, including staphylococci, Haemophilus influenzae, streptococci, gonococci, and viruses such as adenoviruses. Treatment in all of these cases, when possible, is thus to the underlying infectious agent.
Rheumatoid arthritis is an inflammatory bone disease causing destruction of articular cartilage, in which macrophages accumulate in the rheumatoid synovial membrane. Mediators are cytokines, including IL-18 and IL-18, and IFN-.
Pneumonia is an inflammation of the lungs that can be caused by viruses (such as respiratory syncytial, parainfluenza, and influenza), bacteria, fungi, mycoplasmas, rickettsias (especially Q fever), Chlamydia, or parasites. It can also occur as a hypersensitivity, or allergic response, to agents such as mold, humidifiers, and animal excreta, and in such a case would be treated with anti-allergic agents.
Other inflammations in the respiratory system include CF, adult respiratory distress syndrome, asthma, and bronchitis.
Myocarditis is an inflammation of the muscular middle layer of the heart (myocardium) Viruses, bacteria, and noninfectious diseases can cause it. Treatment is primarily supportive e.g. drugs may be used to improve the heart's ability to contract and to remove extra fluids from the body. Unless the underlying infectious agent itself is treatable, this inflammation is not itself treated.
Glossitis is inflammation of the tongue. Local causes of glossitis include bacterial or viral infection, mechanical irritation or injury from burns, rough edges of teeth or dental and oral appliances, or other trauma; exposure to irritants (tobacco, alcohol, hot foods, or spices), and sensitization (to e.g. toothpaste, mouthwash, breath fresheners, dyes in candy, plastic in dentures or retainers) anemia and other B vitamin deficiencies, erythema multiform, pemphigus vulgaris, syphilis, and other disorders. It can be inherited. Corticosteroids such as prednisone may be given to reduce the inflammation. Antibiotics, antifungal medications, or other antimicrobials may be prescribed if the cause of glossitis is an infection. Anemia and nutritional deficiencies must be treated, often by dietary changes or other supplements.
Meningitis is an inflammation of the outer covering of the brain and spinal cord. Virtually any known infectious agent can cause it. Thus, if it were caused by Haemophilus influenzae or Neisseria meningitis, the antibiotic derivative rifampin would be used.
Encephalitis is an inflammation of the brain itself. It is most often caused by a group of arboviruses. Treatment of encephalitis is largely supportive because no specific antiviral agents, except for that which works against herpes simplex virus, are available for therapy.
Hepatitis is an inflammation of the liver, usually caused by viral invasion, notably hepatitis A, B and C, but sometimes Epstein-Barr virus; herpes simplex viruses; measles, mumps, and chicken pox viruses; and cytomegaloviruses. Treatment, when possible, is with antivirals. Inflammation of the liver also takes the form of alcoholic hepatitis. Lupoid hepatitis is an autoimmune disorder.
Hemorrhoids are an enlarged or varicose condition of the hemorrhoidal veins and tissues around the anus, either internal or external. Anything that obstructs the free circulation of the blood in the portal system will give rise to hemorrhoids. Constipation, straining at stool, diarrhea, dysentery, rough toilet paper, uncleanness, pelvic tumors, displacement of the uterus and pregnancy are among the most common causes.
There is a series of inflammatory problems directly connected to neutrophil-endothelial cell adhesion (NECA). These include frostbite injury, bacterial meningitis, acute airway inflammation, allograft rejection, hemorrhagic shock, septic shock, ischemia, and reperfusion injuries.
Urethritis is an inflammation of the duct that leads from the bladder to the exterior of the body. It is often due to fecal contamination or irritation due to physical or chemical substances (e.g. introduction of foreign bodies into the urethra, bubble bath, or soap) or gonorrhea. Treatment may simply involve the withdrawal of the offending chemical agent, or the administration of antibiotics, when Neisseria gonorrhoeae is involved.
Inflammation can arise from the eruption of teeth in a child (teething).
Inflammation of the nails can arise from chronic paronychia, fungus (especially Candida albicans), trauma, impaired circulation, and dermatitis.
Bright's disease (or glomerulonephritis) is inflammation of the glomeruli and the nephrons, the structures in the kidney that produce urine. It usually results from an infection, such as a streptococcal infection, that occurs somewhere else in the body. There is no real treatment beyond relief of the symptoms.
Thyroiditis is an inflammation of the thyroid gland, and takes three forms. Hashimoto's Thyroiditis (chronic lymphocytic thyroiditis) is the most common type of thyroiditis. It is an autoimmune disorder, and treatment is to start thyroid hormone replacement. For De Quervain's Thyroiditis (subacute or granulomatous thyroiditis), treatment is usually bed rest and aspirin to reduce inflammation. Occasionally cortisone and thyroid hormone may be used. Silent Thyroiditis usually arises following pregnancy. Treatment is usually bed rest with beta-blockers.
