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Restrict the search for
angiotensin ii
to a specific field?
Status:
Investigational
Source:
NCT00600275: Phase 1/Phase 2 Interventional Completed Solid Tumors
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
BGT 226 is an orally available, small molecule, the dual inhibitor of mammalian target of rapamycin (mTOR) and phosphatidylinositol 3'kinase (PI3K), developed by Novartis for the treatment of solid tumors, including advanced breast cancer. A phase I/II trial was completed in the US, Canada, and Spain, and a phase I trial was completed in Japan. However, development appears to have been discontinued.
Status:
Investigational
Source:
NCT01039597: Phase 1/Phase 2 Interventional Unknown status Mild to Moderate Ulcerative Colitis
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Ore Pharmaceuticals developed ORE1001 previously known as MLN-4760 as an orally administered, small molecule compound, for the treatment of inflammatory bowel diseases. ORE1001 is a specific angiotensin-converting enzyme 2 inhibitor. It was shown that ORE1001 markedly decreased tissue myeloperoxidase activity, a well-known marker of inflammation. As a result, ORE1001 was studied as a treatment of gastrointestinal inflammatory conditions. ORE1001 was involved in phase I clinical trial to investigate its safety and activity in subjects with ulcerative colitis. In addition, the drug was studied for NSAID-induced ulcer and obesity. However, all these studies were discontinued.
Status:
Investigational
Source:
NCT02266745: Phase 2 Interventional Active, not recruiting Advanced Solid Tumors
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02953639: Phase 2 Interventional Completed Schizophrenia
(2016)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Basmisanil (INN) (developmental code names RG-1662, RO5186582) is a highly selective inverse agonist/negative allosteric modulator of α5 subunit-containing GABAA receptors which is under development by Roche for the treatment of cognitive impairment associated with Down syndrome. The phase II trials were recently terminated due to lack of efficacy. This outcome suggests either that the α5-NAM was insufficiently effective to restore neuronal plasticity or alternatively that the hypothesis of excessive GABAergic inhibition obstructing neuronal plasticity does not extend to individuals with DS.
Status:
Investigational
Source:
NCT03193853: Phase 2 Interventional Completed Triple Negative Breast Cancer
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Serabelisib (INK1117 and TAK-117) is an orally bioavailable, PI3K p110α- isoform-specific inhibitor with an in vitro IC50 of 15 nM, highly selective against other isoforms (p110β, p110γ, and p110δ) and mTOR (no significant inhibitions at 1 μM concentration). It displayed significant efficacy in several PI3Kα mutant-specific preclinical mouse xenograft tumor models, and blocked signaling to Akt and inhibited the growth of cancer cells harboring wild-type or mutated p110α. Preclinical studies showed TAK-117 to have the low potential for disrupting glucose metabolism or for causing cardiac adverse events; in rats and monkeys, doses up to 50 mg/kg/day were well tolerated. Serabelisib is currently under clinical evaluation.
Status:
Investigational
Source:
JAN:COBALT PROTOPORPHYRIN [JAN]
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Cobalt protoporphyrin (CoPP) is a potent HO-1 inducer and generally known to be an antioxidant in various cell types. CoPP has been shown to downregulate various
cytochrome P450 isoforms, and various mechanisms
of action have been attributed to its ability to induced HO-
1. It has also been used to promote endogenous carbon
dioxide (CO) generation and protect against myocardial
infarction in vivo. CoPP also participated in regulating
the inflammatory response in CNS which mainly suppressed
inflammatory component. It has been demonstrated
that CoPP reduced LPS/Interleukin 13 (IL-13)-induced
microglial death.
Status:
Investigational
Source:
NCT03042013: Phase 2 Interventional Withdrawn Subjects With NSCLC With an EGFR Activating Mutation
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Naquotinib (ASP8273) is an orally available, irreversible, mutant-selective, epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Naquotinib was found by mass spectrometry to covalently bind to a mutant EGFR (L858R/ T790M) via cysteine residue 797 in the kinase domain of EGFR with long-lasting inhibition of EGFR phosphorylation for 24 h. In the NSCLC cell lines harboring the above EGFR mutations, Naquotinib had IC50 values of 8-33 nM toward EGFR mutants, more potently than that of WT EGFR (IC50 value of 230 nM). In mouse xenograft models, Naquotinib induced complete regression of the tumors after 14 days of treatment. ASP8273 even showed activity in mutant EGFR cell line which is resistant to other EGFR TKIs. Naquotinib is in phase III clinical trials for the oral treatment of EGFR mutated non-small cell lung cancer (NSCLC).
Status:
Investigational
Source:
NCT01626924: Phase 2 Interventional Terminated Perinatal Asphyxia
(2012)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
2-Iminobiotin (2-IB) is a cyclic guanidino analog of biotin (Vitamin B7) and combined neuronal and inducible (but not endothelial) nitric oxide synthase inhibitor that has been demonstrated to improve neuroprotection in animal models of hypoxic-ischemic Brain Injury. While the exact mechanism of action has yet to be defined, 2-Iminobiotin potentially protects against hypoxic-ischemic brain damage by preventing nitric oxide or peroxynitrite-induced mitochondrial damage. In preclinical models, 2-Iminobiotin provides gender-specific neuroprotection against hypoxia-ischemia in neonatal rats by a NO-independent mechanism.
Status:
Investigational
Source:
NCT01218477: Phase 1/Phase 2 Interventional Completed Leukemia
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
BMS-833923 was discovered by Exelixis and was out-licensed to Bristol-Myers Squibb. BMS-833923 is an orally bioavailable Smoothened antagonist. BMS-833923 reduces hedgehog pathway activity, decreases cell proliferation and induces apoptosis via the intrinsic pathway in esophageal adenocarcinoma (EAC) cell lines. BMS-833923 dose-dependently affects canonical and prostate hedgehog signature gene transcription in vitro. BMS-833923 is in phase II clinical trials for the treatment of chronic myeloid leukaemia.
Status:
Investigational
Source:
NCT00579384: Phase 2 Interventional Completed Photosensitive Epilepsy
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)