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Restrict the search for
sulfisoxazole acetyl
to a specific field?
Status:
Investigational
Source:
NCT04231266: Phase 2 Interventional Active, not recruiting GNE Myopathy
(2022)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
N-acetylmannosamine (ManNAc), a hexosamine monosaccharide, is the first committed biological precursor of Neu5Ac. N-acetylmannosamine is being investigated as a potential treatment for GNE myopathy. N-acetylmannosamine has being reported to improve the cognitive function in aged animals. It has potential therapeutic application for cognitive dysfunction. N-acetylmannosamine is under investigation for GNE myopathy.
Class (Stereo):
CHEMICAL (ABSOLUTE)
Gestaclone was developed as a progesterone receptor agonist; however, this compound has never been marketed. Information about the current use of this compound is not available.
Status:
Investigational
Source:
NCT00264433: Phase 2 Interventional Completed Neoplasms
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Exherin is a small, cyclic pentapeptide vascular-targeting agent with potential antineoplastic and antiangiogenic activities. ADH-1 selectively and competitively binds to and blocks N-cadherin, which may result in disruption of tumor vasculature, inhibition of tumor cell growth, and the induction of tumor cell and endothelial cell apoptosis. In murine melanoma xenografts, ADH-1 in combination with melphalan significantly reduced tumor growth up to 30-fold over melphalan alone. ADH-1 enhancement of response to melphalan was associated with increased formation of DNA adducts, increased apoptosis, and intracellular signaling changes. In a pilot study (phase I trial), ADH-1 intravenous pretreatment before chemotherapy in metastatic melanoma completely destroyed tumors in half of patients
Status:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Nolpitantium (SR-140333) is a highly selective nonpeptide antagonist of neurokinin-1 (NK1) receptor. Nolpitantium potently, selectively and competitively inhibited substance P binding to NK1 receptors from various animal species, including humans. In vitro, it was a potent antagonist in functional assays for NK1 receptors such as [Sar9, Met(O2)11]substance P-induced endothelium-dependent relaxation of rabbit pulmonary artery and contraction of guinea-pig ileum. Up to 1 mkM, Nolpitantium had no effect in bioassays for NK2 and NK3 receptors. The antagonism exerted by Nolpitantium toward NK1 receptors was apparently non-competitive, with pD2' values between 9.65 and 10.16 in the different assays. Nolpitantium also blocked in vitro [Sar9, Met(O2)11]substance P-induced release of acetylcholine from rat striatum. In vivo, Nolpitantium exerted highly potent antagonism toward [Sar9, Met(O2)11]substance P-induced hypotension in dogs, bronchoconstriction in guinea-pig) and plasma extravasation in rats. Nolpitantium was found to be effective in the modulation of the inflammatory response and airway remodeling in mice. Nolpitantium is reported to cause antagonism of the SP-induced relaxations of human isolated intralobar pulmonary arterial rings. Nolpitantium also blocked the activation of rat thalamic neurons after nociceptive stimulation. Nolpitantium has been shown to reduce the severity of inflammation in trinitrobenzene sulfonic acid-induced colitis in the rat colon. Nolpitantium inhibited mustard oil-induced plasma protein extravasations in the dorsal skin of the rat hind paw. Nolpitantium had been in some phase II clinical trials but further studies were discontinued.
Status:
Investigational
Source:
NCT02837900: Phase 2 Interventional Completed Knee Osteoarthritis
(2016)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT01020006: Phase 2 Interventional Completed Pancreatic Cancer
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
PCI-27483 is a reversible small-molecule inhibitor of activated factor VII (factor VIIa) with potential antineoplastic and antithrombotic activities. FVII, a serine protease, becomes activated (FVIIa) upon binding with TF forming the FVIIa/TF complex, which induces intracellular signaling pathways by activating protease activated receptor 2 (PAR-2). Upon subcutaneous administration, factor VIIa inhibitor PCI-27483 selectively inhibits factor FVIIa in the VIIa/TF complex, which may prevent PAR-2 activation and PAR2-mediated signal transduction pathways, thereby inhibiting tumor cell proliferation, angiogenesis, and metastasis of TF-overexpressing tumor cells. A phase I study in healthy volunteers was conducted
to assess the PD and PK profiles of PCI-
27483 following a single, SC injection. The halflife
of PCI-27483 was 10-12 h. The International
Normalized Ratio (INR) was strongly correlated
with drug plasma concentration. PCI-27483 was
well tolerated. This compound has being evaluated in a phase Ib/II trial in patients with pancreatic cancer receiving treatment with gemcitabine. However, no recent development has been reported. The compound was originally developed by Celera, then licensed to Pharmacyclics (acquired by Abbvie in 2015) later.
In 2012, the product was licensed to Novo Nordisk by Pharmacyclics for disease outside of oncology.
Status:
Investigational
Source:
NCT01150812: Phase 1 Interventional Terminated Thrombin Inhibition
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02100527: Phase 2 Interventional Withdrawn Acne Vulgaris
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
PF-05175157 exhibited good potencies against the two isoforms of the Acetyl-CoA carboxylase enzyme (ACC1 and ACC2) from human and rat. PF-05175157 has undergone multiple clinical trials in healthy volunteers and for the treatment of diabetes mellitus. PF-05175157 was in the phase II when the development was discontinued due to safety concerns. Among potential barriers for the use of ACC inhibitors in humans include concerns of increased risk of myocardial injury following an ischemic event. PF-05175157 reduced the multiplication of West Nile virus (WNV), dengue virus (DENV), and Zika virus (ZIKV) in cultured cells, which is compatible with the predicted broad spectrum of host targeting antivirals. PF-05175157 reduced the peak of viremia in WNV-infected mice, supporting that ACC is a valuable target for antiviral intervention. PF05175157 also reduced the viral burden in the kidney of infected mice.
Status:
Investigational
Source:
NCT01588756: Phase 1/Phase 2 Interventional Completed Healthy
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
