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Restrict the search for
angiotensin ii
to a specific field?
Status:
Investigational
Source:
INN:declopramide [INN]
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Declopramide is an apoptosis inducer. Also, it inhibits NFkappaB activation by inhibition of IkappaBbeta breakdown. In preclinical research, Declopramide demonstrated strong antitumor properties. It had been in phase II clinical trials for the treatment of colorectal cancer. However, this research has been discontinued.
Status:
Investigational
Source:
NCT00096239: Phase 2 Interventional Completed Fallopian Tube Cancer
(2004)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Pfizer's CP-547632 is a selective inhibitor of VEGFR-2 tyrosine kinase that was discovered during Pfizer's collaboration with OSI Pharmaceuticals. CP-547632, was identified as a potent inhibitor of the VEGFR-2 and basic fibroblast growth factor (FGF) kinases (IC(50) = 11 and 9 nM, respectively). It is selective relative to epidermal growth factor receptor, platelet-derived growth factor beta, and other related TKs. It also inhibits VEGF-stimulated autophosphorylation of VEGFR-2 in a whole cell assay with an IC(50) value of 6 nM. After oral administration of CP-547632 to mice bearing NIH3T3/H-ras tumors, VEGFR-2 phosphorylation in tumors was inhibited in a dose-dependent fashion (EC(50) = 590 ng/ml). CP-547,632 is a well-tolerated, orally-bioavailable inhibitor presently under clinical investigation for the treatment of human malignancies. CP-547632 is in phase I for the treatment of diabetic retinopathy and age-related macular degeneration.
Status:
Investigational
Source:
NCT03598309: Phase 2 Interventional Recruiting Lung Diseases
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Demethoxycurcumin is a derivative or curcumin and represents one of the major active components of curcumin products isolated from Curcumae sp. In preclinical models, Demethoxycurcumin inhibits LPS-induced nitric oxide (NO) production, and expression of iNOS and COX2 in RAW264.7 cells by blocking NF-kB activation. Demethoxycurcumin also inhibits NF-kB dependent iNOS, TNFα and IL-1β expression in LPS-treated rat microglial cells. Demethoxycurcumin suppresses the expression of MMPs and ICAM-1 in MDA-MB-231 human breast cancer cells by inhibition of NF-kB. Demethoxycurcumin is currently in Phase I clinical trials.
Status:
Investigational
Source:
NCT00116909: Phase 2 Interventional Completed Locally Recurrent or Metastatic Cancer of the Head and Neck
(2004)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
OSI-7904L is a liposomal formulation of the highly specific, noncompetitive thymidylate synthase inhibitor OSI-7904 (also known as GW1843, BW1843U89, and GS7904). The liposome formulation was developed to enhance the therapeutic index and dose schedule convenience of this potent antifolate compound. This drug was studied in phase II clinical trial in patients to treat head and neck cancer, gastroesophageal adenocarcinoma and advanced biliary cancer, but these studies were discontinued. As an example in case of OSI-7904L, was revealed that its activity was below a level of clinical relevance in advanced biliary tract cancer, providing only a small degree of disease stabilization.
Status:
Investigational
Source:
NCT00978250: Phase 2 Interventional Completed Head and Neck Neoplasms
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
5-Fluoro-2-deoxycytidine is a fluorinated pyrimidine analog antimetabolite with potential antineoplastic activity. As a prodrug, 5-fluoro-2-deoxycytidine is converted by intracellular deaminases to the cytotoxic agent 5-fluorouracil (5-FU). 5-FU is subsequently metabolized to active metabolites including 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP). FdUMP binds to and inhibits thymidylate synthase, thereby reducing the production of thymidine monophosphate, which leads to depletion of thymidine triphosphate and the inhibition of DNA synthesis and cell division. FUTP competes with uridine triphosphate (UTP) for incorporation into the RNA strand, which results in the inhibition of RNA and protein synthesis and cell proliferation. 5-Fluoro-2-deoxycytidine undergoing trials to test its effectiveness in treating cancer that has not responded to standard therapies.
