41 research outputs found
Composition and formulations and their use as nociceptic, anti-anxiolytic and anabolic agents
Composition and formulations comprising a first agent such as folinic acid, pharmaceutically acceptable salts thereof or mixtures thereof, and a second agent(s) such as analgesics, muscle relaxants, mood disorder agents, anti-inflammatories, anti-migraine agents, anti-emetics, diuretics, high protein composites, and the like. The products are suitable as nociceptics and for the treatment of wasting disorders, bulimia, anorexia nervosa, anxiety, irritability and other symptoms associated with Pre Menstrual Syndrome, as well as for administration either in conjunction with steroids or to compensate adenosine depletion and/or bizarre behavior or aggression common in steroid users
Method of treating adenosine depletion
A method of treating adenosine depletion in a subject in need of such treatment is disclosed. The method comprises administering to the subject folinic acid or a pharmaceutically acceptable salt thereof in an amount effective to treat adenosine depletion. A method of treating asthma in a subject in need of such treatment is also disclosed. The method comprises administering to the subject dehydroepiandrosterone, analogs thereof, or pharmaceutically acceptable salts thereof in an amount effective to treat asthma
Low adenosine anti-sense oligonucleotide, compositions, kit and method for treatment of airway disorders associated with bronchoconstriction, lung inflammation, allergy(ies) and surfactant depletion
An in vivo method of selectively delivering a nucleic acid to a target gene or mRNA comprises the topical admistration, e.g. to the respiratory system, of a subject of a therapeutic amount of an oligonucleotide that is antisense to the initiation codon region, coding region, 5' or 3' inton-exon junctions or regions within 2 to 10 nucleotides of the junctions of the target gene, or antisense to a mRNA complementary to the target gene in an amount effective to reach the target polynucleotide and reducing or inhibiting expression. Additionally, a method of treating and adenosine mediated effect is described also utilizing the delivery of antisense and in order to minimize triggering adenosine receptors by their metabolism, the administered oligos have a low content of or are essentially free of adenosine. The agent, composition and formulations are used for prophlactic, preventive and therapeutic treatment of ailments associated with impaired respiration, lung allergies and/or vasoconstriction, inflammation, allergies, allergic rhynitis, asthma, impeded respiration, lung pain, cystic fibrosis and bronchoconstriction
Method of inhibiting carcinogenesis by treatment with dehydroepiandrosterone and analogs thereof
A method of combatting cancer in a subject comprising administering to said subject dehydroepiandrosterone (DHEA) or an analog thereof in an amount effective to combat cancer is disclosed in which heart failure induced by the DHEA or analog thereof is combatted by administering to the subject a ubiquinone, in an amount effective to combat heart failure induced by the DHEA or analog thereof. A prefered DHEA analog for carrying out the invention is 16 alpha-fluoroepiandrosterone, and a preferred ubiquinone for carrying out the invention is Coenzyme Q.sub.10
Method for reducing adenosine levels with a dehydroepiandrosterone and optionally a ubiquinone
A method and composition for reducing adenosine levels comprises administering a dehydroepiandrosterone, and optionally a ubiquinone
Agent and method for treating disorders associated with cytidine deaminase or deoxycytidine deaminase overexpression
An agent of the chemical formula C.sub.7 N.sub.3 H.sub.8 O.sub.2 R.sup.1 R.sup.2 XX.sup.1, wherein X and X.sup.1 are each independently C or N but not simultaneously, R.sup.1 is lower alkyl, alkenyl or alkynyl, halogen or haloalkyl, and R.sup.2 is H, --N.sub.3 --OH, amino or halogen; or pharmaceutically acceptable salts thereof. A method of treating a disorder associated with the overexpression of cytidine deaminase or deoxycytidine deaminase comprises administering to a subject in need of the treatment a compound of the chemical formula ##STR1## wherein X and X.sub.1 are each independently C or N; R.sup.1 is lower alkyl, lower alkenyl, lower alkynyl, halogen, or haloalkyl; and R.sup.2 H, --N.sub.3, --OH, amino, or halogen; or a pharmaceutically acceptable salt thereof in an amount effective to treat the disorder. Pharmaceutical formulations useful in the method of the present invention are also disclosed
Compositions & formulations with a non-glucocorticoid steroid &/or a ubiquinone & kit for treatment of respiratory & lung disease
A composition comprises as the active agent a Non-glucocorticoid steroid, analogue thereof, a ubiquinone, or their salts, in an amount effective for reducing levels of, or hypersensitivity to, adenosine, increasing levels of lung surfactant or ubiquinone, or for preventing or treating respiratory, lung and cancer diseases. The present treatment is useful for treating asthma, rhinitis, COPD, CF, RDS, pulmonary fibrosis, cancer and other diseases
Composition, formulations & method for prevention & treatment of diseases and conditions associated with bronchoconstriction, allergy(ies) & inflammation
A pharmaceutical composition effective for preventing and alleviating bronchoconstriction, lung allergy(ies) and inflammation comprises a surfactant and an oligonucleotide anti-sense to an adenosine receptor gene, flanking regions or regions bridging the intro/exon borders, analogues which bind thymidine but have low adenosine content or exhibit lower or no adenosine receptor agonist activity, or antisense to the corresponding mRNA, combinations, sales or mixtures thereof, and a carrier, and optionally other therapeutic agents and formulation products. The composition is formulated for administration by a multiplicity of routes, and finds applications in the prevention and treatment of asthma, kidney damage or failure, ARDS, pulmonary vasoconstriction, inflammation, allergies, impeded respiration, respiratory distress syndrome, pain, cystic fibrosis, pulmonary hypertension, pulmonary vasoconstriction, emphysema, chronic obstructive pulmonary disease (COPD), and cancer, to counter the renal damage and failure associated with ischemic conditions and the administration of certain drugs and radio active diagnostic and therapeutic agents, as well as a joint therapy with the administration of adenosine and adenosine-like agents in the treatment of arrhythmias such as SVT and in cardiovascular function tests (stress tests). The present agent(s) is (are) also suitable for administration before, during and after other treatments, including radiation, chemotherapy, antibody therapy, phototherapy and cancer, and other types of surgery
Autoinflammatory Reaction in Dogs Treated for Cancer via G6PD Inhibition
Glucose-6-phosphate dehydrogenase (G6PD) is an oncoprotein that is overexpressed in cancer cells to provide the NADPH required for their increased anabolism. NADPH, sourced from G6PD fuels nucleotide biosynthesis, maintains redox potential of thioredoxin and glutathione and drives the mevalonate pathway that powers many of the basic mechanisms by which cancer cells escape host control. G6PD is thus a target for cancer treatment being addressed by many groups around the world. We have discovered that systemic inhibition of G6PD by high dose dehydroepiandrosterone (DHEA) causes a severe autoinflammatory response in dogs, which does not occur in mice or rats. Since dogs more closely model the human adrenal androgen system than do common laboratory animals, this finding is relevant to the design of G6PD-inhibiting drugs for humans. The autoinflammatory reaction observed closely resembles mevalonate kinase deficiency (MKD), a rare autosomal recessive disease in humans characterized by recurrent febrile attacks, arthralgia, skin rash, and aphthous ulcers of mucocutaneous tissues. In a manner comparable to animal models of MKD, the reconstitution of protein geranylgeranylation blocked the autoinflammatory reaction caused by systemic G6PD inhibition. This autoinflammatory response to systemic G6PD inhibition represents an unexpected result that must be taken into consideration when targeting this oncoprotein