Regional enteritis (Crohn's disease or ileitis) is an autoimmune disorder, which is associated with the presence of Mycobacterium paratuberculosis. It can affect any part of the gastrointestinal tract but most commonly affects the ileum. The inflammation is controlled primarily by regulation of diet, antibiotics if abscesses and fistulas are present, sometimes Prednisone and other corticosteroids, and surgery.
Stomatitis, inflammation of the mouth, and mucositis, inflammation of the mucosa can arise from sources as diverse as Candida albicans, dentures, chemotherapy, and radiation therapy to the head, neck or mouth (“Radiation mucositis”). It may be secondary to infection, trauma, systemic diseases or autoimmune mechanisms. These come in many forms, such as aphthous ulcers, Acute Necrotizing Ulcerative Gingivitis i.e. "trench mouth", and Lichen Planus. Herpetiform ulcers treatment has ranged from antibiotics, immunosuppressants and yogurt, to Lactobacillus capsules, tetracycline and systemic steroids. Palliative measures include topical anesthetics, Vitamin E, analgesics, and coating agents. Antiviral agents may be used if viral origin is established.
Pancreatitis is inflammation of the pancreas and can arise from abdominal trauma, or the formation of gallstones that obstruct the common bile duct. It can be associated with excessive ingestion of alcohol; with disorders such as cystic fibrosis or Reye's syndrome; or with scorpion stings. Infectious causes include mycoplasmas, Epstein-Barr viruses, Coxsackie viruses, leptospirosis, hepatitis viruses, mumps, congenital German measles, Ascaris worms, and syphilis. The inflammation per se is generally not treatable. Treatment is usually supportive and consists of the management of pain and intravenous feeding.
Neuroretinitis is inflammation of the retina and optic nerve of the eye (“optic neuritis”). It is often idiopathic. It frequently arises secondary to some kind of infection, such as Hepatitis B, HSV, EBV, influenza A, mumps, Coxsackie B, TB, salmonella, Lyme disease, syphilis, leptospirosis, Histoplasmosis, Toxoplasmosis, toxocara, Sarcoidosis, and cat-scratch disease. Treatment is thus to the underlying cause. For example, diffuse unilateral subacute neuroretinitis (DUSN) arises from nematodes deep in the retina or in the subretinal space. Anthelminthic treatment is then used. When the origin is Toxoplasmosis, then anti-Toxoplasma medications such as Pyrimethamine.
Other eye inflammations include scleritis and episcleritis, inflammation of tissues on the sclera; choroiditis, inflammation of the middle coat (choroid) of the eyeball, and uveitis, which is inflammation of the parts of the eyes that make up the iris.
Gastritis is inflammation to the stomach lining. Atrophic gastritis is characterized by the loss of the stomach cells that are responsible for manufacturing acid, pepsin, and intrinsic factor. This condition occurs in older people or those suffering from Helicobacter pylori. Erosive (hemorrhagic) gastritis occurs when shallow ulcers or sores develop on the upper layer of the stomach lining, usually because of the excessive ingestion of a stomach irritant such as aspirin or alcohol.
There can also be mentioned appendicitis, which can occur when a hard piece of stool blocks the opening of the appendix, causing swelling and inflammation.
The great majority of skin problems involve some type of inflammation, such as response to physical injury (e.g. sunburn, ticks, abrasion, or a bee string), acute allergic contact dermatitis (such as poison ivy), and infections (such as boils and cold sores). Ingrown hairs, or pili incarnati, can cause acute pustular reactions. Cancerous lesions of the skin frequently show some degree of inflammatory response. The inflammation of acne is caused by leakage of sebum and keratin debris outside the distended pilosebaceous duct. The bacillus Propionibacterium acnes, which populate the lesions, may also contribute indirectly to this inflammation by metabolizing the sebum to produce irritant fatty acids. Inflammation in skin problems is usually the result of the release of chemical mediators in the skin, notably histamine, peptides (kinins) and fatty acids (prostaglandins and leukotrienes), that are formed enzymatically in response to e.g., injury. Medications designed to counteract inflammation in the skin may or may not antagonize the effects of the particular type of mediator involved, if that is known. The inflammation can take many different forms, including redness, (from dilation of blood vessels); heat, (from increased blood flow); swelling (from leakage of fluid from the small blood vessels); whealing reactions (hives, nettle rash, urticaria) in which vascular changes predominate, and pain or itching. Blisters (from enzymes released from inflammatory cells, resident cells of the skin, or blood plasma components) can cause the breakdown of proteins responsible for the structural integrity of the skin, leading to serious inflammatory disorders such as pemphigus. In addition, the affected skin may feel indurated (hardened) because of the deposition of the coagulation protein fibrin and the infiltration by inflammatory blood cells (lymphocytes, histiocytes, and polymorphonuclear leukocytes).
