Drug results: 49

hexyldecanoic acid viscous oil
mandelic acid
methyl aminolevulinate
methyl salicylate used in over-the-counter liniments, ointments, lotions for relief of musculoskeletal aches and pains; has hemolytic effect on human & sheep erythrocytes; RN given refers to parent cpd; structure in Merck Index, 9th ed, #5990
salicylic acid A compound obtained from the bark of the white willow and wintergreen leaves. It has bacteriostatic, fungicidal, and keratolytic actions.
valproic acid A fatty acid with anticonvulsant and anti-manic properties that is used in the treatment of EPILEPSY and BIPOLAR DISORDER. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of VOLTAGE-GATED SODIUM CHANNELS.
fumaric acid see also record for ferrous fumarate; use FUMARATES for general fumaric acid esters
fosfosal reagent for testing the activity of certain enzymes
dimecrotic acid
tidiacic
glycine A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter.
salicylamide
methylparaben used as a preservative in cosmetics but potentiates UV-induced damage of skin; RN given refers to parent cpd
chromocarb treatment for certain forms of hemorrhagic anal inflammations
phenpromethamine
menadione
taurine A conditionally essential nutrient, important during mammalian development. It is present in milk but is isolated mostly from ox bile and strongly conjugates bile acids.
ethinylestradiol sulfonate
magnesium aspartate
dimethyl fumarate A fumarate derivative that is used as a DERMATOLOGIC AGENT in the treatment of PSORIASIS and SKIN DISEASES. It also may be used as an IMMUNOSUPPRESSIVE AGENT in the treatment of MULTIPLE SCLEROSIS.
mesalazine An anti-inflammatory agent, structurally related to the SALICYLATES, which is active in INFLAMMATORY BOWEL DISEASE. It is considered to be the active moiety of SULPHASALAZINE. (From Martindale, The Extra Pharmacopoeia, 30th ed)
methylhexaneamine sympathomimetic aliphatic amine with vasoconstrictor activity
propiolactone Disinfectant used in vapor form to sterilize vaccines, grafts, etc. The vapor is very irritating and the liquid form is carcinogenic.
(2-benzhydryloxyethyl)diethyl-methylammonium iodide
salicylanilide
dichloroacetic acid A derivative of ACETIC ACID that contains two CHLORINE atoms attached to its methyl group.
choline fenofibrate metabolite of lipantyl; structure; salt of cholesterylamine & 2-(4-(p-chlorobenzoyl)phenoxy)2-methylpropionic acid
kainic acid (2S-(2 alpha,3 beta,4 beta))-2-Carboxy-4-(1-methylethenyl)-3-pyrrolidineacetic acid. Ascaricide obtained from the red alga Digenea simplex. It is a potent excitatory amino acid agonist at some types of excitatory amino acid receptors and has been used to discriminate among receptor types. Like many excitatory amino acid agonists it can cause neurotoxicity and has been used experimentally for that purpose.
adenosine phosphate Adenine nucleotide containing one phosphate group esterified to the sugar moiety in the 2'-, 3'-, or 5'-position.
hematoporphyrin Iron-free derivatives of heme with 4 methyl groups, 2 hydroxyethyl groups and 2 propionic acid groups attached to the pyrrole rings. Some of these PHOTOSENSITIZING AGENTS are used in the PHOTOTHERAPY of malignant NEOPLASMS.
monoctanoin dissolution agent for retained cholesterol bile duct stones; RN in Chemline for octanoic acid, ester with 1,2,3-propanetriol, MF unknown: 11140-04-8; RN for octanoic acid, 2,3-dihydroxypropyl ester (1-monooctanoin): 502-54-5; RN in 9th CI Form Index for (+-)-1-monooctanoin: 19670-49-6
piroctone 2(1H)-pyridinone, 1-hydroxy-4-methyl-6-(2,4,4-trimethylpentyl)- combined with 2-aminoethanol; used to treat pityriasis; structure given in first source
thiamine 3-((4-Amino-2-methyl-5-pyrimidinyl)methyl)-5-(2- hydroxyethyl)-4-methylthiazolium chloride.
