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Search results for m root_codes_WIKIPEDIA in WIKIPEDIA (approximate match)
Status:
Investigational
Class (Stereo):
CHEMICAL (ABSOLUTE)
Ajulemic acid, designated as Resunab™, is being developed by Corbus Pharmaceuticals, for the treatment of cystic fibrosis, systemic sclerosis, systemic lupus erythematosus.Ajulemic acid (AJA) is a first-in-class, synthetic, orally active, cannabinoid-derived drug that preferentially binds to the CB2 receptor and is nonpsychoactive. In preclinical studies, and in Phase 1 and 2 clinical trials, AJA showed a favorable safety, tolerability, and pharmacokinetic profile. It also demonstrated significant efficacy in preclinical models of inflammation and fibrosis. It suppresses tissue scarring and stimulates endogenous eicosanoids that resolve chronic inflammation and fibrosis without causing immunosuppression. AJA is currently being developed for use in 4 separate but related indications including systemic sclerosis (SSc), cystic fibrosis, dermatomyositis (DM), and systemic lupus erythematosus. Phase 2 clinical trials in the first 3 targets demonstrated that it is safe, is a potential treatment for these orphan diseases and appears to be a potent inflammation-resolving drug with a unique mechanism of action, distinct from the nonsteroidal anti-inflammatory drug (NSAID), and will be useful for treating a wide range of chronic inflammatory diseases.
Status:
Investigational
Source:
NCT02097706: Phase 2 Interventional Recruiting Borderline Personality Disorder
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
N-Methyl-D-aspartic acid is an amino acid derivative acting as a specific agonist at the NMDA receptor, and therefore mimics the action of the neurotransmitter glutamate on that receptor. Unlike glutamate, NMDA only binds to and regulates the NMDA receptor and has no effect on other glutamate receptors (such as those for AMPA and kainate). NMDA receptors are particularly important when they become overactive during withdrawal from alcohol as this causes symptoms such as agitation and, sometimes, epileptiform seizures. NMDA is a water-soluble synthetic substance that is not normally found in biological tissue.
Status:
Investigational
Source:
NCT04530643: Phase 2 Interventional Completed Atopic Dermatitis
(2020)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Sodium taurodeoxycholate is a bile salt-related, anionic detergent used for isolation of membrane proteins including inner mitochondrial membrane proteins. It is formed by the conjugation of ursodeoxycholic acid (UDCA) with taurine. Sodium taurodeoxycholate and ursodeoxycholic acid are major constituents of black bear bile, which has been used in traditional Chinese medicine for thousands of years. Bear bile was historically employed to treat a number of diseases including jaundice, summer diarrhea, abdominal pain due to hepatobiliary diseases and gastric malfunction, biliary ascariasis, infectious skin diseases, the common cold, intestinal worms, and inflammation of the throat. Sodium taurodeoxycholate has been shown to inhibit apoptosis by modulating mitochondrial membrane perturbation and pore formation, B cell lymphoma 2 (Bcl-2)-associated protein X (BAX) translocation, cytochrome c release, and caspase activation. Sodium taurodeoxycholate inhibits amyloid beta (Ab)-induced apoptosis and attenuates the endoplasmic reticulum (ER) stress, which are thought to be key components of the pathological process in certain diseases. In clinical studies, Sodium taurodeoxycholate is shown to be very safe with oral administration of 1500 mg/day for up to 6 months. In a more recent clinical study, a dose of 1750 mg/day for up to 4 weeks was well tolerated in healthy obese persons. One of the major adverse effects of Sodium taurodeoxycholate is diarrhea. Based on the related information from ursodeoxycholic acid, other gastrointestinal side effects are possible including abdominal pain, flatulence, nausea, dyspepsia, and anorexia.
