Drug results: 49

allopurinol A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.
caffeine A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes SMOOTH MUSCLE, stimulates CARDIAC MUSCLE, stimulates DIURESIS, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide PHOSPHODIESTERASES, antagonism of ADENOSINE RECEPTORS, and modulation of intracellular calcium handling.
paraldehyde A hypnotic and sedative with anticonvulsant effects. However, because of the hazards associated with its administration, its tendency to react with plastic, and the risks associated with its deterioration, it has largely been superseded by other agents. It is still occasionally used to control status epilepticus resistant to conventional treatment. (From Martindale, The Extra Pharmacopoeia, 30th ed, p608-9)
glycerol A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, or sweetening agent.
ethinylestradiol sulfonate
pheniprazine
glucurolactone
methylhexaneamine sympathomimetic aliphatic amine with vasoconstrictor activity
phloroglucinol A trinitrobenzene derivative with antispasmodic properties that is used primarily as a laboratory reagent.
theophylline A plant genus of the family ASTERACEAE. The name "prickly burweed" is sometimes used but causes confusion with AMSINCKIA.
carfimate
propiolactone Disinfectant used in vapor form to sterilize vaccines, grafts, etc. The vapor is very irritating and the liquid form is carcinogenic.
oxiniacic acid
benzalamide
amfetamine A powerful central nervous system stimulant and sympathomimetic. Amphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulation of release of monamines, and inhibiting monoamine oxidase. Amphetamine is also a drug of abuse and a psychotomimetic. The l- and the d,l-forms are included here. The l-form has less central nervous system activity but stronger cardiovascular effects. The d-form is DEXTROAMPHETAMINE.
trientine An ethylenediamine derivative used as stabilizer for EPOXY RESINS, as ampholyte for ISOELECTRIC FOCUSING and as chelating agent for copper in HEPATOLENTICULAR DEGENERATION.
phenmetrazine A sympathomimetic drug used primarily as an appetite depressant. Its actions and mechanisms are similar to DEXTROAMPHETAMINE.
verteporfin A benzoporphyrin derivative that is used in PHOTOCHEMOTHERAPY to treat wet type MACULAR DEGENERATION.
phenelzine One of the MONOAMINE OXIDASE INHIBITORS used to treat DEPRESSION; PHOBIC DISORDERS; and PANIC.
octodrine 1,3-dimethylamylamine (1,3-DMAA) analog
euflavine 3,6-Diamino-10-methylacridinium chloride mixt. with 3,6-acridinediamine. Fluorescent dye used as a local antiseptic and also as a biological stain. It intercalates into nucleic acids thereby inhibiting bacterial and viral replication.
rezafungin Rezafungin is a semi-synthetic echinocandin. Rezafungin inhibits the 1,3-beta-D glucan synthase enzyme complex, which is present in fungal cell walls but not in mammalian cells. This results in inhibition of the formation of 1,3-beta-D-glucan, an essential component of the fungal cell wall of many fungi, including Candida species (spp.). Inhibition of 1,3-beta-D-glucan synthesis results in concentration-dependent in vitro fungicidal activity against Candida spp., however, the clinical significance of this activity is unknown.
isosorbide 1,4:3,6-Dianhydro D-glucitol. Chemically inert osmotic diuretic used mainly to treat hydrocephalus; also used in glaucoma.
