{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
Restrict the search for
icosapent ethyl
to a specific field?
Status:
Investigational
Source:
NCT00243230: Phase 2 Interventional Completed HIV Infections
(2005)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Vicriviroc or SCH 417690 is a potent and selective antagonist of the CCR5 receptor. vicriviroc binds specifically to the CCR5 receptor and prevents infection of target cells by CCR5-tropic HIV-1 isolates. In antiviral assays, vicriviroc showed potent, broad-spectrum activity against genetically diverse and drug-resistant HIV-1 isolates and was consistently more active than SCH-C in inhibiting viral replication. This compound demonstrated synergistic anti-HIV activity in combination with drugs from all other classes of approved antiretrovirals. Competition binding assays revealed that vicriviroc binds with higher affinity to CCR5 than SCH-C. Functional assays, including inhibition of calcium flux, guanosine 5'-[35S]triphosphate exchange, and chemotaxis, confirmed that vicriviroc acts as a receptor antagonist by inhibiting signaling of CCR5 by chemokines. Finally, vicriviroc demonstrated diminished affinity for the human ether a-go-go related gene transcript ion channel compared to SCH-C, suggesting a reduced potential for cardiac effects. Vicriviroc represented a promising new candidate for the treatment of HIV-1 infection. Vicriviroc for HIV treatment was previously in Phase III studies but has since been discontinued.
Class (Stereo):
CHEMICAL (ACHIRAL)
LAPRAFYLLINE is a xanthine derivative with bronchodilating effect. It might exert its action by inhibiting cAMP phosphodiesterase.
Class (Stereo):
CHEMICAL (ACHIRAL)
Clormecaine is a local anesthetic drug.
Class (Stereo):
CHEMICAL (MIXED)
Iodetryl is fatty acid derivative patented by Russian company OOO "Nauchno-Proizvodstvennaya Firma "I. M. A." as a colloidal contrast agent.
Status:
Investigational
Source:
NCT00069875: Phase 2 Interventional Completed Carcinoma, Non-Small-Cell Lung
(2003)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Etalocib (LY-293111 or VML 295) is a potent and orally active leukotriene B4 receptor antagonist of the biphenylphenol class. It efficiently blocks neutrophil activation and subsequent inflammation. Additionally, it exerts antineoplastic properties through induction of cell cycle arrest and apoptosis in tumor cells. Etalocib was being developed for the treatment of inflammatory diseases and solid tumors.
Status:
Investigational
Source:
INN:cyprodenate [INN]
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Cyprodenate is a stimulant drug, developed by the French company Les Laboratoires Albert Rolland. Cyprodenate was used in the clinical practice to correct the tranquilizing action of benzodiazepine drugs. Upon administration, cyprodenate is hydrolyzed to produce dimethylethanolamine (deanol), which is a precursor of choline, and may enhance central acetylcholine formation.
Status:
Investigational
Source:
NCT01037556: Phase 1/Phase 2 Interventional Unknown status Acute Myelogenous Leukemia
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
PR-104 is a phosphate ester dinitrobenzamide mustard pre-prodrug that is rapidly hydrolyzed systemically to PR-104A, a bioreductive prodrug. PR-104A is in turn activated via reduction by NADPH:cytochrome P450 oxidoreductase and other one-electron reductases in hypoxic cells, and by aldo-keto reductase 1C3 (AKR1C3) independently of oxygen, to the corresponding hydroxylamine (PR-104H) and amine (PR-104M) metabolites. Subsequently, these reactive nitrogen mustards crosslink DNA and cause cytotoxicity in cells. PR-104 is known to have preclinical anti-tumor activity in human tumor xenograft models as mono-therapy and in combination with radiotherapy and chemotherapy. Thrombocytopenia, and to a lesser extent neutropenia, was the dose-limiting toxicity of weekly PR-104. Combination of PR-104 with docetaxel or gemcitabine caused dose-limiting and severe myelotoxicity in patients with advanced solid tumors. PR-104 had been in phase II clinical trial for the treatment of acute myeloid leukemia.
Status:
Class (Stereo):
CHEMICAL (ACHIRAL)
Pretamazium is thiazolium derivative patented by UK pharmaceutical company Wellcome Foundation Ltd. as antiphrastic compound, that active against parasitic nematodes.
Status:
Investigational
Source:
NCT04020224: Not Applicable Interventional Withdrawn Safety Issues
(2024)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Amustaline (S-303) is a quinacrine mustard compound with potential antineoplastic activity. Amustaline binds to, intercalates and crosslinks DNA and RNA. This agent is mainly used for ex vivo purposes, specifically for the inactivation of pathogens such as viruses, protozoa and bacteria in red blood cells (RBCs). When S-303 is added to red blood cells, the compound rapidly passes through membranes, including those of cells and viral envelopes, due to its amphipathic character, and intercalates into helical regions of the nucleic acids of pathogens and white blood cells. TERCEPTTMBlood System usingamustaline (S-303) and glutathione (GSH) was able to inactivate high levels of DENV and ZIKV in RBCs. S-303 system has been shown to effectively inactivate a broad spectrum of pathogens, while maintaining RBC quality.
Class (Stereo):
CHEMICAL (RACEMIC)
Dopropidil is an antianginal calcium ion modulating agent, possessing intracellular calcium antagonist activity and anti-ischemic effects in several predictive animal models. Dopropidil had similar vasorelaxant potency as bepridil in the rabbit aorta depolarized by K(+), but was less potent than verapamil, nifedipine, and diltiazem in this respect. Dopropidil has an unusual pharmacological profile, which includes both antiarrhythmic and anti-atherosclerotic properties. In vitro studies show that dopropidil inhibits both smooth and cardiac muscle contractions induced by activation of voltage operated channels, and inhibits the “slow” inward calcium current in the latter tissue, suggesting that dopropidil blocks membrane calcium ion channels. Dopropidil-induced inhibition of collagen and thrombin-induced platelet aggregation at higher concentrations also suggests actions other than calcium channel blockade since platelets lack voltage operated channels. Dopropidil also reduces fatty streak formation in the aorta of cholesterol fed rabbits, an action which may be related to the demonstrated antioxidant properties of this compound. Long-term toxicity studies in rats and dogs showed only mild toxic signs, notably a decrease in food consumption, slight sedation, and some vomiting in the latter species. Dopropidil had been in phase II clinical trials for the treatment of angina pectoris and arrhythmias. However, these studies were discontinued.