Status:
Investigational
Source:
NCT03678116: Not Applicable Interventional Completed Energy Metabolism
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT00555074: Phase 2 Interventional Completed Obesity
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Tungstic acid is a fairly strong acid, it catalyzes the oxidation by hydrogen peroxide of alkenes to the corresponding epoxides. Tungstic acid is widely used in the production of tungsten metal, alloys, and is used as a mordant for textiles and plastics. Tungstic acid has been reported to
rapidly precipitate the quaternary ammonium cations in cholinergic nerve terminals, such as ACh or choline. Also, tungsten dietary supplementation has successfully
been used to reduce xanthine oxide (XO) activity,
resulting in decreased gastrointestinal (GI) mucosal damage because of lowered XO activity. Tungstic acid has been shown to effectively antagonize stress-induced gastric ulcers, possibly by decreasing motility and mass cell degranulation. Tungstic acid gel has been used as an epileptogenic agent since 1960. Epilepsy produced by this agent is characterized by good localization, short latency and limited duration. It is effective in cerebral cortex, brain stem and spinal cord.
Status:
Investigational
Source:
NCT01971385: Phase 1 Interventional Completed Herpes Labialis
(2013)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Squaric acid is a dibasic organic acid and useful intermediate in a variety of synthetic reactions involving the synthesis of photosensitive squarylium dyes and inhibitors of protein tyrosine phosphatases. Medically, squaric acid dibutyl ester or dibutyl squarate derives from a squaric acid is used for the treatment of warts.
Status:
Investigational
Source:
Clin Pharmacol Ther. May 2021;109(5):1274-1281.: Not Applicable Human clinical trial Completed Multiple System Atrophy/blood
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02929901: Phase 2/Phase 3 Interventional Completed Type 2 Diabetes Nonalcoholic Fatty Liver
(2016)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Z-Chlorogenic acid better known as cis-5-caffeoylquinic acid is a cinnamate ester formed by condensation fo the carboxy group of cis-caffeic acid with the 5-hydroxy group of (+)-quinic acid. It is a naturally occurring isomer of Chlorogenic acid and can be extracted from Nerium indicum flowers, coffee plant, Purpurascen leaves, Artemisia pectinata, and tobacco. In some but not all extractions cis-5caffeoylquinic content is increased after UV exposure of plant or cells.
Status:
Investigational
Source:
NCT04462666: Phase 2 Interventional Unknown status Gouty Arthritis
(2020)
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Status:
Investigational
Source:
NCT01898884: Phase 1 Interventional Completed Friedreich's Ataxia
(2013)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
3-Indolepropionic acid (IN-OX1; Indole-3-propionic acid; OX-1; Oxigon; SHP 22; SHP-622; VP-20629), an endogenous substance produced by bacteria in the intestine, is a deamination product of Tryptophan (T947200) that protects the hippocampus (studied in gerbils) from ischemic damage and oxidative stress. It’s ability to protect the neurons in this way is attributed to its potent antioxidative effects. 3-Indolepropionic acid is also hypothesized to have protective effects on the thyroid gland. 3-Indolepropionic acid is being studied for therapeutic use in Alzheimer's disease. 3-Indolepropionic acid (IPA) completely protected primary neurons and neuroblastoma cells against oxidative damage and death caused by exposure to Abeta, by inhibition of superoxide dismutase, or by treatment with hydrogen peroxide. In kinetic competition experiments using free radical-trapping agents, the capacity of IPA to scavenge hydroxyl radicals exceeded that of melatonin, an indoleamine considered to be the most potent naturally occurring scavenger of free radicals. In contrast with other antioxidants, IPA was not converted to reactive intermediates with pro-oxidant activity. In 2011, Intellect redirected the focus of the OX1 program from Alzheimer's disease to FA (Friedreich's Ataxia). Research suggests that the symptoms associated with FA are the result of oxidative stress caused by the abnormal accumulation of iron. OX1's ability to neutralize ROS could be an effective agent to reduce oxidative stress in FA, thereby eliminating the symptoms of FA and increasing both quality of life and longevity in affected individuals.