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
mesterolone 17 beta-Hydroxy-1 alpha-methyl-5 alpha-androstan-3-one. A synthetic steroid with anabolic and androgenic activities.
caspofungin Caspofungin, an echinocandin, inhibits the synthesis of beta (1,3)-D-glucan, an essential component of the cell wall of susceptible Aspergillus species and Candida species. Beta (1,3)-D-glucan is not present in mammalian cells. Caspofungin has shown activity against Candida species and in regions of active cell growth of the hyphae of Aspergillus fumigatus.
doxepin A dibenzoxepin tricyclic compound. It displays a range of pharmacological actions including maintaining adrenergic innervation. Its mechanism of action is not fully understood, but it appears to block reuptake of monoaminergic neurotransmitters into presynaptic terminals. It also possesses anticholinergic activity and modulates antagonism of histamine H(1)- and H(2)-receptors.
teplizumab Teplizumab-mzwv binds to CD3 (a cell surface antigen present on T lymphocytes) and delays the onset of Stage 3 type 1 diabetes in adults and pediatric patients aged 8 years and older with Stage 2 type 1 diabetes. The mechanism may involve partial agonistic signaling and deactivation of pancreatic beta cell autoreactive T lymphocytes. Teplizumab-mzwv leads to an increase in the proportion of regulatory T cells and of exhausted CD8+ T cells in peripheral blood.
ibrexafungerp Ibrexafungerp, a triterpenoid antifungal agent, inhibits glucan synthase, an enzyme involved in the formation of 1,3-beta-D-glucan, an essential component of the fungal cell wall. Ibrexafungerp has concentration-dependent fungicidal activity against Candida species as measured by time kill studies. Ibrexafungerp retains in vitro antifungal activity when tested at pH 4.5 (the normal vaginal pH).
infliximab Infliximab products neutralize the biological activity of TNF-alpha by binding with high affinity to the soluble and transmembrane forms of TNF-alpha and inhibit binding of TNF-alpha with its receptors. Infliximab products do not neutralize TNF-beta (lymphotoxin-alpha), a related cytokine that utilizes the same receptors as TNF-alpha. Biological activities attributed to TNF-alpha include: induction of pro-inflammatory cytokines such as interleukins (IL) 1 and 6, enhancement of leukocyte migration by increasing endothelial layer permeability and expression of adhesion molecules by endothelial cells and leukocytes, activation of neutrophil and eosinophil functional activity, induction of acute phase reactants and other liver proteins, as well as tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Cells expressing transmembrane TNF-alpha bound by infliximab products can be lysed in vitro or in vivo. Infliximab products inhibit the functional activity of TNF-alpha in a wide variety of in vitro bioassays utilizing human fibroblasts, endothelial cells, neutrophils, B and T-lymphocytes and epithelial cells. The relationship of these biological response markers to the mechanism(s) by which infliximab products exert their clinical effects is unknown. Anti-TNF-alpha antibodies reduce disease activity in the cotton-top tamarin colitis model, and decrease synovitis and joint erosions in a murine model of collagen-induced arthritis. Infliximab products prevent disease in transgenic mice that develop polyarthritis as a result of constitutive expression of human TNF-alpha, and when administered after disease onset, allow eroded joints to heal.
tucidinostat An orally bioavailable benzamide-type inhibitor of histone deacetylase (HDAC) isoenzymes 1, 2, 3 and 10, with potential antineoplastic activity. Chidamide binds to and inhibits HDACs, leading to an increase of acetylation levels of histone proteins. This agent also inhibits the expression of kinases in the PI3K/Akt and MAPK/Ras signaling pathways and may result in cell cycle arrest and the induction of tumor cell apoptosis. This may inhibit tumor cell proliferation in susceptible tumor cells. HDACs, a class of enzymes that deacetylate chromatin histone proteins, are upregulated in many tumor types and play key roles in gene expression. Compared to some other benzamide-type HDAC inhibitors, chidamide is more stable, more resistant to degradation and has a longer half-life.
futibatinib Futibatinib is a small molecule kinase inhibitor of FGFR 1, 2, 3, and 4 with IC50 values of less than 4 nM. Futibatinib covalently binds FGFR. Constitutive FGFR signaling can support the proliferation and survival of malignant cells. Futibatinib inhibited FGFR phosphorylation and downstream signaling and decreased cell viability in cancer cell lines with FGFR alterations including FGFR fusions/rearrangements, amplifications, and mutations. Futibatinib demonstrated anti-tumor activity in mouse and rat xenograft models of human tumors with activating FGFR genetic alterations.
