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Restrict the search for
glutathione disulfide
to a specific field?
Status:
Investigational
Source:
NCT03694444: Phase 1/Phase 2 Interventional Completed Gingivitis
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT03220217: Phase 2 Interventional Completed Gastro-Enteropancreatic Neuroendocrine Tumor
(2017)
Source URL:
Class (Stereo):
CHEMICAL (EPIMERIC)
Status:
Investigational
Source:
NCT03773133: Phase 1/Phase 2 Interventional Terminated Small Cell Lung Cancer and Breast Cancer
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02166242: Phase 1 Interventional Completed Carcinoma, Non-small Cell Lung
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT02204085: Phase 1/Phase 2 Interventional Active, not recruiting Acute Myeloid Leukemia, in Relapse
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
GO-203-2c is a cell-penetrating peptide that binds to MUC1, a protein that causes cancer (oncoprotein). MUC1 is over-expressed in many human cancers, such breast, prostate, lung, colon, pancreas, and ovary cancer, and has been associated with poor prognosis. GO-203-2c blocks homodimerization of the MUC1-C subunit required for nuclear translocation and downstream signaling. This binding eventually leads to cell death (in laboratory setting). Since MUC1 is over-expressed in many cancers, the potential of GO-203-2c in treatment of cancers is being investigated. A phase I clinical trial has been completed in which GO-203-2c was shown to be safe and demonstrating both anti-leukemia and immunomodulatory effects. A phase II study is investigating its potential in the treatment of Acute Myeloid Leukemia.
Status:
Investigational
Source:
NCT01612676: Phase 2 Interventional Completed Septic Shock
(2012)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Selepressin (FE 202158) was designed as a selective and short-acting vasopressin type 1a receptor (V(1a)R) agonist. This drug was developed for the treatment of vasodilatory hypotension in shock. Selepressin successfully completed phase IIa clinical trial, where was found that in septic shock patients, selepressin 2.5 ng/kg/minute was able to rapidly replace norepinephrine, improve fluid balance and shorten the time of mechanical ventilation.
Status:
Investigational
Source:
NCT02824419: Phase 2/Phase 3 Interventional Unknown status Pulmonary Sarcoidosis
(2016)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
INN:invopressin [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
INN:phencyclidine [INN]
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Phencyclidine is an illegal, hallucinogenic drug that was initially used as an anesthetic agent in the 1950s and early 1960s, but was then withdrawn in 1965 because of dissociative hallucinogenic effects that were often disturbing and sometimes severe and prolonged. Phencyclidine is a noncompetitive NMDA (N-methyl-D-aspartate) receptor antagonist and glutamate receptor antagonist, but also interacts with other receptor sites, and may have effects with dopamine, opioid and nicotinic receptors. Phencyclidine disrupts the functioning of receptors for the neurotransmitter glutamate, which plays a major role in the perception of pain as well as in learning, memory, and emotion. It also influences the actions of the neurotransmitter dopamine, which causes the euphoria associated with drug use. Phencyclidine overdose deaths may occur after taking a large dose, though many phencyclidine related deaths result from delusions and other psychological consequences of the drug’s use. There have been reports of death due to accidental drowning, leaping from high places, and motor vehicle accidents in addition to violent episodes of self-mutilation, suicides, and homicides.
Status:
Investigational
Source:
NCT02414516: Phase 1 Interventional Unknown status Solid Tumor
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
OBP-801 (spiruchostatin A) is an inhibitor of histone deacetylase (HDAC) enzymes, with potential antineoplastic activity. OBP-801 was originally identified as an enhancer of PAI-1 gene expression and was established as a new HDAC inhibitor by a p21 promoter reporter screen. Upon administration, OBP-801 inhibits the activity of HDACs; this results in an accumulation of highly acetylated chromatin histones, the induction of chromatin remodeling and an altered pattern of gene expression. This leads to selective transcription of tumor suppressor genes, tumor suppressor protein-mediated inhibition of tumor cell division and induction of tumor cell apoptosis. This may inhibit proliferation of susceptible tumor cells. HDAC, which is upregulated in many tumor cell types, deacetylates chromatin histone proteins. OBP‑801 induces M‑phase arrest and apoptosis in rhabdomyosarcoma cells. OBP‑801 is expected to show anticancer effect by promoting an expression of tumor suppressor genes in cancer cell and inducing apoptotic and autophagic cell death. The results of pre-clinical studies on OBP-801 indicated the most potent HDAC inhibitory activity as compared to other HDAC inhibitors including and Zolinza® and Istodax®, and its efficacy on a wide range of cancers is expected. Furthermore, Oncolys has been exploring the potential ophthalmic use of OBP-801 in collaboration with Kyoto Prefectural University of Medicine. OBP-801 has been used in trials studying the treatment of solid tumor.
