U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

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Showing 811 - 820 of 34988 results

Status:
Investigational
Source:
INN:eciruciclib [INN]
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Status:
Investigational
Source:
INN:suricapavir [INN]
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)

Status:
Investigational
Source:
INN:potrasertib [INN]
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Status:
Investigational
Source:
NCT04652518: Phase 2 Interventional Terminated Covid19
(2020)
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Status:
Investigational
Source:
NCT04472897: Phase 1 Interventional Recruiting Tuberculosis
(2020)
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Status:
Investigational
Source:
INN:aminoquinuride
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)


Aminoquinuride (Surfen) binds to glycosaminoglycans (GAGs) and has been shown to influence their function, and the function of proteoglycans (complexes of GAGs linked to a core protein). Surfen was first described in 1938 as a component of depot insulin; however, subsequent studies have revealed its efficacy in binding to glycosaminoglycans (GAGs). Surfen contains four quinoline rings that contain positively charged amino or methyl groups. Surfen was found to bind with greatest avidity to heparin. There are now a handful of studies on the biological effects of surfen, many of which relate to its ability to block the interaction between GAGs and signaling proteins, including effects on growth factors (fibroblast growth factor and vascular endothelial growth factor) and fibrils associated with the binding of human immunodeficiency virus (HIV)-1 to target cells. Surfen inhibits the action of SEVI (semen-derived enhancer of HIV viral infection). Because SEVI can increase HIV infectivity by several orders of magnitude, supplementing current HIV microbicide candidates with SEVI inhibitors, such as surfen, might greatly increase their potency. Surfen has also been shown to reduce inflammation but inhibits remyelination in murine models of multiple sclerosis.
Status:
Investigational
Source:
NCT00085826: Phase 3 Interventional Completed Non-Small Cell Lung Cancer
(2001)
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)



Exisulind (tentative trade name Aptosyn) is an antineoplastic agent, which was originally developed by Cell Pathways. This drug is an inhibitor of phosphodiesterase (PDE) isozymes: PDE5 and PDE4. Inhibition of PDE5 appears to be pharmacologically relevant, which leads to increase cGMP and activate protein kinase G at doses that induce apoptosis, whereas cyclic AMP levels were not changed. Exisulind has been in phase III clinical trials for the treatment of Non-Small Cell Lung Cancer and for the treatment of polyps in patients who have familial adenomatous polyposis (Colorectal Cancer and Small Intestine Cancer). In addition, this drug was in phase II/III for the treatment of Prostate Cancer, however, there studies have been discontinued.
Status:
Investigational
Source:
INN:femoxetine
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)

Femoxetine is a selective serotonin re-uptake inhibitor. It was being studied in the treatment of narcolepsy, migraine, depressive states and eating disorder. Femoxetine development has been discontinued.
Status:
Investigational
Source:
INN:carsatrin [INN]
Source URL:

Class (Stereo):
CHEMICAL (RACEMIC)

Carsatrin (also known as RWJ 24517) is purinylpiperazine derivative patented by Ortho Pharmaceutical Corp. as cardiotonic and antiarrhythmic. Carsatrin acts as positive inotropic agent that increases twitch tension and prolongs the action potential (AP) duration of ventricular muscle without affecting the Na+,K+-ATPase, adenylyl cyclase, phosphodiesterase isozymes, or cardiac myofilaments. Carsatrin’s positive inotropic effect can be prevented by tetrodotoxin but not by the adrenergic antagonists timolol, yohimbine, or prazosin