Drug results: 29

aminopicoline
hexyldecanoic acid viscous oil
salicylanilide
heptaminol An amino alcohol that has been used as a myocardial stimulant and vasodilator and to relieve bronchospasm. Its most common therapeutic use is in orthostatic hypotension. The mechanism of heptaminol's therapeutic actions is not well understood although it has been suggested to affect catecholamine release or calcium metabolism.
methylhexaneamine sympathomimetic aliphatic amine with vasoconstrictor activity
enbucrilate A tissue adhesive that is applied as a monomer to moist tissue and polymerizes to form a bond. It is slowly biodegradable and used in all kinds of surgery, including dental.
exalamide
cycloserine Antibiotic substance produced by Streptomyces garyphalus.
kinetin A furanyl adenine found in PLANTS and FUNGI. It has plant growth regulation effects.
phenpromethamine
pyrithione split from cephalosporin molecule; some metal complexes of this have fumarate reductase inhibitory activity and may be useful against trypanosomes; RN given refers to parent cpd; structure
etilamfetamine
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)
hemin Chloro(7,12-diethenyl-3,8,13,17-tetramethyl-21H,23H-porphine-2,18-dipropanoato(4-)-N(21),N(22),N(23),N(24)) ferrate(2-) dihydrogen.
bunaftine N-Butyl-N-(2-(diethylamino)ethyl)-1-naphthamide. A proposed antiarrhythmic that prolongs myocardial refractory period and stabilizes cell membranes.
peginterferon beta-1a an interferon beta-1a to which a single, linear 20,000 dalton methoxy poly(ethyleneglycol)-O-2-methylpropionaldehyde molecule is covalently attached to the alpha amino group of the N-terminal amino acid residue. A possible role for IFNs in prophylaxis or early treatment of COVID-19 has been suggested to compensate for possibly insufficient endogenous IFN production. However, the efficacy and safety of IFNs for treatment or prevention of COVID-19 were not established.
thyrotropin alfa A highly purified recombinant glycoprotein form of human THYROID-STIMULATING HORMONE, produced by recombinant DNA technology comprising two non-covalently linked subunits, an alpha subunit of 92 amino acid residues containing two N-linked glycosylation sites, and a beta subunit of 118 residues containing one N-linked glycosylation site. The amino acid sequence of thyrotropin alfa is identical to that of human pituitary thyroid stimulating hormone.
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.
somatostatin A 14-amino acid peptide named for its ability to inhibit pituitary GROWTH HORMONE release, also called somatotropin release-inhibiting factor. It is expressed in the central and peripheral nervous systems, the gut, and other organs. SRIF can also inhibit the release of THYROID-STIMULATING HORMONE; PROLACTIN; INSULIN; and GLUCAGON besides acting as a neurotransmitter and neuromodulator. In a number of species including humans, there is an additional form of somatostatin, SRIF-28 with a 14-amino acid extension at the N-terminal.
tetracosactide A synthetic peptide that is identical to the 24-amino acid segment at the N-terminal of ADRENOCORTICOTROPIC HORMONE. ACTH (1-24), a segment similar in all species, contains the biological activity that stimulates production of CORTICOSTEROIDS in the ADRENAL CORTEX.
thiamine 3-((4-Amino-2-methyl-5-pyrimidinyl)methyl)-5-(2- hydroxyethyl)-4-methylthiazolium chloride.
teriparatide A polypeptide that consists of the 1-34 amino-acid fragment of human PARATHYROID HORMONE, the biologically active N-terminal region. The acetate form is given by intravenous infusion in the differential diagnosis of HYPOPARATHYROIDISM and PSEUDOHYPOPARATHYROIDISM. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1995)
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.
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.
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.
baloxavir marboxil Baloxavir marboxil is a prodrug that is converted by hydrolysis to baloxavir, the active form that exerts anti-influenza virus activity. Baloxavir inhibits the endonuclease activity of the polymerase acidic (PA) protein, an influenza virus-specific enzyme in the viral RNA polymerase complex required for viral gene transcription, resulting in inhibition of influenza virus replication. The 50% inhibitory concentration (IC50) of baloxavir was 1.4 to 3.1 nM (n=4) for influenza A viruses and 4.5 to 8.9 nM (n=3) for influenza B viruses in a PA endonuclease assay. Viruses with reduced susceptibility to baloxavir have amino acid substitutions in the PA protein. It was investigated as a potential treatment during the early stages of the COVID-19 pandemic but in vitro antiviral activity against SARS-CoV-2 was not confirmed.
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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