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Restrict the search for
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Status:
Investigational
Source:
NCT02123290: Phase 2 Interventional Completed Plasmodium Falciparum Malaria
(2016)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
DSM265 is an experimental antimalarial that selectively inhibits the parasite dihydroorotate dehydrogenase (DHODH). DSM265 is the first DHODH inhibitor to reach clinical development for treatment of malaria. DSM265 is highly selective toward DHODH of the malaria parasite Plasmodium, efficacious against both blood and liver stages of P. falciparum, and active against drug-resistant parasite isolates. The only possible DSM265-related adverse event was a moderate transient elevation in serum bilirubin.
Status:
Investigational
Source:
NCT02933372: Phase 2 Interventional Completed Parkinson's Disease
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT04546633: Phase 2 Interventional Completed Uncomplicated Plasmodium Falciparum Malaria
(2021)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
GNF-156 (ganaplacide or KAF-156) is an antimalarial agent that is part of the imidazolopiperazine family. It exerts activity against pre-erythrocytic liver stages, asexual and sexual blood stages. An improvement compared to existing antimalarial drug combinations is that this compound shows promising single-dose antimalarial activity, and no serious safety and tolerability concerns in humans are known so far. Phase II clinical trials have been completed for GNF-156. Its potential is also being investigated in combination with lumefantrine (an aryl-amino alcohol) in LUM-KAF156.
Status:
Investigational
Source:
NCT00868790: Phase 2 Interventional Terminated Type 2 Diabetes Mellitus
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
MK 3577 is an orally active glucagon receptor antagonist which was under development by Merck & Co for the treatment of type 2 diabetes mellitus. MK 3577 demonstrate activity in cellular models and preclinical trials. In phase II clinical trials MK 3577 shows good efficacy and acceptable level of adverse events, but no further development reports were published.
Status:
Investigational
Source:
NCT03318809: Phase 1 Interventional Completed Heart Failure
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT04358393: Phase 1/Phase 2 Interventional Recruiting AML
(2020)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT01915576: Phase 1 Interventional Completed Neoplasms
(2013)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
BAY-1125976 is an orally bioavailable inhibitor of the serine/threonine protein kinase AKT (protein kinase B) isoforms 1 and 2 (AKT1/2) with potential antineoplastic activity. AKT1/2 inhibitor BAY1125976 selectively binds to and inhibits the phosphorylation and activity of AKT1/2 in a non-ATP competitive manner, which may result in the inhibition of the phosphatidylinositol 3 (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway. This may lead to both the reduction of cell proliferation and the induction of cell apoptosis in AKT-overexpressing tumor cells. The AKT signaling pathway is often deregulated in cancer and is associated with tumor cell proliferation, survival, and migration. BAY 1125976 is equally potent against Akt1 and Akt2 isoforms and up to 86 fold less potent against Akt3 It inhibits the Akt1 and Akt2 by binding into an allosteric binding pocket formed by kinase and PH domain. It inhibits cell proliferation in a broad panel of human cancer cell lines, particularly in breast and prostate cancer cell lines expressing estrogen or androgen receptors. It effectively blocks Akt signaling by inhibiting the phosphorylation of Akt and the downstream effectors, including eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1), glycogen synthase kinase 3 beta (GSK3s), proline-rich Akt substrate 40 kDa (PRAS40), S6 ribosomal protein (S6RP), and 70 kDa ribosomal protein S6 kinase 1 (70S6K). BAY 1125976 exhibits strong in vivo efficacy in both cell line and patient-derived xenograft models such as the KPL4 breast cancer model (PIK3CAH1074R mutant), the MCF7 and HBCx-2 breast cancer models, and the AktE17K mutant driven prostate cancer (LAPC-4) and anal cancer (AXF 984) models.
Status:
Investigational
Source:
NCT01525212: Phase 1 Interventional Withdrawn Chronic Hepatitis C
(2012)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Bristol-Myers Squibb developed BMS-929075 as a selective, orally bioavailable hepatitis C virus (HCV) NS5B polymerase inhibitor for the treatment of chronic HCV infection. BMS-929075 was involved in phase I clinical trials for hepatitis C virus (HCV) infected patients; however, the company withdrew a study prior to enrolment.
Status:
Investigational
Source:
NCT02254707: Phase 1/Phase 2 Interventional Completed Hepatitis C, Chronic
(2004)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT00827190: Phase 1 Interventional Completed Acute Ischemic Stroke
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
ILS 920 (previously known as WAY-265920) was developed for the treatment of stroke. ILS-920 binds selectively to the immunophilin FKBP52 and to the β1-subunit of L-type voltage-gated calcium channels (VGCC). ILS 920 successfully completed phase I clinical trial where was determine the safety, tolerability, pharmacokinetics, and pharmacodynamics after administration of ascending single intravenous (IV) doses to healthy adult subjects. However, information about the further development of this drug is not available.