Prostatitis, inflammation of the prostate, comes in several different forms, including those of bacterial origins, and those, which are not, including chronic abacterial prostatitis and asymptomatic inflammatory prostatitis. Certain types of anti-inflammatory agents, such as non-steroidal anti-inflammatory medications (Ibuprofen and naproxen) along with muscle relaxants can be used in the non-bacterial cases.
The above list is by no means complete, but demonstrates the extraordinary breadth of causes, mechanisms, and treatment (or lack thereof) for inflammation. Thus, the scope of claims is enormous.
Now let’s turn to autoimmune disease:
The primary function of the immune system is to fight infection. It has also evolved to maintain homeostasis and regulate commensal microbes that normally inhabit the body, primarily beneficial or benign bacteria. Failure to do this at a normal level constitutes immunodeficiency. There are a substantial number of immunodeficiency disorders, in two very different categories.
Primary immunodeficiency disorders are caused by inherited functional defects in the cells of the immune system.
The primary immunodeficiencies commonly involve defects in lymphocyte development,
and these can be divided into 4 categories: 1. Severe combined immunodeficiencies. These
include a. Absence of all myeloid and lymphoid cells (Reticular dysgenesis), b. Absence of all
lymphoid populations (Adenosine Deaminase deficiency), c. Absence of T and NK cells (X-
linked SCID; γc deficiency), d. Absence of T and NK cells (autosomal SCID; JAK-3 deficiency),
e. Absence of T and NK cells (autosomal SCID: unknown mechanism), f. Absence of T and B
cells (Alymphocytosis; Rag gene defects), g. Absence of T and B cells (Alymphocytosis; non-
RAGrecombination defect), and h. Absence of T cells (T-B+NK+ SCID; IL-7R deficiency). 2.
Combined Immunodeficiencies. These include a. DiGeorge syndrome, b. Purine nucleotide
phosphorylase deficiency, c. ZAP-70 mutations, d. DNA ligase I deficiency, e. CD3 ε deficiency,
f. CD3 γ deficiency, g. HLA class II deficiency (CIITA, RFX5), h. Class I deficiency (TAP2), i. Ataxia telangiectasia, j. Cartilage hair hypoplasia. 3. Humoral Immunodeficiencies. These include a. X-linked agammaglobulinemia (Bruton’s disease), b. Human surrogate light chain and µ heavy chain mutants, c. IgG subclass deficiencies, d. κ chain deficiency, e. X-linked hyper-IgM syndrome; f. Hyper-IgM syndrome (autosomal), g. Selective IgA deficiency, h. Common variable immunodeficiency. 4. Disorders involving aberrant lymphocyte activation. These include a. Wiskott-Aldrich syndrome, b. Autoimmune lymphoproliferative syndrome, c. “Accelerated phase” disorders (notably, Chediak-Higashi syndrome, Familial hemophagocytic lymphohistiocytosis, X-linked lymphoproliferation, and Immunodeficiency with partial albinism), and d. Omenn’s syndrome.
Another group is the Phagocytes Defects. These include Chronic Granulomatous Disease (CGD, which comes in forms including gp91 phox Deficiency, p22 phox Deficiency, p47 phox Deficincy, p67 phox Deficiency); Neutrophil G-6PD Deficiency; Myeloperoxidase Deficiency; Specific Granule Deficiency; Shwachman-Diamond Syndrome; Localised Juvenile Periodontitis, and Papillon-Lefevre Syndrome.
There are the Predominantly Antibody Deficiencies, which include Agammaglobulinemia with Absent B Cells (Btk Deficiency, μ Heavy Chain Deficiency, λ5/14.1 Deficiency, Igα Deficiency, Igβ Deficiency, BLNK Deficiency, LRRC8 Deficiency, and other Forms of Agammaglobulinemia); Hypogammaglobulinemia with Normal/Low Number of B Cells (Common Variable Immunodeficiency, ICOS Deficiency, TACI Deficiency, CD19 Deficiency, and other Forms of Hypogammaglobulinemia); Immunoglobulin Class Switch Recombination Deficiencies (Due to Intrinsic B Cell Defects) (AID Deficiency, UNG Deficiency, and other CSR Selective Deficiencies); Selective IgA Deficiency; Other Immunoglobulin Isotypes or Light Chain Deficiencies (Isolated IgG Subclass Deficiency, IgA with IgG Subclass Deficiency, Ig Heavy Chain Deletions, K Light Chain Deficiency); Specific Antibody Deficiency with Normal Immunoglobulin Concentrations; and Transient Hypogammaglobulinemia of Infancy.
