Primaquine is a oral medication used to treat and prevent malaria and to treat Pneumocystis pneumonia. Specifically it is used for malaria due to Plasmodium vivax and Plasmodium ovale along with other medications and for prevention if other options cannot be used. Primaquine is an alternative treatment for Pneumocystis pneumonia together with clindamycin. Primaquine is lethal to P. vivax and P. ovale in the liver stage, and also to P. vivax in the blood stage through its ability to do oxidative damage to the cell. However, the exact mechanism of action is not fully understood. Primaquine is well-absorbed in the gut and extensively distributed in the body without accumulating in red blood cells. Administration of primaquine with food or grapefruit juice increases its oral bioavailibity. In blood, about 20% of circulating primaquine is protein-bound, with preferential binding to the acute phase protein orosomucoid. With a half-life on the order of 6 hours, it is quickly metabolized by liver enzymes to carboxyprimaquine, which does not have anti-malarial activity. Common side effects of primaquine administration include nausea, vomiting, and stomach cramps. Primaquine phosphate is recommended only for the radical cure of vivax malaria, the prevention of relapse in vivax malaria, or following the termination of chloroquine phosphate suppressive therapy in an area where vivax malaria is endemic. Patients suffering from an attack of vivax malaria or having parasitized red blood cells should receive a course of chloroquine phosphate, which quickly destroys the erythrocytic parasites and terminates the paroxysm. Primaquine phosphate should be administered concurrently in order to eradicate the exoerythrocytic parasites in a dosage of 1 tablet (equivalent to 15 mg base) daily for 14 days.

Hydrocortisone is the main glucocorticoid secreted by the adrenal cortex. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). Hydrocortisone is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease.

Hydrocortisone is the main glucocorticoid secreted by the adrenal cortex. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). Hydrocortisone is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease.

Hydrocortisone is the main glucocorticoid secreted by the adrenal cortex. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). Hydrocortisone is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease.

Oxycodone is a semisynthetic opioid used for the management of acute and chronic pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. Oxycodone is a highly selective full agonist of the μ-opioid receptor (MOR), with low affinity for the δ-opioid receptor (DOR) and κ-opioid receptor (KOR). After oxycodone binds to the MOR, a G protein-complex is released, which inhibits the release of neurotransmitters by the cell by reducing the amount of cAMP produced, closing calcium channels, and opening potassium channels. After a dose of conventional (instant-release) oral oxycodone, the onset of action is 10–30 minutes, and peak plasma levels of the drug are attained within roughly 30–60 minutes in contrast, after a dose of OxyContin (an oral controlled-release formulation), peak plasma levels of oxycodone occur in about three hours. The duration of instant-release oxycodone is 3 to 6 hours, although this can be variable depending on the individual. Oxycodone in the blood is distributed to skeletal muscle, liver, intestinal tract, lungs, spleen, and brain. Serious side effects of oxycodone include reduced sensitivity to pain (beyond the pain the drug is taken to reduce), euphoria, anxiolysis, feelings of relaxation, and respiratory depression. Common side effects of oxycodone include constipation (23%), nausea (23%), vomiting (12%), somnolence (23%), dizziness (13%), itching (13%), dry mouth (6%), and sweating (5%).

Flavin mononucleotide, or riboflavin-5′-phosphate, is a biomolecule produced from riboflavin by the enzyme riboflavin kinase and functions as prosthetic group of various oxidoreductases including NADH dehydrogenase as well as cofactor in biological blue-light photo receptors. Riboflavin (Vitamin B 2) (as riboflavin 5-phosphate sodium) is an ingredient of the FDA approved composition Infuvite Adult, indicated as a daily multivitamin maintenance supplement for adults and children aged 11 and older receiving parenteral nutrition. Infuvite Adult is also indicated in other situations where administration by the intravenous route is required. Such situations include surgery, extensive burns, fractures and other trauma, severe infectious diseases, and comatose states, which may provoke a “stress” situation with profound alterations in the body’s metabolic demands and consequent tissue depletion of nutrients. Flavin mononucleotide is also a component of Cytoflavin, used for the treatment of consequences of cerebral infarction, for the treatment of atherosclerosis, encephalopathy, neurasthenia. Cytoflavin is marketed in Russian Federation.

Flavin mononucleotide, or riboflavin-5′-phosphate, is a biomolecule produced from riboflavin by the enzyme riboflavin kinase and functions as prosthetic group of various oxidoreductases including NADH dehydrogenase as well as cofactor in biological blue-light photo receptors. Riboflavin (Vitamin B 2) (as riboflavin 5-phosphate sodium) is an ingredient of the FDA approved composition Infuvite Adult, indicated as a daily multivitamin maintenance supplement for adults and children aged 11 and older receiving parenteral nutrition. Infuvite Adult is also indicated in other situations where administration by the intravenous route is required. Such situations include surgery, extensive burns, fractures and other trauma, severe infectious diseases, and comatose states, which may provoke a “stress” situation with profound alterations in the body’s metabolic demands and consequent tissue depletion of nutrients. Flavin mononucleotide is also a component of Cytoflavin, used for the treatment of consequences of cerebral infarction, for the treatment of atherosclerosis, encephalopathy, neurasthenia. Cytoflavin is marketed in Russian Federation.

