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Restrict the search for
phenyl aminosalicylate
to a specific field?
Status:
Investigational
Source:
NCT04176848: Phase 2 Interventional Active, not recruiting Breast Cancer
(2020)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Status:
Investigational
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Lorediplon is a novel non-benzodiazepine, the hypnotic drug acting as a GABAA receptor modulator, differentially active at the alpha1-subunit, associated with promoting sleep. As compared with other selective benzodiazepine receptor agonists, lorediplon has demonstrated in pre-clinical studies a potent hypnotic profile with potential advantages in sleep maintenance and sleep architecture preservation associated with a good safety profile, that is, no induction of tolerance, lack of next-day hangover effect, weak effect on muscular tone, and weak interaction with ethanol. Lorediplon demonstrated a minimum of 10-fold and the 6-fold increase in potency (respectively) in the spontaneous motor activation studies, compared with the currently marketed hypnotics (zolpidem and zaleplon). Additionally, when the electroencephalogram (EEG) effects of lorediplon and zolpidem were compared in the sleep-wake cycle in the mouse, lorediplon demonstrated a 10-fold increase in potency compared with zolpidem in the sleep-wake cycle and 13% greater possibility of fewer wake episodes than zolpidem. At concentrations of 1.2mg/kg, lorediplon demonstrated a 57%increased effect on Slow Wave Sleep (SWS), when compared with a placebo. In clinical trials, the clinical safety and tolerability were excellent for all doses tested. In pharmacokinetic studies, after oral administration, lorediplon is rapidly absorbed from the gastrointestinal tract reaching maximum plasma concentrations at approximately 2 h. Lorediplon demonstrated a dose-dependent improvement in sleep, whereas zolpidem showed a more sustained wake after sleep onset effect. No next-day hangover effects were observed. These sleep effects are also consistent with the pharmacokinetic profile of lorediplon.
Status:
Investigational
Source:
NCT01348919: Phase 1/Phase 2 Interventional Completed Multiple Myeloma
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Delanzomib (CEP-18770), a proteasome inhibitor, was being developed by Cepahlon (a subsidiary of Teva) for the treatment of cancer and immunological disorders. Delanzomib (CEP-18770) induces apoptotic cell death in multiple myeloma (MM) cell lines and in primary purified CD138-positive explant cultures from untreated and bortezomib-treated MM patients. In vitro, Delanzomib (CEP-18770) has a strong antiangiogenic activity and potently represses RANKL-induced osteoclastogenesis. Delanzomib represses the proteasomal degradation of a variety of proteins, including inhibitory kappaBalpha (IkappaBalpha), resulting in the cytoplasmic sequestration of the transcription factor NF-kappaB; inhibition of NF-kappaB nuclear translocation and transcriptional up-regulation of a variety of cell growth-promoting factors; and apoptotic cell death in susceptible tumor cell populations. In vitro studies indicate that this agent exhibits a favorable cytotoxicity profile toward normal human epithelial cells, bone marrow progenitors, and bone marrow-derived stromal cells relative to the proteasome inhibitor bortezomib. Delanzomib has been in phase II clinical trials for the treatment of multiple myeloma (MM). However, this research has been discontinued. Currently Delanzomib is on Phase I clinical trial for Non-Hodgkin's lymphoma and Solid tumours.
Status:
Investigational
Source:
NCT00645853: Phase 2 Interventional Completed Persistent or Permanent Nonvalvular Atrial Fibrillation
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Atecegetran metoxil (more widely known as AZD0837), an anticoagulant and a prodrug, converted to a selective and reversible direct thrombin inhibitor (AR-H067637). Atecegetran metoxil participated in phase II clinical trials to prevent the stroke and systemic embolism in patients with non-valvular atrial fibrillation. The development of atecegetran metoxil was discontinued, due to a limitation identified in the long-term stability of the extended-release drug product.
Status:
Investigational
Source:
NCT00599911: Phase 2 Interventional Completed Major Depressive Disorder
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Tedatioxetine (previously known as Lu AA24530) is a multimodal antidepressant that was developed for the treatment of depression and anxiety disorders (generalized anxiety disorder mainly). Tedatioxetine is a monoamine enhancer with reuptake inhibition at monoamine transporters and possesses an antagonist activity at 5-HT3 and 5-HT2c receptors. In 2009, the drug was studied in phase II clinical trials where it showed positive results in major depressive disorder. However, it remains unclear as to whether tedatioxetine development has been postponed and/or abandoned.
Status:
Investigational
Source:
NCT00598390: Phase 1 Interventional Completed Healthy
(2008)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT00884520: Early Phase 1 Interventional Completed Lung Cancer
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT01019928: Phase 2 Interventional Completed Sensitivity in Esophagus
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT04452500: Phase 2 Interventional Recruiting PTSD
(2022)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Status:
Investigational
Source:
NCT00713544: Phase 2 Interventional Completed Rheumatoid Arthritis
(2008)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
AZD5672 was developed by AstraZeneca for the treatment of rheumatoid arthritis. It was found that the drug inhibits P-glycoprotein and is a CCR5 antagonist. Exists hypothesis that inhibition of CCR5 can bring benefits in the treatment of rheumatoid arthritis. In July 2009, Phase-II for Rheumatoid arthritis was discontinued.
