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Total 422235 Results
| Label | Description | ILX | Version | Created CID | Modified Time | ||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| Olmesartan | Olmesartan belongs to the class of medicines called angiotensin II receptor antagonists to treat high blood pressure. It is marketed worldwide by Daiichi Sankyo, Ltd. and in the United States by Daiichi Sankyo, Inc. and Forest Laboratories. Pharmacology: Olmesartan, a specific angiotensin II type 1 antagonist, is used alone or with other antihypertensive agents to treat hypertension. Unlike the angiotensin receptor antagonist losartan, olmesartan does not have an active metabolite or possess uricosuric effects. Blockade of the angiotensin II receptor inhibits the negative regulatory feedback of angiotensin II on renin secretion, but the resulting increased plasma renin activity and circulating angiotensin II levels do not overcome the effect of olmesartan on blood pressure. Mechanism of action: Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation and renal reabsorption of sodium. Olmesartan blocks the vasoconstrictor effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in vascular smooth muscle. Its action is, therefore, independent of the pathways for angiotensin II synthesis. Olmesartan has more than a 12,500-fold greater affinity for the AT1 receptor than for the AT2 receptor. Drug type: Approved. Investigational. Small Molecule. Drug category: Angiotensin II Type 1 Receptor Blockers. Antihypertensive Agents | ILX:0108002 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Olopatadine | Used to treat allergic conjunctivitis (itching eyes), olopatadine inhibits the release of histamine from mast cells. It is a relatively selective histamine H1 antagonist that inhibits the in vivo and in vitro type 1 immediate hypersensitivity reaction including inhibition of histamine induced effects on human conjunctival epithelial cells. Pharmacology: Used to treat allergic conjunctivitis (itching eyes), olopatadine inhibits the release of histamine from mast cells. It is a relatively selective histamine H1 antagonist that inhibits the in vivo and in vitro type 1 immediate hypersensitivity reaction including inhibition of histamine induced effects on human conjunctival epithelial cells. Mechanism of action: Olopatadine is a selective histamine H1 antagonist and binds to the histamine H1 receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine. Olopatadine is devoid of effects on alpha-adrenergic, dopamine and muscarinic type 1 and 2 receptors. Drug type: Approved. Small Molecule. Drug category: Anti-Allergic Agents. Anti-Inflammatory Agents, Non-Steroidal. Antihistamines. Histamine H1 Antagonists. Histamine H1 Antagonists, Non-Sedating | ILX:0108003 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Olsalazine | Olsalazine is an anti-inflammatory drug used in the treatment of Inflammatory Bowel Disease and Ulcerative Colitis. Olsalazine is a derivative of salicylic acid. Inactive by itself (it is a prodrug), it is converted by the bacteria in the colon to mesalamine. Mesalamine works as an anti-inflammatory agent in treating inflammatory diseases of the intestines. Pharmacology: Olsalazine is an anti-inflammatory drug used in the treatment of Inflammatory Bowel Disease and Ulcerative Colitis. Olsalazine reduces the bowel inflammation, diarrhea (stool frequency), rectal bleeding, and abdominal pain. Like Balsalazide, Olsalazine is believed to deliver Mesalazine, or 5-aminosalicylic acid (5-ASA), past the small intestine, directly to the large intestine, which is that active site of disease in ulcerative colitis. Mechanism of action: Orally administered olsalazine is converted to mesalamine which is thought to be the therapeutically active agent in the treatment of ulcerative colitis. The mechanism of action of mesalamine (and sulfasalazine) is unknown, but appears to be topical rather than systemic. Mucosal production of arachidonic acid (AA) metabolites, both through the cyclooxygenase pathways, i.e., prostanoids, and through the lipoxygenase pathways, i.e., leukotrienes (LTs) and hydroxyelcosatetraenoic acids (HETEs) is increased in patients with chronic inflammatory bowel disease, and it is possible that mesalamine diminishes inflammation by blocking cyclooxygenase and inhibiting prostaglandin (PG) production in the colon. Drug type: Approved. Small Molecule. Drug category: Anti-Inflammatory Agents, Non-Steroidal. Gastrointestinal Agents | ILX:0108004 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Omalizumab | A recombinant DNA-derived humanized IgG1k monoclonal antibody that selectively binds to human immunoglobulin E (IgE). Xolair is produced by a Chinese hamster ovary cell suspension culture in a nutrient medium containing the antibiotic gentamicin. Pharmacology: Xolair inhibits the binding of IgE to the high-affinity IgE receptor (FceRI) on the surface of mast cells and basophils. Reduction in surface-bound IgE on FceRI-bearing cells limits the degree of release of mediators of the allergic response. Xolair is used to treat severe, persisten asthma. Mechanism of action: Xolair binds to IgE (a class of antibodies normally secreted in allergic responses), which prevents their binding to mast cells and basophils. Drug type: Approved. Biotech. Investigational. Drug category: Anti-Asthmatic Agents. Immunomodulatory Agents | ILX:0108005 