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Search results for dexamethasone root_protein_modifications_structuralModifications_molecularFragment_refPname in Protein Structural Modification Substance Name (approximate match)
Status:
Investigational
Source:
NCT00791570: Phase 1 Interventional Completed Neovascular Maculopathy
(2008)
Source URL:
Class:
PROTEIN
Status:
Investigational
Source:
NCT02598648: Not Applicable Interventional Recruiting Acute Respiratory Distress Syndrome
(2015)
Source URL:
Class:
PROTEIN
Status:
Investigational
Source:
NCT04262479: Phase 2 Interventional Completed Latent Autoimmune Diabetes in Adults
(2020)
Source URL:
Class:
PROTEIN
Status:
Investigational
Source:
NCT00791570: Phase 1 Interventional Completed Neovascular Maculopathy
(2008)
Source URL:
Class:
PROTEIN
Status:
Investigational
Source:
NCT02672163: Not Applicable Interventional Completed Heart Failure
(2016)
Source URL:
Class:
PROTEIN
Status:
Investigational
Source:
NCT03249207: Phase 3 Interventional Active, not recruiting Subarachnoid Hemorrhage
(2018)
Source URL:
Class:
PROTEIN
Status:
Investigational
Source:
NCT01487915: Phase 2 Interventional Unknown status Advanced Urothelial Carcinoma
(2010)
Source URL:
Class:
PROTEIN
Status:
Investigational
Source:
NCT03428022: Phase 3 Interventional Unknown status NSCLC
(2017)
Source URL:
Class:
PROTEIN
Status:
Investigational
Source:
NCT00996255: Phase 1 Interventional Terminated Advanced/Metastatic Solid Tumors
(2006)
Source URL:
Class:
PROTEIN
Targets:
Conditions:
PHA-793887 is an inhibitor of multiple cyclin dependent kinases (CDK) with activity against CDK2, CDK1 and CDK4. PHA-793887 was cytotoxic for leukemic cell lines in vitro, with IC(50) ranging from 0.3 to 7 uM. In colony assays PHA-793887 showed very high activity against leukemia cell lines, with an IC(50) <0.1 uM indicating that it has efficient and prolonged antiproliferative activity. PHA-793887 induced cell-cycle arrest, inhibited Rb and nucleophosmin phosphorylation. PHA-793887 has promising therapeutic activity against acute leukemias in vitro and in vivo.
Status:
Investigational
Class:
PROTEIN
Dalazatide is a 37-amino acid synthetic peptide, a derivative of ShK, which was originally isolated from the venom of the Carribean Sea Anemone. The drug was first discovered by the University of California at Irvine and further developed by Kineta and KPI Therapeutics. Dazalatide is a specific inhibitor of the voltage-gated Kv1.3 potassium channel. The Kv1.3 potassium channel is highly upregulated on effector memory T-cells (TEM cells), and is involved in regulating their calcium uptake. Chronically activated memory T cells are key mediators of numerous autoimmune diseases, including psoriasis and multiple sclerosis. In vivo studies with dalazatide in a delayed-type hypersensitivity (DTH) model have shown that drug treatment inhibited the DTH response by suppressing TEM cells, but had no effect on naïve or central memory T cells. Dalazatide was investigated in a phase I clinical trials for the treatment of plaque psoriasis. The study indicates that dalazatide is generally well tolerated and can improve psoriatic skin lesions by modulating T cell surface and activation marker expression and inhibiting mediators of inflammation in the blood.