diclofenac etalhyaluronate sodium Diclofenac etalhyaluronate is a 130,000 kDa compound in which the diclofenac molecule is attached via a 2-aminoethanol linker to the glucuronic acid moiety of the hyaluronic acid. Diclofenac is released through hydrolytic cleavage of the ester linkage and it inhibits the synthesis of prostaglandin E2.
mepindolol 2-methyl deriv of pindolol; RN given refers to parent cpd; structure
esketamine Esketamine is the S-enantiomer of racemic ketamine. It is a non-selective, non-competitive, antagonist of the N-methyl-D-aspartate (NMDA) receptor, an ionotropic glutamate receptor. Through NMDA receptor antagonism, esketamine produces a transient increase in glutamate release leading to increases in alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) stimulation and subsequently to increases in neurotrophic signalling which may contribute to the restoration of synaptic function in these brain regions involved with the regulation of mood and emotional behaviour. Restoration of dopaminergic neurotransmission in brain regions involved in the reward and motivation, and decreased stimulation of brain regions involved in anhedonia, may contribute to the rapid response.
lixisenatide A synthetic GLUCAGON-LIKE PEPTIDE-1 RECEPTOR (GLP-1) agonist that binds GLP-1 receptor that is used to control blood sugar levels in patients with TYPE 2 DIABETES; amino acid sequence is H-HGEGTFTSDLSKQMEEEAVRLFIEWLKNGGPSSGAPPSK KKKKK-NH2 (ZP10A).
etesevimab FDA issued an Emergency Use Authorization (EUA) for etesevimab and bamlanivimab on February 9, 2021 that permits combined use of the drugs for the treatment of mild to moderate COVID-19. The EUA of bamlanivimab ALONE was revoked by FDA but the use of bamlanivimab in a combined regimen with etesevimab remains unchanged. Etesevimab is a recombinant neutralizing human IgG1kappa mAb to the spike protein of SARS-CoV-2, with amino acid substitutions in the Fc region (L234A, L235A) to reduce effector function. Etesevimab binds the spike protein and blocks spike protein attachment to the human ACE2 receptor with an IC50value of 0.32 nM (0.046 μg/mL). Bamlanivimab and etesevimab bind to different but overlapping epitopes in the receptor binding domain (RBD) of the S-protein. Using both antibodies together is expected to reduce the risk of viral resistance.
etofibrate analog of clofibrate with nicotinic acid substituted on the 2-carbon of the ethyl ester group; structure; RN given refers to parent cpd
levetiracetam The precise mechanism(s) by which levetiracetam exerts its antiepileptic effect is unknown. The antiepileptic activity of levetiracetam was assessed in a number of animal models of epileptic seizures. Levetiracetam did not inhibit single seizures induced by maximal stimulation with electrical current or different chemoconvulsants and showed only minimal activity in submaximal stimulation and in threshold tests. Protection was observed, however, against secondarily generalized activity from focal seizures induced by pilocarpine and kainic acid, two chemoconvulsants that induce seizures that mimic some features of human complex partial seizures with secondary generalization. Levetiracetam also displayed inhibitory properties in the kindling model in rats, another model of human complex partial seizures, both during kindling development and in the fully kindled state. In vitro and in vivo recordings of epileptiform activity from the hippocampus have shown that levetiracetam inhibits burst firing without affecting normal neuronal excitability, suggesting that levetiracetam may selectively prevent hypersynchronization of epileptiform burst firing and propagation of seizure activity. Levetiracetam at concentrations of up to 10 uM did not demonstrate binding affinity for a variety of known receptors, such as those associated with benzodiazepines, GABA (gamma-aminobutyric acid), glycine, NMDA (N-methyl-D-aspartate), re-uptake sites, and second messenger systems. Furthermore, in vitro studies have failed to find an effect of levetiracetam on neuronal voltage-gated sodium or T-type calcium currents and levetiracetam does not appear to directly facilitate GABAergic neurotransmission. However, in vitro studies have demonstrated that levetiracetam opposes the activity of negative modulators of GABA- and glycine-gated currents and partially inhibits N-type calcium currents in neuronal cells. A saturable and stereoselective neuronal binding site in rat brain tissue has been described for levetiracetam. Experimental data indicate that this binding site is the synaptic vesicle protein SV2A, thought to be involved in the regulation of vesicle exocytosis. Although the molecular significance of levetiracetam binding to synaptic vesicle protein SV2A is not understood, levetiracetam and related analogs showed a rank order of affinity for SV2A which correlated with the potency of their antiseizure activity in audiogenic seizure-prone mice. These findings suggest that the interaction of levetiracetam with the SV2A protein may contribute to the antiepileptic mechanism of action of the drug.
