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Restrict the search for
betamethasone phosphate
to a specific field?
Status:
Investigational
Source:
JAN:DERSIMELAGON PHOSPHORIC ACID [JAN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT01225536: Phase 1 Interventional Completed Solid Tumor
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
INN:emavusertib [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
INN:fosifloxuridine nafalbenamide [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
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NCT00482287: Phase 2 Interventional Withdrawn Hypotension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:
INN:roducitabine [INN]
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
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Navoximod (formerly NLG 919, GDC 0919), a small molecule, orally bioavailable, immune checkpoint inhibitor, is being developed by NewLink Genetics for the treatment of solid tumours. Navoximod is a potent IDO (indoleamine-(2,3)-dioxygenase) pathway inhibitor with Ki/EC50 of 7 nM/75 nM. Upon administration, navoximod targets and binds to IDO1, a cytosolic enzyme responsible for the oxidation of the essential amino acid tryptophan into kynurenine. By inhibiting IDO1 and decreasing kynurenine in tumor cells, this agent increases tryptophan levels, restores the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells, and T-lymphocytes, and causes a reduction in tumor-associated regulatory T-cells (Tregs). Activation of the immune system, which is suppressed in many cancers, may induce a cytotoxic T-lymphocyte (CTL) response against the IDO1-expressing tumor cells. IDO1 is overexpressed by a variety of tumor cell types and plays an important role in immunosuppression. Tryptophan depletion is associated with immunosuppression caused by T-cell suppression. Navoximod is under investigation in clinical trial NCT02048709 (Indoleamine 2,3-Dioxygenase (IDO) inhibitor in advanced solid tumors).
Status:
Investigational
Source:
NCT01060475: Phase 1 Interventional Completed Healthy
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
