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Restrict the search for
amphotericin b
to a specific field?
Status:
Investigational
Source:
NCT01468324: Phase 1 Interventional Completed Glioblastoma Multiforme
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
INN:tracazolate [INN]
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Tracazolate (ICI 136,753), a pyrazolopyridine, is a non-benzodiazepine with anxiolytic-like activity in animal models. It is known to interact with gamma-aminobutyric acid (GABA)(A) receptors, adenosine receptors, and phosphodiesterases. Its intrinsic efficacy, potentiation, or inhibition is determined by the nature of the third subunit (gamma1-3, delta, or epsilon) within the GABA(A) receptor complex.
Status:
Investigational
Source:
NCT01379287: Phase 1 Interventional Completed Solid Tumors
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
KOSN-1724, also known as iso-fludelone, is the third-generation epothilone B analogue. It binds to tubulin and induces microtubule polymerization/reduces microtubule depolymerization, resulting in the inhibition of cell division and induction of apoptosis. KOSN-1724 is in phase I clinical trials for the treatment of solid tumors.
Status:
Investigational
Source:
NCT00784875: Phase 2 Interventional Completed Primary Insomnia
(2008)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT02656849: Phase 2 Interventional Withdrawn Solid Tumor
(2016)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Roniciclib (BAY1000394) is a pan-cyclin-dependent kinase inhibitor that has been developed for treatment in small cell lung carcinoma and solid tumors. Roniciclib targets certain key proteins that are essential for the survival of cancer cells, resulting in decreased tumor growth. Phase I studies to evaluate the safety, tolerability and pharmacokinetics of roniciclib have been completed successfully. In phase II studies, roniciclib was found to be well tolerated and showed promising efficacy when combined with chemotherapy in small cell lung carcinoma patients. However, due to an observed safety signal (treatment-emergent adverse events) in one phase II study, other clinical trials have been discontinued and further development of roniciclib was terminated.
Status:
Investigational
Source:
NCT00858377: Phase 1 Interventional Completed Advanced Malignancy
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Amgen is developing AMG-900, an orally active, small molecule aurora kinase A, B and C inhibitor for the treatment of solid tumours and haematological malignancies. In tumor cells, AMG-900 inhibited autophosphorylation of aurora-A and -B as well as phosphorylation of histone H3 on Ser(10), a proximal substrate of aurora-B. The predominant cellular response of tumor cells to AMG-900 treatment was aborted cell division without a prolonged mitotic arrest, which ultimately resulted in cell death. AMG-900 inhibited the proliferation of 26 tumor cell lines, including cell lines resistant to the antimitotic drug paclitaxel and to other aurora kinase inhibitors (AZD1152, MK-0457, and PHA-739358), at low nanomolar concentrations. Furthermore, AMG-900 was active in an AZD1152-resistant HCT116 variant cell line that harbors an aurora-B mutation (W221L). Oral administration of AMG-900 blocked the phosphorylation of histone H3 in a dose-dependent manner and significantly inhibited the growth of HCT116 tumor xenografts. Importantly, AMG-900 was broadly active in multiple xenograft models, including 3 multidrug-resistant xenograft models, representing 5 tumor types. AMG-900 has entered clinical evaluation in adult patients with advanced cancers and has the potential to treat tumors refractory to anticancer drugs such as the taxanes.
Status:
Investigational
Source:
NCT02204644: Phase 3 Interventional Completed CML, CML-CP,MMR,TKI
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Flumatinib (HHGV678) is an orally bioavailable antineoplastic tyrosine kinase inhibitor. Flumatinib inhibits the wild-type forms of Bcr-Abl, platelet-derived growth factor receptor (PDGFR) and mast/stem cell growth factor receptor (SCFR; c-Kit) and forms of these proteins with certain point mutations. Flumatinib was extensively metabolized after oral administration, and the major metabolic pathways observed were amide hydrolysis, demethylation, oxidation, and glucuronide conjugation. It is in phase III clinical trials for the treatment of Chronic myeloid leukemia (in China).
Status:
Investigational
Source:
NCT00002243: Phase 1 Interventional Completed HIV Infections
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Calanolide A is a new non-nucleoside reverse transcriptase inhibitor (NNRTI) originally extracted from a tropical tree (Calophyllum lanigerum) in the Malaysian rain forest. Viral life-cycle studies indicate that calanolide A acts early in the infection process, similar to the known HIV reverse transcriptase (RT) inhibitor 2', 3'-dideoxycytidine. In enzyme inhibition assays, calanolide A potently and selectively inhibits recombinant HIV type 1 RT but not cellular DNA polymerases or HIV type 2 RT within the concentration range tested. Phase I studies have found that calanolide A is well tolerated. Consequently, it has potential clinical applications in combination with other antiviral drugs to suppress HIV-1 mutants. Nevertheless, the development of calanolide A has been delayed due to its low therapeutic index (range: 16–279), non-ideal antiviral activity, and the complexity of its extraction from plants
Status:
Investigational
Source:
NCT04044001: Phase 1/Phase 2 Interventional Completed Pulmonary Tuberculoses
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
BTZ-043 efficiently inhibits Mtb cell wall synthesis by blocking the decaprenyl- phosphoribose-2′-epimerase (DprE1), necessary for the synthesis of D-Arabinofuranose, a component of arabinogalactan and arabinomannan. Due to this mechanism it is highly selective for Mycobacteria species and does not affect the gut flora. BTZ-043 binds covalently to the enzyme and blocks it irreversibly. BTZ-043 is active against all tested Mtb strains including clinical isolated from MDR and XDR patients. The in vitro MIC ranges between ~0.1 - 80 ng/ml for fast growers, and from 1 - 30 ng/ml for members of the M. tuberculosis complex. In vivo BTZ-043 shows superior activity to INH in mouse models, most prominent after 2 months and thereafter. Synergistic effects with Rifampicin were detected in vitro as well as in vivo. In preclinical toxicology (GLP) studies, BTZ-043 showed a low toxicologic potential, it was well tolerated up to 180 mg/kg in rats. BTZ-043 showed no interaction with the CYP450 enzymes or the hERG channel. Genotoxicity and mutagenicity studies were negative. In vitro metabolism studies implicate an acceptable stability in the human organism with only one main metabolite. Protocols for GMP production in industrial scale are available and high purity of the substance can be achieved easily. Currently the final tolerability studies in two animal models are completed and studies in mice are conducted to better describe the pharmacodynamic drivers.
Status:
Investigational
Source:
NCT01573819: Phase 1 Interventional Completed Huntington Disease
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
GlaxoSmithKline is developing GSK-356278 as a selective, brain-penetrant phosphodiesterase 4 (PDE4) inhibitor that demonstrates anxiolytic and cognition-enhancing effects. Small molecule phosphodiesterase (PDE) 4 inhibitors have long been known to show therapeutic benefit in various preclinical models of psychiatric and neurologic diseases because of their ability to elevate cAMP in various cell types of the central nervous system. The drug was studied for the treatment of Huntington's disease, depressive and anxiety disorders. GSK-356278 has completed phase I clinical trials for evaluation of the safety, tolerability, and pharmacokinetics in male volunteers with the therapeutic dose for future clinical development.
