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Restrict the search for
l-glutamine
to a specific field?
Status:
Investigational
Source:
NCT03712124: Phase 2 Interventional Completed Gastroparesis
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Status:
Investigational
Source:
NCT02588105: Phase 1 Interventional Completed Advanced Solid Tumours
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Status:
Investigational
Source:
NCT02106338: Phase 1 Interventional Completed Clostridium Difficile Infection
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
CRS-3123, also known as REP-3123, is a methionyl-tRNA synthetase inhibitor potentially for the treatment of enteric infections. CRS-3123 is in Phase 1 clinical development for the treatment of Clostridium difficile Infection (CDI). CRS-3123 is a small molecule protein synthesis inhibitor that acts on the novel target methionyl-tRNA synthetase (MetRS). REP-3123 has been shown to be active in vitro against clinical
isolates of C. difficile including epidemic strains such as B1/
NAP1/027; MIC values of REP-3123 for C. difficile are
typically 0.5 -- 1.0 mg/l. REP-3123 is also active against a range of clinically important aerobic Gram-positive bacteria
including methicillin-susceptible and -resistant Staphylococcus
aureus (MIC90 values of 0.06 and 0.25 mg/l, respectively),
Streptococcus pyogenes (MIC90 0.5 mg/l) and enterococci
(MIC90 32 mg/l). CRS-3123 has numerous potential advantages over current CDI therapies. In addition to being highly potent against all clinical isolates of C. difficile tested, CRS-3123 has several desirable qualities for the treatment of CDI which include:
Narrow spectrum for C. difficile, which may substantially reduce the disruption of normal intestinal flora compared to current therapies;
Inhibition of toxin production, potentially leading to lower morbidity and mortality;
Inhibition of sporulation, potentially leading to lower rates of transmission and recurrence;
A novel mechanism of action, which means that its use will not compromise the utility of systemic antibiotics while maintaining activity against pre-existing resistance mechanisms.
Status:
Investigational
Source:
NCT02898779: Phase 1 Interventional Completed Malaria
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02067793: Phase 2 Interventional Completed Major Depressive Disorder
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT03725722: Phase 2 Interventional Completed Atopic Dermatitis
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02503423: Phase 1/Phase 2 Interventional Active, not recruiting Solid Tumors
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Status:
Investigational
Source:
NCT02666963: Phase 1 Interventional Completed Healthy
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02687152: Phase 1/Phase 2 Interventional Completed Type 2 Diabetes Mellitus
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
N(ω)-hydroxy-nor-L-arginine (nor-NOHA), an arginase inhibitor, has therapeutic potential in the treatment of cardiovascular and obstructive airway diseases. Nor-NOHA is a reversible, competitive arginase inhibitor. The affinity of nor-NOHA for the to the arginase active site was found in the nanomolar range. Nor-NOHA has proven to be one of the strongest arginase inhibitors. Inhibition by nor-NOHA is ten times more potent on arginase II than on arginase I. The pharmacokinetics of nor-NOHA is characterized by high bioavailability, close to 100% after multiple dose and rapid elimination resulting in t1/2 of 15–30 min after intravenous and intraperitoneal administration to rats. Arginase inhibition with Nor-NOHA increased circulating arginine levels and decreased hepatic damage during liver I/R injury. Arginase blockade represents a potentially novel strategy to combat hepatic I/R injury associated with liver transplantation. Nor-NOHA is under investigation in clinical trial NCT02009527 (Arginase inhibition in ischemia-reperfusion injury).
Status:
Investigational
Source:
NCT03371680: Not Applicable Interventional Completed ARDS
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
