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Restrict the search for
clindamycin phosphate
to a specific field?
Status:
Investigational
Source:
NCT00725933: Phase 1 Interventional Completed Advanced Solid Tumors
(2008)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT01466322: Phase 1 Interventional Completed Multiple Sclerosis, Relapsing-Remitting
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT00482287: Phase 2 Interventional Withdrawn Hypotension
(2008)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
TrioxBio's API, S-ethylisothiouronium diethylphosphate, MTR-104 (MTR- 105), is a nitric oxide synthase (NOS) inhibitor which blocks the production of nitric oxide, preventing the dilation of blood vessels and the other detrimental effects caused by excessive NOS activity. MTR-105, a
fast-acting synthetic NOS inhibitor with rapid onset of action when administered parenterally, has
been effective in alleviating hypotension experimentally
and in several observational studies while reducing NO
production. MTR-105 is registered and approved for clinical use in the Republic of Moldova where data have been
collected from 434 patients exposed to the drug in pre- and postapproval clinical investigations.
Status:
Investigational
Source:
NCT03189914: Phase 1/Phase 2 Interventional Completed Metastatic Pancreatic Cancer
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Fluorocyclopentenylcytosine (RX-3117) is a novel small molecule nucleoside compound that is incorporated into DNA or RNA of cancer cells and inhibits both
DNA and RNA synthesis which induces apoptotic cell death of tumor cells. Fluorocyclopentenylcytosine also mediates the down-regulation of DNA
methyltransferase 1 (DNMT1), an enzyme responsible for the methylation of cytosine residues on newly synthesized DNA and
also a target for anticancer therapies. Preclinical studies have shown Fluorocyclopentenylcytosine to be effective in both inhibiting the growth of
various human cancer xenograft models, including colon, lung, renal and pancreas, as well as overcoming chemotherapeutic
drug resistance.
Fluorocyclopentenylcytosine has demonstrated a broad spectrum anti-tumor activity against 50 different human cancer cell lines and efficacy in 12
different mouse xenograft models. The efficacy in the mouse xenograft models was superior to that of gemcitabine. In addition,
in human cancer cell lines made resistant to the anti-tumor effects of gemcitabine, Fluorocyclopentenylcytosine still retains its full anti-tumor
activity.
In August 2012, Rexahn reported the completion of an exploratory Phase I clinical trial of Fluorocyclopentenylcytosine in cancer patients conducted
in Europe, to investigate the oral bioavailability, safety and tolerability of the compound. In this study, oral administration of Fluorocyclopentenylcytosine demonstrated an oral bioavailability of 34-58% and a plasma half-life (T1/2) of 14 hours. In addition, Fluorocyclopentenylcytosine was safe
and well tolerated in all subjects throughout the dose range tested. Fluorocyclopentenylcytosine is in phase I/II clinical trials by Rexahn for the treatment of bladder cancer and pancreatic cancer. This compound was granted Orphan Drug Designation by the U.S. Food and Drug Administration (FDA) for the treatment of patients with pancreatic cancer in September 2014.
Status:
Investigational
Source:
NCT02471846: Phase 1 Interventional Completed Solid Tumor
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
NLG919 is a novel small-molecule IDO-pathway inhibitor. NLG919 potently inhibits this pathway in vitro and in cell-based assays. It is orally bioavailable and has a favorable pharmacokinetic and toxicity profile. In mice, a single oral administration of NLG919 reduces the concentration of plasma and tissue Kyn by ∼ 50%. Using IDO-expressing human monocyte-derived DCs in allogeneic MLR reactions, NLG919 potently blocked IDO-induced T cell suppression and restored robust T cell responses with an ED50=80 nM. Similarly, using IDO-expressing mouse DCs from tumor-draining lymph nodes, NLG919 abrogated IDO-induced suppression of antigen-specific T cells (OT-I) in vitro. In vivo, in mice bearing large established B16F10 tumors, administration of NLG919 markedly enhanced the anti-tumor responses of naïve, resting pmel-1 cells to vaccination with cognate hgp100 peptide plus CpG-1826 in IFA
Status:
Investigational
Source:
NCT01060475: Phase 1 Interventional Completed Healthy
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT01226407: Phase 1 Interventional Unknown status Solid Tumour
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
CG-200745 is a novel inhibitor of histone deacetylases (HDACs), initially developed by CrystalGenomics, Inc for treatment of various hematological and solid cancers. Combinations of CG-200745 with SN38 (the active form of irinotecan), or oxaliplatin were more effective than the agents alone when used to inhibit the growth of HCT116 cells. The protein expressions of acetyl-H3, p21, caspase-3, -8, and -9, PARP, and XIAP were affected in a time- and dose-dependent manner in HCT116 cells treated with the CG-200745 alone or combined CG-200745 and SN-38. In HCT116 xenografts, the HDACI CG-200745 in combination with irinotecan dramatically inhibited tumor growth without showing additive toxicity.
Status:
Investigational
Source:
NCT03742037: Phase 2 Interventional Completed Systemic Lupus Erythematosus
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Cenerimod is an orally available sphingosine-1-phosphate receptor 1 (S1P1) modulator that is being developed by Idorsia Pharmaceuticals for the treatment of systemic lupus erythematosus. Sphingosine-1-phosphate (S1P), a lipid mediator, regulates lymphocyte migration between lymphoid tissue and blood. Cenerimod is a potent, selective, safe and orally administrable S1P1 receptor modulator, which reportedly reduced blood lymphocytes and attenuated murine experimental autoimmune encephalomyelitis (EAE) in a murine model. Cenerimod has potential as novel therapy with an improved safety profile for autoimmune diseases with a high unmet medical need.
Status:
Investigational
Source:
NCT03387215: Phase 1/Phase 2 Interventional Completed Heart Failure, Systolic
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Status:
Investigational
Source:
NCT02106338: Phase 1 Interventional Completed Clostridium Difficile Infection
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
CRS-3123, also known as REP-3123, is a methionyl-tRNA synthetase inhibitor potentially for the treatment of enteric infections. CRS-3123 is in Phase 1 clinical development for the treatment of Clostridium difficile Infection (CDI). CRS-3123 is a small molecule protein synthesis inhibitor that acts on the novel target methionyl-tRNA synthetase (MetRS). REP-3123 has been shown to be active in vitro against clinical
isolates of C. difficile including epidemic strains such as B1/
NAP1/027; MIC values of REP-3123 for C. difficile are
typically 0.5 -- 1.0 mg/l. REP-3123 is also active against a range of clinically important aerobic Gram-positive bacteria
including methicillin-susceptible and -resistant Staphylococcus
aureus (MIC90 values of 0.06 and 0.25 mg/l, respectively),
Streptococcus pyogenes (MIC90 0.5 mg/l) and enterococci
(MIC90 32 mg/l). CRS-3123 has numerous potential advantages over current CDI therapies. In addition to being highly potent against all clinical isolates of C. difficile tested, CRS-3123 has several desirable qualities for the treatment of CDI which include:
Narrow spectrum for C. difficile, which may substantially reduce the disruption of normal intestinal flora compared to current therapies;
Inhibition of toxin production, potentially leading to lower morbidity and mortality;
Inhibition of sporulation, potentially leading to lower rates of transmission and recurrence;
A novel mechanism of action, which means that its use will not compromise the utility of systemic antibiotics while maintaining activity against pre-existing resistance mechanisms.
