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Total 393357 Results
| Label | Description | ILX | Version | Created CID | Modified Time | ||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| ALX receptor | ILX:0100523 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| Alzheimers disease | A neurodegenerative disease resulting in the insidious onset of dementia. Impairment of memory, judgement, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (adapted from MSH) | ILX:0100524 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Amacrine neuron | A neuron characterized by amacrine extensions. Discovered first by Herophilus (335-263 BC) in the retina. Considered initially without axon, now they are commonly found in nerve nets, where they may have an axon and/or dendrite.Adapted from Swanson, 2013. | ILX:0100525 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Ambenonium | Ambenonium is a cholinesterase inhibitor used in the management of myasthenia gravis. (Wikipedia) Pharmacology: Ambenonium, similar to pyridostigmine and neostigmine, is used for the treatment of muscle weakness and fatigue in people with myasthenia gravis. It is postulated to exert its therapeutic effect by enhancing cholinergic function by inhibiting the hydrolysis of acetylcholine by acetylcholinesterase. Increased levels of acetylcholine has peripheral effects, as acetylcholine is also used in the brain, where it tends to cause excitatory actions. The glands that receive impulses from the parasympathetic part of the autonomic nervous system are also stimulated in the same way. This is why an increase in acetylcholine causes a decreased heart rate and increased production of saliva. Ambenonium is used less commonly than neostigmine or pyridostigmine but may be preferred in patients hypersensitive to the bromide ion. Ambenonium produces fewer muscarinic side effects than neostigmine, but more than pyridostigmine. Mechanism of action: Ambenonium exerts its actions against myasthenia gravis by competitive, reversible inhibition of acetylcholinesterase. The disease myasthenia gravis occurs when the body inappropriately produces antibodies against acetylcholine receptors, and thus inhibits proper acetylcholine signal transmission (when acetylcholine binds to acetylcholine receptors of striated muscle fibers, it stimulates those fibers to contract). Ambenonium reversibly binds acetylcholinesterase, and as acetylcholinesterase is responsible for the hydrolysis of acetylcholine, this inhibition increases levels of acetylcholine. In turn this facilitates transmission of impulses across the myoneural junction and effectively treats the disease. Drug type: Approved. Small Molecule. Drug category: Antiarrhythmic Agents. Antimyasthenics | ILX:0100527 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Amcinonide | Amcinonide is a corticosteroid. (Wikipedia) Pharmacology: Amcinonide is a topical corticosteroid. The topical corticosteroids constitute a class of primarily synthetic steroids used as anti-inflammatory and antipruritic agents. Amcinonide reduces or inhibits the actions of chemicals in the body that cause inflammation, redness, and swelling. The mechanism of anti-inflammatory activity of the topical corticosteroids is unclear. Various laboratory methods, including vasoconstrictor assays, are used to compare and predict potencies and/or clinical efficacies of the topical corticosteroids. There is some evidence to suggest that a recognizable correlation exists between vasoconstrictor potency and therapeutic efficacy in man. When in an ointment form, amcinonide also helps the skin maintain moisture. Mechanism of action: The mechanism of the anti-inflammatory activity of the topical steroids, in general, is unclear. However, corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor, arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2. Amcinonide has affinity for the glucocorticoid receptor. It has weak affinity for the progesterone receptor, and virtually no affinity for the mineralocorticoid, estrogen, or androgen receptors. Drug type: Approved. Small Molecule. Drug category: Corticosteroids, topical | ILX:0100528 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Amdinocillin | Amidinopenicillanic acid derivative with broad spectrum antibacterial action. It is poorly absorbed if given orally and is used in urinary infections and typhus. (PubChem) Pharmacology: Amdinocillin is a novel, semisynthetic penicillin effective against many gram-negative bacteria. The antibacterial activity of amdinocillin is derived from its ability to bind specifically and avidly to Penicillin Binding Protein-2 (PBP 2). Amdinocillin is active alone against many gram-negative organisms. Pseudomonas and non-fermenting gram-negative bacteria, however, are usually resistant. Amdinocillin, in combination with many beta-lactams, exhibits marked synergy against many enterobacteriaceae. No such synergy can be demonstrated for gram-positive organisms or pseudomonas species. Amdinocillin is not beta-lactamase stable. Organisms which produce high levels of plasma-mediated beta-lactamase are resistant to the drug. Co-administration of probenecid results in markedly elevated plasma levels of amdinocillin and delays its excretion. Mechanism of action: Amdinocillin is a stong and specific antagonist of Penicillin Binding Protein-2 (PBP 2). Drug type: Approved. Small Molecule. Drug category: Anti-Bacterial Agents. Anti-Infective Agents, Urinary. Penicillins | ILX:0100529 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| American cockroach | ILX:0100530 | 5 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| American lobster | ILX:0100531 | 5 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| Amiculum of dentate nucleus | ILX:0100532 | 14 | scicrunch | 06/23/2020 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| Amifostine | A phosphorothioate