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Restrict the search for
alpha-tocopherol
to a specific field?
Status:
Investigational
Source:
NCT02648178: Not Applicable Interventional Completed Nicotine Dependence, Other Tobacco Product
(2016)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT01638403: Phase 3 Interventional Completed Treatment of Excessive Daytime Sleepiness in Narcolepsy
(2010)
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Diclobutrazol is the active ingredient of a broad-spectrum systemic fungicide for use on cereals. Diclobutrazol sprays appear promising for the control of coffee rust, apple mildew and scab, grape powdery mildew and various other crop diseases. Diclobutrazol has a systemic action and is translocated mainly acropetally. It eradicative action, increased by vapour effect, is very strong. Diclobutrazol is of low toxicity to mammals and other animals. It is also of low toxicity to birds, fish and invertebrates. Diclobutrazol inhibited spore germination and mycelia growth of a wide range of fungi. Stereoselective inhibition of human CYP3A4 and Candida albicans CYP51 was observed with enantiomers of the azole antifungal compound diclobutrazol. The RR(+) configuration at its asymmetric carbon center was most active.
Status:
Investigational
Source:
NCT01460420: Phase 1/Phase 2 Interventional Completed Hematologic Malignancies
(2011)
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
(±)-quinuclidinyl benzilate (3-quinuclidinyl benzilate), is a specific muscarinic cholinergic receptor antagonist. It binds potently but reversibly to the muscarinic cholinergic receptors of mammalian brain and peripheral tissues. 3-quinuclidinyl benzilate was invented by Hoffmann-La Roche Inc in 1951, while investigating antispasmodic agents resembling tropine for the treatment of gastrointestinal conditions. In the 1960s 3-quinuclidinyl benzilate, was developed and weaponized as a new chemical agent for battlefield use as a psychochemical. Assigned the NATO code BZ it is classified as a hallucinogenic chemical warfare agent that affects both the peripheral and central nervous systems (CNS). It is one of the most potent anticholinergic psychomimetics known, with only small doses necessary to produce incapacitation. The primary route of absorption is through the respiratory system but absorption also can occur through the skin or gastrointestinal tract. BZ is odorless and is usually disseminated as an aerosol. Data regarding the health effects of BZ in humans following inhalation exposure are limited to military application studies. Pharmacologic activity of 3-quinuclidinyl benzilate is similar to other anticholinergic drugs (eg, atropine) but with a much longer duration of action. It was shown that I[3H]-3-quinuclidinyl benzilate accumulated in various brain regions after intravenous injection. The specific binding of [3-3H]3-quinuclidinyl-benzilate and [125I]3-quinuclidinyl-(3-iodo-4-hydroxy-benzilate) to rat brain subcellular fractions is parallel in myelin, synaptic plasma membrane and mitochondrial fractions with a 3-4-fold enrichment observed in synaptic plasma membrane over crude mitochondrial fractions. These findings suggested the use of 3-quinuclidinyl benzilate as a binding probe useful in assaying low levels of muscarinic receptor in tissue culture and other biological sources including labeling the receptor in vivo for autoradiographic studies. M2 muscarinic acetylcholine receptor (M2 receptor), essential for the physiologic control of cardiovascular function through activation of G protein-coupled inwardly-rectifying potassium channels, was shown to bind 3-quinuclidinyl benzilate with high affinity in vitro.
Status:
Investigational
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT03881059: Phase 2 Interventional Completed Active Psoriatic Arthritis
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
BMS-191011, an opener of the cloned large-conductance, Ca2+-activated potassium (maxi-K) channel, demonstrated efficacy in in vivo stroke models, which led to its nomination as a candidate for clinical evaluation. Its maxi-K channel opening properties were consistent with its structural topology, being derived by combining elements from other known maxi-K openers. BMS-191011 demonstrated efficacy as an opener of the cloned large-conductance Ca2+-activated potassium (maxi-K) channel in in vivo stroke models
Status:
Investigational
Source:
NCT04434937: Phase 2 Interventional Completed Lymphoma
(2020)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02808390: Phase 2 Interventional Terminated Ulcerative Colitis
(2016)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT01440517: Phase 2 Interventional Terminated Diabetes Mellitus
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Maraciclatide Tc-99m is radiolabelled with technetium 99m cyclic peptide maraciclatide (NC100692 or diamine dioxime-Lys-Cys-Arg-Gly-Asp-Cyc-Phe-Cys-polyethylene glycol). Maraciclatide Tc-99m binds vitronectin receptors (αvβ3 and αvβ5 integrins) with high affinity. Maraciclatide Tc-99m is used in single-photon emission computed tomography (SPECT) imaging of vitronectin receptors that are upregulated and expressed preferentially on proliferating endothelial cells. Maraciclatide Tc-99m is being developed as a diagnostic agent to determine neoplasia and cardiovascular diseases.
Status:
Investigational
Source:
NCT02929862: Phase 1/Phase 2 Interventional Completed Cancer
(2016)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT04120116: Phase 2 Interventional Completed Sensorineural Hearing Loss
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
CHIR 99021 is a selective, pyridimidine-based, glycogen synthase kinase 3 inhibitor that is effective at low nanomolar concentrations in enzyme assays and submicromolar concentrations in isolated cells and tissues. Chiron was developing CHIR 99021 for potential use in the treatment of type 2 diabetes mellitus. CHIR 99021 promoted insulin-mediated glucose uptake and increased glucose disposal in rodent models of diabetes. However, there has been no recent development reported.
