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

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

Showing 171 - 180 of 2696 results

Status:
Investigational
Source:
INN:fosmidomycin
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)



Fosmidomycin (3-(formylhydroxyamino)-propylphosphonic acid mono-sodium salt, 3-(N-formyl-N-hydroxyamino)-propylphosphonic acid mono-sodium salt, FR-31564) is a potent inhibitor of P. falciparum 1-deoxy-D-xylulose-5-phosphate reductoisomerase (PfDXR), developed by Albert Schweitzer Hospital for P. falciparum malaria treatment. Fosmidomycin was originally isolated as natural antibiotic from Streptomyces lavendulae. Fosmidomycin is active against a broad range of enterobacteria, but not against Gram-positive organisms or anaerobes. Fosmidomycin was developed as far as an early phase II study for the treatment of urinary tract infections by Fujisawa Pharmaceutical Company (Osaka, Japan) in the early eighties, but these trials have been discontinued. In recent clinical studies, it was shown that fosmidomycin is effective in curing uncomplicated Plasmodium falciparum malaria in humans. The treatment was well tolerated and resulted in a fast parasite and fever clearance. However, the high rate of recrudescence precludes the use of fosmidomycin as a monotherapy. In drug combination studies, the synergy of fosmidomycin with clindamycin was observed. Clinical studies with a fosmidomycin-clindamycin combination are currently ongoing.
Status:
Investigational
Source:
INN:fosopamine
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Fosopamine (also known as Sim 2055), is a prodrug of epinine was studied for the treatment of renal failure and of essential hypertension. However, phase II of clinical trials in Italy was discontinued in 1995. Information about the current development of this drug is not available.
Status:
Investigational
Source:
NCT00002422: Phase 1 Interventional Completed HIV Infections
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)



16alpha-Bromoepiandrosterone (HE2000) is a synthetic steroid that limits non-productive inflammation, enhances protective immunity and improves survival in clinical studies of patients with human immunodeficiency virus (HIV), malaria and tuberculosis infections. HE 2000 had also shown activity in vitro against cytomegalovirus, polio, hepatitis B and C and influenza virus. 16alpha-Bromoepiandrosterone inhibits glucose-6-phosphate dehydrogenase (G6PD) and cell proliferation. HE 2000 was in phase II development for the Hepatitis B in Malaysia and Singapore, but it was suspended.
Status:
Investigational
Source:
JAN:ERITORAN SODIUM [JAN]
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)

Eritoran (E-5564) is a synthetic lipid A analog that has been designed to antagonize the effects of lipopolysaccharide (LPS) and has been found to do this by interacting with Toll-like receptor 4, the cell surface receptor for LPS. Preclinical in vitro and in vivo studies of eritoran tetrasodium indicate it can limit excessive inflammatory mediator release associated with LPS and improve survival in sepsis models. Clinically, eritoran was being investigated for the treatment of severe sepsis, septic shock, and other endotoxin-mediated indications. Eritoran development has been discontinued.
Edelfosine is a synthetic alkyl-lysophospholipid, a potent immunomodulator and an effective inhibitor of tumor cell proliferation. The cytotoxic effect of edelfosine has been evaluated in a large variety of both tumor (leukemic and solid) and normal cell types, showing a high degree of selectivity towards tumor cells. Like all alkyl-lysophospholipids, Edelfosine incorporates into the cell membrane and does not target the DNA. In many tumor cells, Edelfosine causes selective apoptosis, sparing healthy cells. Edelfosine can activate the Fas/CD95cell death receptor, can inhibit the MAPK/ERK mitogenic pathway and the Akt/protein kinase B (PKB) survival pathway. Edelfosine apoptosis-inducing abilities were studied with several types of cancer, among them multiple myeloma and non-small and small cell lung carcinoma cell lines. In vivo activity against human solid tumors in mice was shown against malignant gynecological tumor cells, like ovarian cancer, and against breast cancer. In vivo biodistribution studies demonstrated a “considerably higher” accumulation of Edelfosine in tumor cells than in other analyzed organs. Several clinical trials were conducted. Among them, a phase I trials with solid tumors or leukemias and phase II with non-small-cell lung carcinomas (NSCLC). In Phase II clinical trial for use of Edelfosine in treating leukemia with bone marrow transplants, it was found to be safe and 'possibly effective'. A phase II trial for the treatment of brain cancers was also reported. It showed encouraging results in stopping the growth of the tumor and a considerable improvement in the “quality of life” of the patients. A phase II trial on the effect of Edelfosine on advanced non-small-cell bronchogenic carcinoma had a “remarkable” “high proportion of patients with stationary tumor status” as result, stable disease after initial progression in 50% of the patients.
Clofilium is a quaternary ammonium compound that acts as potassium channel blocker. Clofilium is a class III agent. Clofilium increases atrial and ventricular effective refractory period without changing conduction time and, despite no apparent change in premature ventricular complex frequency, it can abolish the ability to induce ventricular tachycardia by programmed stimulation and is also well tolerated.
Status:
Investigational
Source:
USAN:METRONIDAZOLE PHOSPHATE [USAN]
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Conditions:

Metronidazole phosphate is a water-soluble prodrug of metronidazole.
Status:
Investigational
Source:
USAN:TRIAMCINOLONE ACETONIDE SODIUM PHOSPHATE [USAN]
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)

Triamcinolone acetonide- 21-dihydrogen phosphate is the long-acting derivative of a synthetic glucocorticoid triamcinolone. Triamcinolone acetonide has eight times more potency than prednisolone. Triamcinolone acetonide- 21-dihydrogen phosphate used for intravenous injection. It is supposed to be hydrolyzed rapidly in the body to form the free corticoid alcohol.
Status:
Investigational
Source:
NCT03074435: Phase 3 Interventional Unknown status Malaria
(2016)
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)


Conditions:

Chlorpyrifos (CPF) is a crystalline organophosphate insecticide. It was introduced in 1965 by Dow Chemical Company and is known by many trade names (see table), including Dursban and Lorsban. It acts on the nervous system of insects by inhibiting acetylcholinesterase. Chlorpyrifos is an organophosphate, with potential for both acute toxicity at larger amounts and neurological effects in fetuses and children even at very small amounts. For acute effects, the EPA classifies chlorpyrifos as Class II: moderately toxic. CPF is a strongly genotoxic agent that induces DNA damage and cell apoptosis.
Status:
Investigational
Source:
INN:mifobate [INN]
Source URL:

Class (Stereo):
CHEMICAL (RACEMIC)



SR 202 is an antagonist of peroxisome proliferator-activated receptor γ (PPARγ) transcriptional activity induced by troglitazone but not of basal PPARγ activity. It is selective for PPARγ, not affecting basal or agonist-induced transcriptional activity of PPARα, PPARβ, or the farnesoid X receptor (FXR). It inhibits PPARγ-dependent differentiation of preadipocyte 3T3-L1 cells in a dose-dependent manner. SR 202 (400 mg/kg) decreases the amount of weight gained and white adipose tissue mass accumulated by mice fed a standard or high-fat diet for ten weeks and is associated with lower PPARγ mRNA levels. It protects against high-fat diet-induced insulin resistance in wild-type mice and improves insulin sensitivity in ob/ob mice.