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

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Showing 541 - 550 of 1728 results

Status:
Investigational
Source:
INN:tivanidazole
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Tivanidazole is metronidazole derivative. It is antiprotozoal drug. Tivanidazole was used as trichomonacide.
Status:
Investigational
Source:
INN:tivirapine
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)

Tivirapine, also known as R-86183, is a HIV-1 specific reverse transcriptase inhibitor. It inhibits the replication of HIV-1, but not HIV-2, in a variety of CD4+ T-cell lines and peripheral blood lymphocytes. Whereas an HIV-1 strain containing the Leu-100-->Ile mutation in the RT gene is about 400-fold less susceptible, R86183 still inhibits the replication of an HIV-1 strain containing the Tyr-181-->Cys RT mutation by 50% at a concentration of 130 nM. Tivirapine had been in phase I clinical trial for the treatment of HIV-1 infection. However, this development was discontinued.
Status:
Investigational
Source:
INN:sulfaclorazole
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Sulfaclorazole is a benzenesulfonamide derivative patented by Farbwerke Hoechst A.-G. as an antibacterial agent that active against Streptococcus pyogenes.
Status:
Investigational
Source:
INN:opiniazide [INN]
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

OPINIAZIDE (also known as saluzid) was used for the treatment of meningeal tuberculosis in adults and in children. Information about the current use of this drug is not available.
Status:
Investigational
Source:
INN:oxifungin
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Oxifungin was developed as an antifungal agent. However, information about the current use of this compound is not available.
Status:
Investigational
Source:
USAN:Ancriviroc
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Ancriviroc (SCH 351125) is a small-molecule antagonist of the human immunodeficiency virus type 1(HIV-1) coreceptor CCR5. It has in vitro activity against R5 viruses with 50% inhibitory concentrations ranging from 1.0 to 30.9 nM. Ancriviroc is an orally bioavailable small molecule inhibitor of HIV-1 entry via CCR5 coreceptor interaction. Ancriviroc has potent activity against RANTES binding (K(i) = 2 nM), possesses subnanomolar activity in blocking viral entry and has excellent antiviral potency versus a panel of primary HIV-1 viral isolates. Ancriviroc had been in phase I clinical trials by Schering-Plough (subsidiary of Merck Sharp & Dohme) for the treatment of HIV infection. However, this research has been discontinued.
Status:
Investigational
Source:
NCT00002413: Phase 2 Interventional Completed HIV Infections
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)


MKC-442 (6-benzyl-1-(ethoxymethyl)-5-isopropyl-uracil) is a highly potent and selective inhibitor of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT). Emivirine structurally is a nucleoside analog (NRTI) molecule, but it functions as a non-nucleoside reverse transcriptase inhibitor (NNRTI). Emivirine had reached phase 3 clinical trials for the treatment of HIV-1 infections before its further development was stopped.
Status:
Investigational
Source:
INN:triafungin
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Triafungin is the antifungal agent.
Status:
Investigational
Source:
JAN:NANAFROCIN [JAN]
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)


Conditions:

Nanafrocin (nanaomycin A) belongs to the class of quinone antibiotics isolated from a strain OS-3966 of Streptomyces rosa var. notoensis. Nanafrocin (nanaomycin A) mode of action is dependent on its reduction by the respiratory chain-linked NADH or flavin dehydrogenase of the organism. The reduced form of nanafrocin (nanaomycin A) is quickly auto-oxidized by molecular oxygen producing singlet molecular oxygen (O2−). The ability to produce O2− is related to the antimicrobial activity of nanafrocin (nanaomycin A).
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.