There are assorted Complement Deficiencies, including Deficiencies of Classical Pathway Components (C1q/C1r/C1s Deficiencies, C4 Deficiency, C2 Deficiency); Deficiencies of Lectin Pathway Components (MBL Deficiency, MASP2 Deficiency); Deficiencies of Alternative Pathway Components (Factor D Deficiency, Properdin Deficiency); Deficiency of Complement Component C3; Deficiencies of Terminal Pathway Components (C5-9 Deficiencies); and Deficiencies of Complement Regulatory Proteins (C1 Inhibitor Deficiency, Factor I Deficiency, Factor H Deficiency, CD46 Deficiency, CD55 Deficiency, CD59 Deficiency).
There are syndromes associated with defective DNA repair, chromosome instability, or both such as Ataxia-Telangiectasia, Ataxia-Like Syndrome, Nijmegen Breakage Syndrome, Bloom's Syndrome, ICF Syndrome, DNA Ligase IV Deficiency, and Fanconi Pancytopenia
There are the Hyper-IgE syndromes: Stat3 Deficiency, Tyk2 Deficiency, and HIES with Unknown Origin, although there are other systems for classifying these.
There are assorted inborn errors of metabolism associated with immunodeficiency, including Adenosine Deaminase Deficiency, Glycogen Storage Disease Ib/Ic, Barth Syndrome, Galactosemia, Branched-Chain Amino Acidurias, and Lysinuric Protein Intolerance.
There are some Interferon- gamma /IL-12 Pathway deficiencies and some Natural Killer Cell deficiencies which are primary immunodeficiency disorders. There are others which fall into the categories of Toll-like Receptor (TLRS) defects, and still others are Mannose-binding lectin (MBL) deficiencies, and there are also Growth Hormone Pathway Defects. Still others arise from Caspase 8 deficiency and from defects of NF-κB regulation.
There is Immunodeficiency with thymoma (Good's syndrome), Antibody deficiency with Transcobalamin II Deficiency; Warts, Hypogammaglobulinemia, Infection, Myelokathexis (WHIM) syndrome, Roifman Syndrome 1, Roifman-Costa Syndrome (Roifman Syndrome 2); Spondyloenchondrodysplasia; Kabuki Syndrome; CHARGE Association; Rubinstein-Taybi Syndrome; Mulvihill-Smith Syndrome; OLEDAID Syndrome (which exists in three genetically distinct forms); Dyskeratosis Congenita; Hermansky-Pudlak Syndrome, Type II; Griscelli Syndrome, Type 2; Short-Limb Skeletal Dysplasia with Combined Immunodeficiency; Høyeraal- Hreidarsson Syndrome; Cohen Syndrome and many, many other syndromes.
II. Secondary immunodeficiencies are acquired defects in immune function resulting from a wide variety of sources. These include drugs (e.g. cancer chemotherapeutic agents, Cyclosporin, and corticosteroids), infections of immune system cells (most notably HIV, but also HTLV-1, EBV, and some others), disseminated cancers (malignancies that invade the bone marrow may crowd out immune system cells and their precursors), radiation therapy (causing bone marrow suppression, lymphocyte toxicity), splenectomy (increased susceptibility to infection by encapsulated microorganisms), severe burns (loss of immunoglobulins through damaged skin), chronic renal disease, and aging.
Immunodeficiency can be secondary to metabolic disorders, such as Type 2 diabetes, hyperadrenocorticism (Cushing's syndrome, in which excess cortisol suppresses the immune system), uremia and pregnancy.
Some are the result of Endocrine disorders, notably GH deficiency as well as estrogen toxicity.
Others arise from nutritional disorders, especially zinc, iron and vitamin E deficiency.
These can also arise from systemic viral infections such as canine distemper virus, canine parvovirus, FeLV, feline panleukopenia virus, equine herpes 1, BVD, FIV and BIV, as well as some bacterial infections, notably Mycobacterium paratuberculosis. Parasites (e.g. Eperythrozoonsis, Trypanosomiasis, Demodex canis, and Ehrlichia spp.) as well as toxins such as mycotoxins, and bracken fern toxicosis, can trigger secondary immunodeficiencies.
(2) The nature of the invention and predictability in the art:
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).