Status:
Investigational
Source:
NCT00064142: Phase 2 Interventional Completed AIDS-related Kaposi Sarcoma
(2003)
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Halofuginone is a low molecular weight quinazolinone alkaloid, and a potent inhibitor of collagen alpha1(I) and matrix metalloproteinase 2 (MMP-2) gene expression. Halofuginone also effectively suppresses tumor progression and metastasis in mice. Halofuginone is a potent inhibitor of collagen a1(I) and matrix metalloproteinase 2 (MMP-2) gene expression. Halofuginone also suppresses extracellular matrix deposition and cell proliferation. Also was shown that halofuginone increased apoptosis in α smooth muscle actin- and prolyl 4-hydroxylase β-expressing cells in mdx diaphragm and in myofibroblasts, the major source of extracellular matrix. The profound antitumoral effect of halofuginone is attributed to its combined inhibition of tumour-stromal support, vascularization, invasiveness, and cell proliferation. HT-100 (delayed-release halofuginone), currently in clinical phase 1b/2a in five U.S. hospitals, is a small molecule drug candidate taken orally for the treatment of Duchenne muscular dystrophy (DMD) patients primarily through its ability to reduce fibrosis and inflammation and promote muscle fiber regeneration. The medicine candidate has been granted orphan drug designation in the U.S. and the EU — meaning it has been commercially undeveloped due to its limited profitability — and fast-track designation in the U.S. — an FDA process that aims to facilitate the development and patients’ reach to novel therapies for unmet medical needs.
Status:
Investigational
Source:
NCT00318500: Phase 2 Interventional Completed Dysmenorrhea
(2006)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Prinaberel is a selective agonist of estrogen receptor beta. Although initially developed for the treatment of endometriosis, the drug was also shown to be effective in vitro in other inflammatory diseases. Phase II clinical studied revealed its effectiveness in case of Crohn's disease and endometriosis, but the drug failed to demonstrate antiinflammatory efficacy in RA patients.
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Fandofloxacin is a difluoroquinolone derivative. This compound possesses an antibacterial spectrum comparable to those of rufloxacin and ciprofloxacin in vivo. Fandofloxacin showed a rapid and nearly complete absorption, and a long residence time in the body. Because it has been reported that the in vivo antibacterial activity of Fandofloxacin is comparable or superior to other quinolones, despite the fact that its in vitro activity is significantly lower than that of the other compounds, the pharmacokinetics of this antibiotic may be responsible, at least in part, for the enhanced in vivo antibacterial activity of Fandofloxacin. Fandofloxacin is an inhibitor of bacterial DNA gyrase. The toxicities and adverse effects of Fandofloxacin observed in various toxicology studies and clinical trials were less than those of commercially available drugs. It has been in phase II clinical trial for the treatment of Urinary tract infections. However, this research has been discontinued in 2008.
Status:
Investigational
Source:
INN:pralnacasan [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Pralnacasan is a potent, non-peptide inhibitor of interleukin-1beta converting enzyme (ICE, aka Caspase-1). It was originally discovered by Vertex Pharmaceuticals and licensed for development to Aventis Pharma. In 2003 Aventis and Vertex Pharmaceuticals agreed to voluntarily discontinue development based on results from a 9-month animal toxicity trial that showed liver abnormalities due to chronic high doses of pralnacasan. Pralnacasan has also been investigated for the treatment of Partial Epilepsy; advancing to Phase II clinical trials.
Status:
Investigational
Source:
NCT03292406: Phase 2 Interventional Completed Cutaneous T Cell Lymphoma
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Resiquimod is an imidazoquinolinamine and Toll-like receptor (TLR) agonist with potential immune response modifying activity. Resiquimod exerts its effect through the TLR signaling pathway by binding to and activating TLR7 and 8 mainly on dendritic cells, macrophages, and B-lymphocytes. This induces the nuclear translocation of the transcription activator NF-kB as well as activation of other transcription factors. This may lead to an increase in mRNA levels and subsequent production of cytokines, especially interferon-alpha (INF-a) and other cytokines, thereby enhancing T-helper 1 (Th1) immune responses. In addition, topical application of resiquimod appears to activate Langerhans' cells, leading to an enhanced activation of T-lymphocytes. Resiquimod is used as a topical gel[1] in the treatment of skin lesions[2] such as those caused by the herpes simplex virus[3][4] and cutaneous T cell lymphoma. Due to its immunostimulatory activity, this agent may potentially be used as a vaccine adjuvant.