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
aducanumab Aducanumab-avwa is a human, immunoglobulin gamma 1 (IgG1) monoclonal antibody directed against aggregated soluble and insoluble forms of amyloid beta. The accumulation of amyloid beta plaques in the brain is a defining pathophysiological feature of Alzheimer’s disease. ADUHELM reduces amyloid beta plaques, as evaluated in Studies 1, 2, and 3.
selpercatinib Selpercatinib is a kinase inhibitor. Selpercatinib inhibited wild-type RET and multiple mutated RET isoforms as well as VEGFR1 and VEGFR3 with IC50 values ranging from 0.92 nM to 67.8 nM. In other enzyme assays, selpercatinib also inhibited FGFR 1, 2, and 3 at higher concentrations that were still clinically achievable. In cellular assays, selpercatinib inhibited RET at approximately 60-fold lower concentrations than FGFR1 and 2 and approximately 8-fold lower concentration than VEGFR3
tasurgratinib Tasurgratinib succinate is an orally active, small molecule inhibitor of fibroblast growth factor receptors (FGFRs) 1, 2, and 3 being developed for the treatment of solid tumors, including cholangiocarcinoma (i.e., bile duct cancer) and breast cancer.
tegomil fumarate Riulvy, active substance tegomil fumarate, is a medicine used to treat multiple sclerosis, a disease in which the immune system (the body’s natural defences) attacks the protective insulation around nerves (myelin) in the brain and spinal cord, causing inflammation and damage to the nerves themselves. The mechanism by which tegomil fumarate exerts therapeutic effects in multiple sclerosis is not fully understood. Tegomil fumarate acts via the major active metabolite, monomethyl fumarate. Preclinical studies indicate that monomethyl fumarate pharmacodynamic responses appear to be primarily mediated through activation of the Nuclear factor (erythroid derived 2)-like 2 (Nrf2) transcriptional pathway. Dimethyl fumarate has been shown to up regulate Nrf2-dependent antioxidant genes in patients (e.g. NAD(P)H dehydrogenase, quinone 1; [NQO1]).
elinzanetant Elinzanetant is a non-hormonal, selective neurokinin 1 (NK-1) and 3 (NK-3) receptors antagonist. It blocks NK-1 and NK-3 receptors signalling on kisspeptin/neurokinin B/dynorphin (KNDy) neurons, which is postulated to normalise neuronal activity involved in thermo- and sleep regulation.
setmelanotide Setmelanotide is an 8 amino acid cyclic peptide analog of endogenous melanocortin peptide alpha-MSH (alpha-melanocyte stimulating hormone). It is a melanocortin 4 (MC4) receptor agonist, with 20-fold less activity at the melanocortin 3 (MC3) and melanocortin 1 (MC1) receptors.
chloroprocaine Chloroprocaine, like other local anesthetics, blocks the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse, and by reducing the rate of rise of the action potential. In general, the progression of anesthesia is related to the diameter, myelination, and conduction velocity of affected nerve fibers. Clinically, the order of loss of nerve function is as follows: (1) pain, (2) temperature, (3) touch, (4) proprioception, and (5) skeletal muscle tone.
relatlimab Relatlimab is a human IgG4 monoclonal antibody that binds to the LAG-3 receptor, blocks interaction with its ligands, including MHC II, and reduces LAG-3 pathway-mediated inhibition of the immune response. Antagonism of this pathway promotes T cell proliferation and cytokine secretion. Binding of the PD-1 ligands, PD-L1 and PD-L2, to the PD-1 receptor found on T cells, inhibits T-cell proliferation and cytokine production. Upregulation of PD-1 ligands occurs in some tumors, and signaling through this pathway can contribute to inhibition of active T-cell immune surveillance of tumors. Nivolumab is a human IgG4 monoclonal antibody that binds to the PD-1 receptor, blocks interaction with its ligands PD-L1 and PD-L2, and reduces PD-1 pathwaymediated inhibition of the immune response, including the anti-tumor immune response. In syngeneic mouse tumor models, blocking PD-1 activity resulted in decreased tumor growth. The combination of nivolumab (anti-PD-1) and relatlimab (anti-LAG-3) results in increased T-cell activation compared to the activity of either antibody alone. In murine syngeneic tumor models, LAG-3 blockade potentiates the anti-tumor activity of PD-1 blockage, inhibiting tumor growth and promoting tumor regression.