proposed as a radiation-protective agent. It causes splenic vasodilation and may block autonomic ganglia. (PubChem) Pharmacology: Amifostine is an organic thiophosphate cytoprotective agent indicated to reduce the cumulative renal toxicity associated with repeated administration of cisplatin in patients with advanced ovarian cancer or non-small cell lung cancer and also to reduce the incidence of moderate to severe xerostomia in patients undergoing post-operative radiation treatment for head and neck cancer. Amifostine is a prodrug that is dephosphorylated by alkaline phosphatase in tissues to a pharmacologically active free thiol metabolite, believed to be responsible for the reduction of the cumulative renal toxicity of cisplatin and for the reduction of the toxic effects of radiation on normal oral tissues. Healthy cells are preferentially protected because amifostine and metabolites are present in healthy cells at 100-fold greater concentrations than in tumour cells. Mechanism of action: The thiol metabolite is responsible for most of the cytoprotective and radioprotective properties of amifostine. It is readily taken up by cells where it binds to and detoxifies reactive metabolites of platinum and alkylating agents as well as scavenges free radicals. Other possible effects include inhibition of apoptosis, alteration of gene expression and modification of enzyme activity. Drug type: Approved. Investigational. Small Molecule. Drug category: Radiation-Protective Agents | ILX:0100533 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Amiloride | A pyrazine compound inhibiting sodium reabsorption through sodium channels in renal epithelial cells. This inhibition creates a negative potential in the luminal membranes of principal cells, located in the distal convoluted tubule and collecting duct. Negative potential reduces secretion of potassium and hydrogen ions. Amiloride is used in conjunction with diuretics to spare potassium loss. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p705) Pharmacology: Amiloride, an antikaliuretic-diuretic agent, is a pyrazine-carbonyl-guanidine that is unrelated chemically to other known antikaliuretic or diuretic agents. It is an antihypertensive, potassium-sparing diuretic that was first approved for use in 1967 and helps to treat hypertension and congestive heart failure. The drug is often used in conjunction with thiazide or loop diuretics. Due to its potassium-sparing capacities, hyperkalemia (high blood potassium levels) are occasionally observed in patients taking amiloride. The risk is high in concurrent use of ACE inhibitors or spironolactone. Patients are also advised not to use potassium-containing salt replacements. Mechanism of action: Amiloride works by inhibiting sodium reabsorption in the distal convoluted tubules and collecting ducts in the kidneys by binding to the amiloride-sensitive sodium channels. This promotes the loss of sodium and water from the body, but without depleting potassium. Amiloride exerts its potassium sparing effect through the inhibition of sodium reabsorption at the distal convoluted tubule, cortical collecting tubule and collecting duct; this decreases the net negative potential of the tubular lumen and reduces both potassium and hydrogen secretion and their subsequent excretion. Amiloride is not an aldosterone antagonist and its effects are seen even in the absence of aldosterone. Drug type: Approved. Small Molecule. Drug category: Diuretics. Sodium channel blockers | ILX:0100535 | 5 | scicrunch | 08/24/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | troy sincomb |
| Aminergic neuron | Any neuron (FBbt_00005106) that releases as a neurotransmitter, some amine (CHEBI:32952). | ILX:0100536 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Amino Acid | Organic compounds that generally contain an amino (-NH2) and a carboxyl (-COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins (MSH). | ILX:0100537 | 4 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Aminoalkylindole | ILX:0100538 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| Aminocaproic Acid | An antifibrinolytic agent that acts by inhibiting plasminogen activators which have fibrinolytic properties. (PubChem) Pharmacology: Aminocaproic acid works as an antifibrinolytic. It is a derivative of the amino acid lysine. The fibrinolysis-inhibitory effects of aminocaproic acid appear to be exerted principally via inhibition of plasminogen activators and to a lesser degree through antiplasmin activity. Mechanism of action: Aminocaproic acid binds reversibly to the kringle domain of plasminogen and blocks the binding of plasminogen to fibrin and its activation to plasmin. Drug type: Approved. Investigational. Small Molecule. Drug category: Antifibrinolytic Agents | ILX:0100539 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Aminohippurate | The glycine amide of 4-aminobenzoic acid. Its sodium salt is used as a diagnostic aid to measure effective renal plasma flow (ERPF) and excretory capacity. (PubChem) Pharmacology: Aminohippurate (p-aminohippuric acid, PAH, PAHA) is the glycine amide of p-aminobenzoic acid. It is filtered by the glomeruli and is actively secreted by the proximal tubules. At low plasma concentrations (1.0 to 2.0 mg/100 mL), an average of 90 percent of aminohippurate is cleared by the kidneys from the renal blood stream in a single circulation. It is ideally suited for measurement of ERPF since it has a high clearance, is essentially nontoxic at the plasma concentrations reached with recommended doses, and its analytical determination is relatively simple and accurate. Aminohippurate is also used to measure the functional capacity of the renal tubular secretory mechanism or transport maximum (TmPAH). This is accomplished by elevating the plasma concentration to levels (40-60 mg/100 mL) sufficient to saturate the maximal capacity