carotegrast methyl Carotegrast methyl is a small-molecule alpha4 integrin antagonist which received its first approval in Japan for the treatment of moderate ulcerative colitis in patients who had inadequate response to 5-aminosalicylic acid. The active metabolite of carotegrast methyl exerts an anti-inflammatory effect by blocking the interaction of alpha4beta1 or alpha4beta7 integrins and their ligands, VCAM-1 and MAd-CAM-1, thereby inhibiting the adhesion of inflammatory cells, including T cells, to vascular endothelial cells and extravasation into inflammatory sites.
colestilan a 2-methylimidazole-epichlorohydrin polymer; bile acid and methotrexate anion-exchange resin
icosapent ethyl Icosapent ethyl is a stable ethyl ester of the omega-3 fatty acid, eicosapentaenoic acid (EPA). The mechanisms of action contributing to reduction of cardiovascular events with icosapent ethyl are not completely understood. The mechanisms are likely multi-factorial including improved lipoprotein profile with reduction of triglyceride-rich lipoproteins, anti-inflammatory, and antioxidant effects, reduction of macrophage accumulation, improved endothelial function, increased fibrous cap thickness/stability, and antiplatelet effects. Each of these mechanisms can beneficially alter the development, progression, and stabilisation of atherosclerotic plaque, as well as the implications of plaque rupture, and preclinical and clinical studies support such benefits with EPA. Systemic and localised anti-inflammatory effects of EPA may result from displacement of pro-inflammatory arachidonic acid (AA), directing catabolism away from eicosanoids (2-series prostaglandins and thromboxanes, and 4-series leukotrienes) to non- or anti-inflammatory mediators. However, the direct clinical meaning of individual findings is not clear.
bempedoic acid Bempedoic acid is an adenosine triphosphate-citrate lyase (ACL) inhibitor that lowers low-density lipoprotein cholesterol (LDL-C) by inhibition of cholesterol synthesis in the liver. ACL is an enzyme upstream of 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase in the cholesterol biosynthesis pathway. Bempedoic acid and its active metabolite, ESP15228, require coenzyme A (CoA) activation by very long-chain acyl-CoA synthetase 1 (ACSVL1) to ETC-1002-CoA and ESP15228-CoA, respectively. ACSVL1 is expressed primarily in the liver. Inhibition of ACL by ETC-1002-CoA results in decreased cholesterol synthesis in the liver and lowers LDL-C in blood via upregulation of low-density lipoprotein receptors
sipavibart Sipavibart is a recombinant human IgG1 monoclonal antibody that provides passive immunisation by binding the SARS-CoV-2 spike protein receptor binding domain (RBD). Sipavibart is long-acting, with amino acid substitutions to extend antibody half-life (YTE) and to reduce antibody effector function and potential risk of antibody-dependent enhancement of disease (TM). Sipavibart binds to the spike protein RBD of SARS-CoV-2 (BA.2), blocking RBD binding to the human ACE2 receptor. This results in a blockade of virus entry.
omega-3-carboxylic acids Fish oil-derived free fatty acids including multiple omega-3 fatty acids, eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA] being the most abundant. The mechanism of action of omega-3-carboxylic acids is not completely understood. Potential mechanisms of action include inhibition of acyl-CoA:1,2-diacylglycerol acyltransferase, increased mitochondrial and peroxisomal beta-oxidation in the liver, decreased lipogenesis in the liver, and increased plasma lipoprotein lipase activity. Omega-3-carboxylic acids may reduce the synthesis of triglycerides in the liver because EPA and DHA are poor substrates for the enzymes responsible for TG synthesis, and EPA and DHA inhibit esterification of other fatty acids.