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.
azathioprine Azathioprine is an inactive pro-drug of 6-mercaptopurine (6-MP), which acts as a purine antagonist but requires cellular uptake and intracellular anabolism to thioguanine nucleotides (TGNs) for immunosuppression. TGNs and other metabolites (e.g. 6-methylmercaptopurine ribonucleotides) inhibit de novo purine synthesis and purine nucleotide interconversions. The TGNs are also incorporated into nucleic acids and this contributes to the immunosuppressive effects of the medicinal product. Other potential mechanisms of azathioprine include the inhibition of many pathways in nucleic acid biosynthesis, hence preventing proliferation and activity of cells involved in the immune response (B and T lymphocytes). Because of these mechanisms, the therapeutic effect of azathioprine may be evident only after several weeks or months of treatment. Unlike 6-MP, the activity of the azathioprine metabolite 1-methyl-4-nitro-5-thioimidazole has not been clearly determined. However, compared with 6-MP it appears to modify the activity of azathioprine in several systems. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance has been listed as a known carcinogen. (Merck Index, 11th ed)
nafarelin A potent synthetic agonist of GONADOTROPIN-RELEASING HORMONE with 3-(2-naphthyl)-D-alanine substitution at residue 6. Nafarelin has been used in the treatments of central PRECOCIOUS PUBERTY and ENDOMETRIOSIS.
adenosine phosphate Adenine nucleotide containing one phosphate group esterified to the sugar moiety in the 2'-, 3'-, or 5'-position.
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.
entecavir Entecavir, a guanosine nucleoside analogue with activity against HBV reverse transcriptase, is efficiently phosphorylated to the active triphosphate form, which has an intracellular half-life of 15 hours. By competing with the natural substrate deoxyguanosine triphosphate, entecavir triphosphate functionally inhibits all three activities of the HBV reverse transcriptase: (1) base priming, (2) reverse transcription of the negative strand from the pregenomic messenger RNA, and (3) synthesis of the positive strand of HBV DNA. Entecavir triphosphate is a weak inhibitor of cellular DNA polymerases alpha, beta, and delta and mitochondrial DNA polymerase gamma with Ki values ranging from 18 to > 160 microM.
phytomenadione A lipid cofactor that is required for normal blood clotting. Several forms of vitamin K have been identified: VITAMIN K 1 (phytomenadione) derived from plants, VITAMIN K 2 (menaquinone) from bacteria, and synthetic naphthoquinone provitamins, VITAMIN K 3 (menadione). Vitamin K 3 provitamins, after being alkylated in vivo, exhibit the antifibrinolytic activity of vitamin K. Green leafy vegetables, liver, cheese, butter, and egg yolk are good sources of vitamin K.
pexidartinib Pexidartinib is a small molecule tyrosine kinase inhibitor that targets colony stimulating factor 1 receptor (CSF1R), KIT proto-oncogene receptor tyrosine kinase (KIT), and FMS-like tyrosine kinase 3 (FLT3) harboring an internal tandem duplication (ITD) mutation. Overexpression of the CSF1R ligand promotes cell proliferation and accumulation in the synovium. In vitro, pexidartinib inhibited proliferation of cell lines dependent on CSF1R and ligand-induced autophosphorylation of CSF1R. Pexidartinib also inhibited the proliferation of a CSF1R dependent cell line in vivo.

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