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Restrict the search for
amphotericin b
to a specific field?
Status:
Investigational
Source:
NCT00443924: Phase 1 Interventional Completed Ocular Hypertension
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Latrunculin B originates from Latrunculia (now Negombata) magnifica, a sponge from the Red Sea. Latrunculin B inhibits the assembly of actin microfilaments by 1:1 molecular binding of free actin monomers in the cell cytoplasm. It may be a potential therapeutic agent for glaucoma. Latrunculin B induced destabilization of the actin microfilament and apoptosis in a dose-dependent manner, as demonstrated by morphological changes and nuclear condensation in the PC3M cells. In addition, it resulted in an increase in the levels of gamma-H2AX recruitment, implicating the induction of DNA damage, including double-strand breaks. Induction of Bax, with little effect on Bcl-2 expression, indicated that actin disruption causes apoptosis through activation of Bax signaling in PC3M cells. This data might helps to develop the strategy for actin-based anticancer chemotherapy against highly metastatic prostate cancer.
Status:
Investigational
Source:
Pain. Feb 2005;113(3):360-368.: Not Applicable Human clinical trial Completed Pain/chemically induced
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Dextrorphan is an active metabolite of dextromethorphan, is an antitussive agent, which was found in cough medicines. Dextrorphan is a noncompetitive N-methyl-D-aspartate receptor (NMDAR) antagonist, sigma 1 receptor agonist, so as is an agonist of mu and kappa opioid receptors. In addition was found, that dextrorphan possessed anticonvulsive and neuroprotective effects.
Status:
Investigational
Source:
NCT01271270: Phase 1 Interventional Completed Age-Related Macular Degeneration
(2010)
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
RES-529 (previously named Palomid 529, P529) is a phosphoinositide 3-kinase (PI3K)/AKT/mechanistic target of rapamycin (mTOR) pathway inhibitor that interferes with the pathway through both mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2) dissociation. P529 inhibits tumor growth, angiogenesis, and vascular permeability. It retains the beneficial aspects of tumor vascular normalization that rapamycin boasts. This compound is currently being developed in oncology and ophthalmology. The oncology focus is for the treatment of glioblastoma, where it has received orphan designation by the US Food and Drug Administration, and prostate cancer.
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Oxidopamine (6-Hydroxydopamine) is an antagonist of the neurotransmitter dopamine with potential antineoplastic activity. 6-Hydroxydopamine (6-HOD) can be taken up by selective adrenergic terminals, thereby causing acute degeneration of adrenergic terminals that leads to depletion of norepinephrine, and of dopamine in the dopamine-sensitive sites. This agent is auto-oxidated at physiological pH that leads to the formation of reactive free radicals, thereby leading to cytotoxicity in neural cells. 6-Hydroxydopamine is often used to induce CNS and sympathetic neural lesions that model aging and various nervous disorders in animal systems. The growth of C-1300 neuroblastoma was markedly slowed in 6-hydroxydopamine-treated mice. The growth of the A-10 breast adenocarcinoma was also significantly retarded in 6-hydroxydopamine-treated mice but the growth of B-16 melanoma was not affected.
Status:
Investigational
Source:
NCT01827605: Phase 3 Interventional Active, not recruiting Relapsed Follicular Lymphoma
(2012)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Tricyclazole is a systemic fungicide for control of Pyricularia oryzae on rice. Tricyclazole protects plants from infection by P. oryzae by preventing penetration of the epidermis by the fungus. The compound acts by inhibiting melanization within the appressorium, thus causing a lack of rigidity in the appressorial wall. Tricyclazole has no apparent effect on spore germination although sporulation is reduced. Tricyclazole is not curative but is protective in its activity. Tricyclazole can influence the pathogenic ability of aspergillus aculeatus by damaging the cell structure of hyphae and conidia, reducing the melanin production, and altering the expression of pathogenic-related gene. Tricyclazole toxin can impair testosterone secretion and the testicular structure in mice, leaving an adversely effect on sperm production system.
Status:
Investigational
Source:
NCT00935844: Phase 1 Interventional Completed Advanced Solid Tumors
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Millennium (a wholly-owned subsidiary of Takeda) was developing TAK- 901 for the treatment of cancer. TAK-901 is an inhibitor of Aurora A/B with IC50 of 21 nM/15 nM. It is not a potent inhibitor of cellular JAK2, c-Src or Abl. TAK-901 is in phase I clinical trials by Millennium Pharmaceuticals for the treatment of advanced hematological malignancies. TAK-901 had been in phase I clinical trials for solid tumors. However, this study was discontinued.
Status:
Investigational
Source:
NCT01772199: Phase 2 Interventional Completed Multiple Sclerosis, Relapsing-Remitting
(2013)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
GlaxoSmithKline (GSK) was developing GSK-239512 as a histamine H3 receptor antagonist/inverse agonist as a monotherapy treatment for subjects with mild-to-moderate probable Alzheimer's disease (AD), multiple sclerosis and Schizophrenia. However, in March 2017, GSK globally discontinued the study of GSK-239512 at phase II.
Status:
Investigational
Source:
Eur J Cancer Clin Oncol. May 1986;22(5):601-5.: Phase 2 Human clinical trial Completed Breast Neoplasms
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Carubicin (also known as Carminomycin) is an anthracycline antineoplastic antibiotic isolated from the bacterium Actinomadura carminata. Carubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis. The drug is active against a variety of experimental tumors. Pharmacology studies in animals revealed that the drug bound largely to serum proteins and that it was widely distributed. In clinical trials The main toxic effect was myelosuppression but gastrointestinal intolerance and alopecia were also reported. Objective partial responses were seen in two of seven previously untreated patients with non-small cell lung cancer and one of three patients with squamous cell carcinoma of the head and neck previously untreated with chemotherapy.
Status:
Investigational
Source:
NCT01785992: Phase 2 Interventional Completed Locally Advanced Breast Cancer
(2012)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Irosustat is a first-generation, orally active, irreversible steroid sulfatase inhibitor. It did not stimulate the growth of estrogen-sensitive MCF-7 breast cells in vitro. Irosustat was in phase II clinical trials for the treatment of breast cancer and endometrial cancer and phase I clinical trial for the treatment of prostate cancer. However, this research has been discontinued.
Class (Stereo):
CHEMICAL (RACEMIC)
Diacetolol is the major metabolite of the β-adrenoceptor blocking agent, acebutolol. In vitro, the β-adrenoceptor blocking potency of diacetolol was less than that of acebutolol but its cardioselectivity (atrial relative to tracheal tissue) was greater. Diacetolol had weak intrinsic sympathomimetic activity, and no significant membrane-stabilizing activity. It did not restore sinus rhythm to anaesthetized dogs with ouabain-induced arrhythmias but was similar to acebutolol in preventing arrhythmia induced by adrenaline/methylchloroform in anaesthetized cats. Study of diacetolol pharmacokinetics and bioavailability suggests either a first-pass effect or incomplete absorption of diacetolol after oral administration. Diacetolol plasma half-life after oral administration is about 12 h and is not dose-dependent. Diacetolol possesses significant antihypertensive action against moderate essential hypertension in man. Its antihypertensive effect is associated with a reduction in the heart rate and a decrease in plasma renin activity.
