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Restrict the search for
dimethyl fumarate
to a specific field?
Status:
Investigational
Class (Stereo):
CHEMICAL (ACHIRAL)
Safotibant (previously known as LF22-0542) was developed as an antagonist at bradykinin B1 receptor for the topical treatment of diabetic macular edema. This drug participated in phase II clinical trials in Australia, in Belgium and in the Czech Republic. However, further, development was discontinued.
Status:
Investigational
Source:
NCT04176848: Phase 2 Interventional Active, not recruiting Breast Cancer
(2020)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Status:
Investigational
Source:
NCT00005976: Phase 2 Interventional Completed Brain and Central Nervous System Tumors
(2000)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Pyrazoloacridine is a pyrazolo[3,4,5-kl]acridine derivative patented by Warner-Lambert Co. as an anticancer agent. Pyrazoloacridine acts as topoisomerase I and II inhibitor that decrease the formation of topoisomerase-DNA adducts. In vitro experiments, Pyrazoloacridine shows efficacy against multidrug-resistant neuroblastoma doxorubicin-resistant human colon carcinoma and breast cancer cell lines. In clinical trials, Pyrazoloacridine demonstrates moderate efficacy in metastatic breast cancer and a high level of adverse events. The dose-limiting toxicity was grade 4 neutropenia. Other grade 3 and 4 toxicities include vomiting, nausea, neurotoxicity, fatigue, and anemia.
Status:
Investigational
Source:
NCT00684593: Phase 2 Interventional Completed Psoriasis
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT03838926: Phase 1 Interventional Unknown status Relapsed or Refractory Hematologic Malignancies
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Trichostatin A (TSA) was originally isolated as an antifungal antibiotic along with its fermentation congeners trichostatin B ((TSA)3-Fe) and the D-glucopyranosides trichostatin C and D. TSA inhibits HDAC in the low nanomolar range and is an inducer of histone hyperacetylation, both in vitro and in vivo. It inhibits all class I and II deacetylases to a similar extent in both tumor and non-tumor cells, although HDAC4 is slightly resistant when compared with HDAC1 and HDAC6. Class III HDAC is not affected by TSA. It has been shown that TSA dosedependently inhibits growth and induces apoptosis in a plethora of carcinoma cell lines in vitro. Recently, it was also found that TSA inhibits angiogenesis, which is important for the growth and metastasis of solid tumors, both in vivo and in vitro. In HT-29 colon carcinoma cells, a single dose of TSA induced transient hyperacetylation of histone H4 resulting in the induction of p21WAF1/Cip1 and inhibition of cellular proliferation at both the G1 and G2 phases of the cell cycle. Growth inhibition was associated with decreased cyclin D1 mRNA and cdk6 protein levels and increased cyclin D3 protein and p21WAF1/Cip1 mRNA levels. Cyclin D1 protein, cyclin D3 mRNA, cdk2 and cdk4 remained unaffected. In addition, TSA induced apoptosis by upregulating the expression of the pro-apoptotic genes ID1, ID2 and ID3, whereas the expression of the anti-apoptotic genes BclxL and Hsp27 was decreased In vivo, TSA induces differentiation and shows chemotherapeutic activity against N-methylnitrosureainduced rat mammary cancer without toxic side effects. TSA may also have therapeutic potential for the treatment of a variety of genetic and infectious diseases since silenced, transduced genes are reactivated probably due to structural changes of the chromatin on integrated viral sequences.
Status:
Investigational
Source:
NCT04207736: Phase 3 Interventional Completed Allergic Conjunctivitis
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Aldeyra’s lead product candidate, reproxalap (formerly ADX 102 or NS-2), is a small molecule RASP (Reactive Aldehyde Species) inhibitor in Phase 3 clinical development for the treatment of dry eye disease, allergic conjunctivitis, noninfectious anterior uveitis, and Sjögren-Larsson syndrome. NS-2 has been tested in a variety of in vitro and preclinical models, and has
demonstrated the ability to trap free aldehydes, diminish inflammation, reduce healing time, protect key cellular constituents from aldehyde damage, and lower the potential for scarring or fibrosis. NS-2 has been tested in a variety of toxicity studies in animals and appears to be generally safe and well tolerated. NS-2 has an orphan drug status for the treatment of Sjogren-Larsson syndrome.
Status:
Investigational
Source:
NCT03677492: Not Applicable Interventional Completed Infertility
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Cytochalasin D, a tropical fungal metabolite, is a disruptor of actin filament function, resulting in multinucleated cell formation, reversible inhibition of cell movement, and the induction of cellular extrusion. It was shown that cytochalasin D inhibits murine CT26 colorectal carcinoma cells growth and angiogenesis.
Status:
Investigational
Source:
NCT01471665: Phase 2 Interventional Completed Asthma
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Fiboflapon sodium (GSK2190915) is a high affinity 5-lipoxygenase-activating protein inhibitor being developed for the treatment of asthma. The compound was originally developed by Amira Pharmaceuticals. Fiboflapon sodium (GSK2190915) exhibits excellent preclinical toxicology and pharmacokinetics in rat and dog. GSK2190915 also demonstrated an extended pharmacodynamic effect in a rodent bronchoalveolar lavage (BAL) model. Oral administration of Fiboflapon sodium (GSK2190915) (1 mg/kg) resulted in sustained inhibition of ex vivo ionophore-challenged whole blood LTB4 biosynthesis with >90% inhibition for up to 12 h and an EC50 of approximately 7 nM. When rat lungs were challenged in vivo with calcium-ionophore, Fiboflapon sodium inhibited LTB4 and cysteinyl leukotriene (CysLT) production with ED50s of 0.12 mg/kg and 0.37 mg/kg, respectively. Fiboflapon sodium is in Phase-II for Asthma (Adjunctive treatment) in Poland, Ukraine, Bulgaria, USA, United Kingdom and Canada (PO).
Class (Stereo):
CHEMICAL (ABSOLUTE)
Suncillin is an antibacteria and antifungal agent produced in Phytera's laboratory from a cell culture of a plant. Suncillin was patented by Bristol-Myers Co. In 1968 for the Pseudomonas bacteria treatment but was never marketed.
Class (Stereo):
CHEMICAL (ABSOLUTE)
Ezlopitant (CJ-11974) is a non-peptide neurokinin-1 receptor antagonist. Pfizer was developing ezlopitant for the potential treatment of irritable bowel syndrome and chemotherapy-induced emesis. Development of ezlopitant has been discontinued.