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Omeprazole | A highly effective inhibitor of gastric acid secretion used in the therapy of stomach ulcers and zollinger-ellison syndrome. The drug inhibits the H(+)-K(+)-ATPase (H(+)-K(+)-exchanging ATPase) in the proton pump of gastric parietal cells. (PubChem) Pharmacology: Omeprazole is a compound that inhibits gastric acid secretion and is indicated in the treatment of gastroesophageal reflux disease (GERD), the healing of erosive esophagitis, and H. pylori eradication to reduce the risk of duodenal ulcer recurrence. Omeprazole belongs to a new class of antisecretory compounds, the substituted benzimidazoles, that do not exhibit anticholinergic or H2 histamine antagonistic properties, but that suppress gastric acid secretion by specific inhibition of the H+/K+ ATPase enzyme system at the secretory surface of the gastric parietal cell. Because this enzyme system is regarded as the acid (proton) pump within the gastric mucosa, omeprazole has been characterized as a gastric acid-pump inhibitor, in that it blocks the final step of acid production. This effect is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus. Mechanism of action: Omeprazole is a proton pump inhibitor that suppresses gastric acid secretion by specific inhibition of the H+/K+-ATPase in the gastric parietal cell. By acting specifically on the proton pump, omeprazole blocks the final step in acid production, thus reducing gastric acidity. Drug type: Approved. Investigational. Small Molecule. Drug category: Anti-Ulcer Agents. Enzyme Inhibitors. Proton-pump Inhibitors | ILX:0108006 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Oncology | The study of cancer, for example, genes and proteins implicated in cancer. | ILX:0108007 | 5 | FDI Lab - SciCrunch.org | 08/01/2022 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Ondansetron | A competitive serotonin type 3 receptor antagonist. It is effective in the treatment of nausea and vomiting caused by cytotoxic chemotherapy drugs, including cisplatin, and has reported anxiolytic and neuroleptic properties. (PubChem) Pharmacology: Ondansetron is an antinauseant and antiemetic agent indicated for the prevention of nausea and vomiting associated with moderately-emetogenic cancer chemotherapy and for the prevention of postoperative nausea and vomiting. Ondansetron is a highly specific and selective serotonin 5-HT3 receptor antagonist, not shown to have activity at other known serotonin receptors and with low affinity for dopamine receptors. Mechanism of action: Ondansetron is a selective serotonin 5-HT3 receptor antagonist. The serotonin 5-HT3 receptors are located on the nerve terminals of the vagus in the periphery and centrally in the chemoreceptor trigger zone of the area postrema. It is thought that chemotherapeutic agents produce nausea and vomiting by releasing serotonin from the enterochromaffin cells of the small intestine, and that the released serotonin then activates 5-HT3 receptors located on vagal efferents to initiate the vomiting reflex. Therefore Ondansetron works by blocking the reception of serotonin at these 5-HT3 receptors. Drug type: Approved. Small Molecule. Drug category: Anti-anxiety Agents. Antiemetics. Antipruritics. Antipsychotic Agents. Antipsychotics. Serotonin Antagonists | ILX:0108008 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| One dimensional region | ILX:0108009 | 2 | FDI Lab - SciCrunch.org | 01/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex | |
| Ongur, Price, and Ferry (2003) area 10l | ILX:0108010 | 6 | FDI Lab - SciCrunch.org | 06/23/2020 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex | |
| Ongur, Price, and Ferry (2003) area 10o | ILX:0108011 | 5 | FDI Lab - SciCrunch.org | 06/23/2020 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex | |
| Ongur, Price, and Ferry (2003) area 10p | ILX:0108012 | 6 | FDI Lab - SciCrunch.org | 06/23/2020 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex | |
| Ongur, Price, and Ferry (2003) area 10r | ILX:0108013 | 6 | FDI Lab - SciCrunch.org | 06/23/2020 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex | |
| Ongur, Price, and Ferry (2003) area 11l | ILX:0108014 | 5 | FDI Lab - SciCrunch.org | 06/23/2020 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex | |
| Ongur, Price, and Ferry (2003) area 11m | ILX:0108015 | 5 | FDI Lab - SciCrunch.org | 06/23/2020 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex | |
| Ongur, Price, and Ferry (2003) area 13a | ILX:0108016 | 6 | FDI Lab - SciCrunch.org | 06/23/2020 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex | |
| Ongur, Price, and Ferry (2003) area 13b | ILX:0108017 | 5 | FDI Lab - SciCrunch.org | 06/23/2020 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex | |
| Ongur, Price, and Ferry (2003) area 13l | ILX:0108018 | 5 | FDI Lab - SciCrunch.org | 06/23/2020 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex | |
| Ongur, Price, and Ferry (2003) area 13m | ILX:0108019 | 6 | FDI Lab - SciCrunch.org | 06/23/2020 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex | |
| Ongur, Price, and Ferry (2003) area 14c | ILX:0108020 | 6 | FDI Lab - SciCrunch.org | 06/23/2020 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex | |
| Ongur, Price, and Ferry (2003) area 14r | ILX:0108021 | 6 | FDI Lab - SciCrunch.org | 06/23/2020 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
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