of the tubular cells to secrete aminohippurate. Inulin clearance is generally measured during TmPAH determinations since glomerular filtration rate (GFR) must be known before calculations of secretory Tm measurements can be done. Mechanism of action: Aminohippurate is filtered by the renal glomeruli and secreted into the urine by the proximal tubules. By measuring the amount of drug in the urine it is possible to determine functional capacity and effective renal plasma flow. Drug type: Approved. Small Molecule. Drug category: Diagnostic aids. Indicators and Reagents | ILX:0100541 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Aminolevulinic acid | A compound produced from succinyl-CoA and glycine as an intermediate in heme synthesis. It is used as a photochemotherapy for actinic keratosis. (PubChem) Pharmacology: The metabolism of aminolevulinic acid (ALA) is the first step in the biochemical pathway resulting in heme synthesis. Aminolevulinic acid is not a photosensitizer, but rather a metabolic precursor of protoporphyrin IX (PpIX), which is a photosensitizer. The synthesis of ALA is normally tightly controlled by feedback inhibition of the enzyme, ALA synthetase, presumably by intracellular heme levels. ALA, when provided to the cell, bypasses this control point and results in the accumulation of PpIX, which is converted into heme by ferrochelatase through the addition of iron to the PpIX nucleus. Mechanism of action: According to the presumed mechanism of action, photosensitization following application of aminolevulinic acid (ALA) topical solution occurs through the metabolic conversion of ALA to protoporphyrin IX (PpIX), which accumulates in the skin to which aminolevulinic acid has been applied. When exposed to light of appropriate wavelength and energy, the accumulated PpIX produces a photodynamic reaction, a cytotoxic process dependent upon the simultaneous presence of light and oxygen. The absorption of light results in an excited state of the porphyrin molecule, and subsequent spin transfer from PpIX to molecular oxygen generates singlet oxygen, which can further react to form superoxide and hydroxyl radicals. Photosensitization of actinic (solar) keratosis lesions using aminolevulinic acid, plus illumination with the BLU-UTM Blue Light Photodynamic Therapy Illuminator (BLU-U), is the basis for aminolevulinic acid photodynamic therapy (PDT). Drug type: Approved. Small Molecule. Drug category: Photosensitizing Agents | ILX:0100542 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Aminophenazone | A pyrazolone with analgesic, anti-inflammatory, and antipyretic properties but has risk of agranulocytosis. A breath test with 13C-labeled aminopyrine has been used as a non-invasive measure of cytochrome P-450 metabolic activity in liver function tests. (PubChem) Pharmacology: Aminophenazone is a pyrazolone with analgesic, anti-inflammatory, and antipyretic properties but has risk of agranulocytosis. A breath test with 13C-labeled aminopyrine has been used as a non-invasive measure of cytochrome P-450 metabolic activity in liver function tests. Mechanism of action: Not Available Drug type: Approved. Small Molecule. Withdrawn. Drug category: Analgesics. Pyrazolones | ILX:0100543 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Aminophylline | Aminophylline is a drug combination that contains theophylline and ethylenediamine in 2:1 ratio. (Wikipedia) Pharmacology: Aminophylline is the ethylenediamine salt of theophylline. Theophylline stimulates the CNS, skeletal muscles, and cardiac muscle. It relaxes certain smooth muscles in the bronchi, produces diuresis, and causes an increase in gastric secretion. Mechanism of action: Theophylline is structurally related to theobromine and caffeine. The precise mechanism of action of theophylline is not known. Drug type: Approved. Small Molecule. Drug category: Bronchodilator Agents. Cardiotonic Agents. Phosphodiesterase Inhibitors. Respiratory Smooth Muscle Relaxants | ILX:0100544 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Aminosalicylic Acid | An antitubercular agent often administered in association with isoniazid. The sodium salt of the drug is better tolerated than the free acid. (PubChem) Pharmacology: Aminosalicylic acid is an anti-mycobacterial agent used with other anti-tuberculosis drugs (most often isoniazid) for the treatment of all forms of active tuberculosis due to susceptible strains of tubercle bacilli. The two major considerations in the clinical pharmacology of aminosalicylic acid are the prompt production of a toxic inactive metabolite under acid conditions and the short serum half life of one hour for the free drug. Aminosalicylic acid is bacteriostatic against Mycobacterium tuberculosis (prevents the multiplying of bacteria without destroying them). It also inhibits the onset of bacterial resistance to streptomycin and isoniazid. Mechanism of action: There are two mechanisms responsible for aminosalicylic acid's bacteriostatic action against Mycobacterium tuberculosis. Firstly, aminosalicylic acid inhibits folic acid synthesis (without potentiation with antifolic compounds). The binding of para-aminobenzoic acid to pteridine synthetase acts as the first step in folic acid synthesis. Aminosalicylic acid binds pteridine synthetase with greater affinity than para-aminobenzoic acid, effectively inhibiting the synthesis of folic acid. As bacteria are unable to use external sources of folic acid, cell growth and multiplication slows. Secondly, aminosalicylic acid may inhibit the synthesis of the cell wall component, mycobactin, thus reducing iron uptake by M. tuberculosis. Drug type: Approved. Small Molecule. Drug category: Antitubercular Agents. Antituberculosis Agents | ILX:0100545 | 5 | scicrunch | 08/24/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | troy sincomb |
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