(3) Direction or Guidance: That provided is very limited. The dosage range information provided in paragraph [1808] of the specification is generic at best.
(4) State of the Prior Art: The claimed compounds are substituted 1,2,6a,6b,7,8,8a,8b,11a,12,12a,12b-dodecahydro-4H-naphtho[2’,1’:4,5]indeno[1,2-d][1,3]dioxol-4-ones. So far as the examiner is not aware of 1,2,6a,6b,7,8,8a,8b,11a,12,12a,12b-dodecahydro-4H-naphtho[2’,1’:4,5]indeno[1,2-d][1,3]dioxol-4-one compounds that have been successfully used as inflammatory disease and autoimmune disease, etc.
(5) Working Examples: There are 46 examples.
(6) Skill of those in the art: The attempts to find compounds to treat the various inflammatory diseases or autoimmune diseases.
(7) The quantity of experimentation needed: Given the fact that, historically, the development
of new drugs for the treatment of inflammatory diseases and autoimmune diseases has been difficult and time consuming, and especially in view of factors 1 and 4 and 6, 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 view of the lack of direction provided in the specification regarding starting materials,
the lack of working examples, and the general unpredictability of chemical reaction, it would
take an undue amount of experimentation for one skilled in the art to make the claimed
compounds and therefore practice the invention. To be enabling, the specification of a patent
must teach those skilled in the art how to make and use the scope of the claimed invention
without undue experimentation. The applicants are not entitled to preempt the efforts of others.
The test for determining compliance with 35 U.S.C. § 112, is whether the applicants have clearly defined their invention.
It is difficult to treat many of the disorders claimed herein. Instant claim language embraces disorders not only for treatment but the prevention, which is not remotely enabled. It is presumed in the prevention of the diseases and/or disorders claimed herein there is a way of identifying those people who may develop a inflammatory bowel disease, asthma, COPD, rheumatoid arthritis, etc. There is no evidence of record, which would enable the skilled artisan in the identification of the people who have the potential of becoming afflicted with the disorders claimed herein.
Where the utility is unusual or difficult to treat or speculative, the examiner has authority
to require evidence that tests relied upon are reasonably predictive of in vivo efficacy by those
skilled in the art. See In re Ruskin, 148 USPQ 221; Ex parte Jovanovics, 211 USPQ 907;
MPEP 2164.05(a).
Patent Protection is granted in return for an enabling disclosure of an invention, not for
vague intimations of general ideas that may or may not be workable. Tossing out the mere germ
of an idea does not constitute enabling disclosure. Genentech Inc. v. Novo Nordisk 42 USPQ2d
1001.
As stated in the MPEP, 2164.08 "[t]he 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). Nevertheless, not everything necessary to practice the
invention need be disclosed. In fact, what is well known is best omitted. In re Buchner, 929
F.2d 660, 661, 18 USPQ2d 1331, 1332 (Fed. Cir. 1991). All that is necessary is that one skilled
in the art be able to practice the claimed invention, given the level of knowledge and skill in the
art. Further the scope of enablement must only bear a reasonable correlation to the scope of
the claims. See, e.g., In re Fisher, 427 F.2d 833, 839,166 USPQ 18, 24 (CCPA 1970). As
concerns the breadth of a claim relevant to enablement, the only relevant concern should be
whether the scope of enablement provided to one skilled in the art by the disclosure is
commensurate with the scope of protection sought by the claims. In re Moore, 439 F.2d 1232,
1236, 169 USPQ 236, 239 (CCPA 1971). See also Plant Genetic Sys., N.V. v. DeKalb Genetics
Corp., 315 F.3d 1335, 1339, 65 USPQ2d 1452, 1455 (Fed. Cir. 2003) (alleged pioneer status of invention irrelevant to enablement determination.”
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 12, 20, 22-26, 45, 47, 50, 52, 57 and 58 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. The following reasons apply:
Claim 1 and claims dependent thereon are vague and indefinite in that it is not known what is meant by the definition of the variable R112 and R113 where there is no variables R112 and R113 in Formula I.
Claim 52 is vague and indefinite in that it is not known what is meant by the double commas on page 13, line 5.
Allowable Subject Matter
Claims 51, 54 and 59 are allowed. None of the prior art of record nor a search in the pertinent art area teaches the compounds and compositions of the compounds as claimed herein.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to BRENDA L COLEMAN whose telephone number is (571)272-0665. The examiner can normally be reached Mon-Fri 10-6 (flex).
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 H. Murray can be reached on 571-272-9023. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/BRENDA L COLEMAN/Primary Examiner, Art Unit 1624
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