U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

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Sodium artesunate, an artemisinin derivative, is used in malaria treatment. Artesunate, has been licensed in Thailand for the treatment of falciparum malaria since 1990. It is a potent antimalarial drug that can reduce parasitaemia by 90% within 24 h of administration. Sodium artesunate was first isolated in China, it is a water soluble antimalaria used clinically in China.
Streptozotocin (Streptozocin, STZ, Zanosar) is a naturally occurring chemical that is particularly toxic to the insulin-producing beta cells of the pancreas in mammals. It is used in medicine for treating certain cancers of the Islets of Langerhans and used in medical research to produce an animal model for hyperglycemia in a large dose as well as Type 1 diabetes with multiple low doses. Streptozocin inhibits DNA synthesis in bacterial and mammalian cells. In bacterial cells, a specific interaction with cytosine moieties leads to degradation of DNA. The biochemical mechanism leading to mammalian cell death has not been definitely established; streptozocin inhibits cell proliferation at a considerably lower level than that needed to inhibit precursor incorporation into DNA or to inhibit several of the enzymes involved in DNA synthesis. Although streptozocin inhibits the progression of cells into mitosis, no specific phase of the cell cycle is particularly sensitive to its lethal effects. Streptozocin is active in the L1210 leukemic mouse over a fairly wide range of parenteral dosage schedules. In experiments in many animal species, streptozocin induced a diabetes that resembles human hyperglycemic nonketotic diabetes mellitus. This phenomenon, which has been extensively studied, appears to be mediated through a lowering of beta cell nicotinamide adenine dinucleotide (NAD) and consequent histopathologic alteration of pancreatic islet beta cells. The metabolism and the chemical dissociation of streptozocin that occurs under physiologic conditions has not been extensively studied. When administered intravenously to a variety of experimental animals, streptozocin disappears from the blood very rapidly. In all species tested, it was found to concentrate in the liver and kidney. As much as 20% of the drug (or metabolites containing an N-nitrosourea group) is metabolized and/or excreted by the kidney. Metabolic products have not yet been identified.
Status:
Investigational
Source:
NCT03557138: Not Applicable Interventional Unknown status Type2 Diabetes Mellitus
(2017)
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)

Status:
Investigational
Source:
NCT02557321: Phase 1/Phase 2 Interventional Active, not recruiting Melanoma
(2015)
Source URL:

Class (Stereo):
CHEMICAL (RACEMIC)

Status:
Investigational
Source:
INN:trenbolone
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)

Status:
Investigational
Source:
NCT03089606: Phase 2 Interventional Completed Melanoma
(2017)
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)

Status:
Investigational
Source:
NCT00302731: Phase 2 Interventional Terminated Menopause
(2006)
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)

Status:
Investigational
Source:
NCT02653729: Phase 2 Interventional Completed Psychosis
(2015)
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Status:
Investigational
Source:
NCT00519376: Phase 2 Interventional Completed Pulmonary Disease, Chronic Obstructive
(2007)
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)

VILANTEROL α-PHENYL CINNAMATE (GW642444H), originally developed by GlaxoSmithKline, is a long-acting β2 adrenoceptor agonist for once daily treatment of COPD and asthma. Phase III clinical trials are ongoing. GW642444H is Vilanterol a-phenylcinnimate salt. In clinical studies the study drug may been given as a dry powder in the form of either the ‘H’ salt (with the excipient lactose), or in the form of the ‘M’ salt (with the excipients lactose and cellobiose octaacetate). Its pharmacological effect is attributable to stimulation of intracellular adenylyl cyclase which catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3',5'-adenosine monophosphate (cAMP). Increases in cyclic AMP are associated with relaxation of bronchial smooth muscle and inhibition of release of hypersensitivity mediators from mast cells in the lungs.
Status:
Investigational
Source:
NCT01588756: Phase 1/Phase 2 Interventional Completed Healthy
(2010)
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)