eladocagene exuparvovec Eladocagene exuparvovec is a gene therapy medicinal product that expresses the human aromatic L-amino acid decarboxylase enzyme (hAADC). It is a non-replicating recombinant adeno-associated virus serotype 2 (AAV2) based vector containing the cDNA of the human dopa decarboxylase (DDC) gene under the control of the cytomegalovirus immediate-early promoter.
gabapentin The mechanism by which gabapentin exerts its analgesic action is unknown, but in animal models of analgesia, gabapentin prevents allodynia (pain-related behavior in response to a normally innocuous stimulus) and hyperalgesia (exaggerated response to painful stimuli). In particular, gabapentin prevents pain-related responses in several models of neuropathic pain in rats or mice (e.g., spinal nerve ligation models, streptozocin-induced diabetes model, spinal cord injury model, acute herpes zoster infection model). Gabapentin also decreases pain-related responses after peripheral inflammation (carrageenan footpad test, late phase of formalin test). Gabapentin did not alter immediate pain-related behaviors (rat tail flick test, formalin footpad acute phase, acetic acid abdominal constriction test, footpad heat irradiation test). The mechanism by which gabapentin exerts its anticonvulsant action is unknown, but in animal test systems designed to detect anticonvulsant activity, gabapentin prevents seizures as do other marketed anticonvulsants. Gabapentin exhibits antiseizure activity in mice and rats in both the maximal electroshock and pentylenetetrazole seizure models and other preclinical models (e.g., strains with genetic epilepsy, etc.). Gabapentin is structurally related to the neurotransmitter GABA (gamma-aminobutyric acid) but it does not modify GABAA or GABAB radioligand binding, it is not converted metabolically into GABA or a GABA agonist, and it is not an inhibitor of GABA uptake or degradation. Gabapentin was tested in radioligand binding assays at concentrations up to 100 uM and did not exhibit affinity for a number of other common receptor sites, including benzodiazepine, glutamate, N-methyl-D-aspartate (NMDA), quisqualate, kainate, strychnine-insensitive or strychnine-sensitive glycine, alpha 1, alpha 2, or beta adrenergic, adenosine A1 or A2, cholinergic muscarinic or nicotinic, dopamine D1 or D2, histamine H1, serotonin S1 or S2, opiate mu, delta or kappa, cannabinoid 1, voltage-sensitive calcium channel sites labeled with nitrendipine or diltiazem, or at voltage-sensitive sodium channel sites labeled with batrachotoxinin A 20-alpha-benzoate. Furthermore, gabapentin did not alter the cellular uptake of dopamine, noradrenaline, or serotonin. In vitro studies with radiolabeled gabapentin have revealed a gabapentin binding site in areas of rat brain including neocortex and hippocampus. A high-affinity binding protein in animal brain tissue has been identified as an auxiliary subunit of voltage-activated calcium channels.
riluzole The etiology and pathogenesis of amyotrophic lateral sclerosis (ALS) are not known, although a number of hypotheses have been advanced. One hypothesis is that motor neurons, made vulnerable through either genetic predisposition or environmental factors, are injured by glutamate. In some cases of familial ALS the enzyme superoxide dismutase has been found to be defective. The mode of action of riluzole is unknown. Its pharmacological properties include the following, some of which may be related to its effect: 1) an inhibitory effect on glutamate release, 2) inactivation of voltage-dependent sodium channels, and 3) ability to interfere with intracellular events that follow transmitter binding at excitatory amino acid receptors. Riluzole has also been shown, in a single study, to delay median time to death in a transgenic mouse model of ALS. These mice express human superoxide dismutase bearing one of the mutations found in one of the familial forms of human ALS. It is also neuroprotective in various in vivo experimental models of neuronal injury involving excitotoxic mechanisms. In in vitro tests, riluzole protected cultured rat motor neurons from the excitotoxic effects of glutamic acid and prevented the death of cortical neurons induced by anoxia. Due to its blockade of glutamatergic neurotransmission, riluzole also exhibits myorelaxant, sedative, and anticonvulsant properties.

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