Ascorbic acid (vitamin C) is a water-soluble vitamin. It occurs as a white or slightly yellow crystal or powder with a slight acidic taste. Ascorbic acid is an electron donor, and this property accounts for all its known functions. As an electron donor, ascorbic acid is a potent water-soluble antioxidant in humans. Ascorbic acid acts as an antioxidant under physiologic conditions exhibiting a cross over role as a pro-oxidant in pathological conditions. Oxidized ascorbic acid (dehydroascorbic acid (DHA) directly inhibits IkappaBalpha kinase beta (IKKbeta) and IKKalpha enzymatic activity in vitro, whereas ascorbic acid did not have this effect. These findings define a function for vitamin C in signal transduction other than as an antioxidant and mechanistically illuminate how vitamin C down-modulates NF-kappaB signaling. Vitamin C is recommended for the prevention and treatment of scurvy. Its parenteral administration is desirable for patients with an acute deficiency or for those whose absorption of orally ingested ascorbic acid (vitamin c) is uncertain. Symptoms of mild deficiency may include faulty bone and tooth development, gingivitis, bleeding gums, and loosened teeth. Febrile states, chronic illness, and infection (pneumonia, whooping cough, tuberculosis, diphtheria, sinusitis, rheumatic fever, etc.) increase the need for ascorbic acid (vitamin c). Hemovascular disorders, burns, delayed fracture and wound healing are indications for an increase in the daily intake.

Ascorbic acid (vitamin C) is a water-soluble vitamin. It occurs as a white or slightly yellow crystal or powder with a slight acidic taste. Ascorbic acid is an electron donor, and this property accounts for all its known functions. As an electron donor, ascorbic acid is a potent water-soluble antioxidant in humans. Ascorbic acid acts as an antioxidant under physiologic conditions exhibiting a cross over role as a pro-oxidant in pathological conditions. Oxidized ascorbic acid (dehydroascorbic acid (DHA) directly inhibits IkappaBalpha kinase beta (IKKbeta) and IKKalpha enzymatic activity in vitro, whereas ascorbic acid did not have this effect. These findings define a function for vitamin C in signal transduction other than as an antioxidant and mechanistically illuminate how vitamin C down-modulates NF-kappaB signaling. Vitamin C is recommended for the prevention and treatment of scurvy. Its parenteral administration is desirable for patients with an acute deficiency or for those whose absorption of orally ingested ascorbic acid (vitamin c) is uncertain. Symptoms of mild deficiency may include faulty bone and tooth development, gingivitis, bleeding gums, and loosened teeth. Febrile states, chronic illness, and infection (pneumonia, whooping cough, tuberculosis, diphtheria, sinusitis, rheumatic fever, etc.) increase the need for ascorbic acid (vitamin c). Hemovascular disorders, burns, delayed fracture and wound healing are indications for an increase in the daily intake.

Ascorbic acid (vitamin C) is a water-soluble vitamin. It occurs as a white or slightly yellow crystal or powder with a slight acidic taste. Ascorbic acid is an electron donor, and this property accounts for all its known functions. As an electron donor, ascorbic acid is a potent water-soluble antioxidant in humans. Ascorbic acid acts as an antioxidant under physiologic conditions exhibiting a cross over role as a pro-oxidant in pathological conditions. Oxidized ascorbic acid (dehydroascorbic acid (DHA) directly inhibits IkappaBalpha kinase beta (IKKbeta) and IKKalpha enzymatic activity in vitro, whereas ascorbic acid did not have this effect. These findings define a function for vitamin C in signal transduction other than as an antioxidant and mechanistically illuminate how vitamin C down-modulates NF-kappaB signaling. Vitamin C is recommended for the prevention and treatment of scurvy. Its parenteral administration is desirable for patients with an acute deficiency or for those whose absorption of orally ingested ascorbic acid (vitamin c) is uncertain. Symptoms of mild deficiency may include faulty bone and tooth development, gingivitis, bleeding gums, and loosened teeth. Febrile states, chronic illness, and infection (pneumonia, whooping cough, tuberculosis, diphtheria, sinusitis, rheumatic fever, etc.) increase the need for ascorbic acid (vitamin c). Hemovascular disorders, burns, delayed fracture and wound healing are indications for an increase in the daily intake.