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Restrict the search for
phenyl aminosalicylate
to a specific field?
Status:
Investigational
Source:
NCT00880217: Phase 2 Interventional Completed Attention Deficit Hyperactivity Disorder
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Bavisant (also known as JNJ-31001074 or BEN-2001), a highly selective, active antagonist of the human H3 receptor that was invented by Johnson & Johnson for the treatment of attention-deficit hyperactivity disorder (ADHD). However, the result of clinical trials did not display significant clinical effectiveness in the treatment of adults with ADHD. BenevolentAI has started phase II clinical trials where investigated bavisant for ameliorating the excessive daytime sleepiness in patients with Parkinson’s disease, using one of the drug side effects is dose-dependent insomnia.
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Mefenidil has been reported to be a selective cerebral vasodilator. It significantly increased cerebral blood flow (without stimulation of O2 uptake) and lowered cerebral vascular resistance without having significant effects in other circulatory regions. Increase in cerebral blood flow is not mediated via the beta-adrenergic receptor as the effect was not blocked by propranolol. However, the clinical usefulness of mefenidil as a cerebral vasodilator may be limited by the accompanying arterial hypotension due to systemic vasodilation, which was most prominent in heart and gut.
Status:
Investigational
Source:
NCT00405054: Phase 2 Interventional Terminated Leukemia
(2006)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Tozasertib, originally developed as VX-680 by Vertex (Cambridge, MA) and later renamed MK-0457 by Merck (Whitehouse Station, NY), was the first aurora kinase inhibitor to be tested in clinical trials. The drug, a pyrimidine derivative, has affinity for all aurora family members at nanomolar concentrations with inhibitory constant values (Ki(app)) of 0.6, 18, and 4.6 nM for aurora A, aurora B, and aurora C, respectively. Preclinical studies confirmed that tozasertib inhibited both aurora A and aurora B kinase activity, and activity has been reported against prostate, thyroid, ovarian, and oral squamous cancer cell lines. Upon treatment with tozasertib, cells accumulate with a 4N DNA content due to a failure of cytokinesis. This ultimately leads to apoptosis, preferentially in cells with a compromised p53 function. Tozasertib is an anticancer chemotherapeutic pan-aurora kinase (AurK) inhibitor that also inhibits FMS-like tyrosine kinase 3 (FLT3) and Abl. Tozasertib is currently in clinical trials as a potential treatment for acute lymphoblastic leukemia (ALL). In cellular models of cancer, tozasertib activates caspase-3 and PARP and decreases expression of HDAC, increasing apoptosis and inhibiting cell growth. In other cellular models, tozasertib inhibits cell proliferation and metastasis by blocking downstream ERK signaling and downregulating cdc25c and cyclin B. This compound also decreases tumor growth in an in vivo model of prostate cancer.
Status:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT00102973: Phase 3 Interventional Completed Ovarian Neoplasms
(2004)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Canfosfamide is a modified glutathione analogue and nitrogen mustard prodrug, with potential antineoplastic activity. Canfosfamide is selectively activated by glutathione S-transferase P1-1 an enzyme that is over-expressed in many human cancers including ovarian cancer. GST P1-1-mediated cleavage leads to an active cytotoxic phosphorodiamidate alkylating metabolite that forms covalent linkages with nucleophilic centers in tumor cell DNA, which may induce a cellular stress response and cytotoxicity, and decrease tumor cell proliferation. Preclinical studies showed that canfosfamide inhibited the growth and was cytotoxic to a wide range of established cancer cell lines including those derived from ovarian cancer (OVCAR3, HEY, SK-OV-3). Canfosfamide treatment inhibited cancer cell proliferation and induced apoptosis through the activation of the cellular stress response kinase pathway. The cytotoxic activity of canfosfamide correlated with the expression of GST P1-1. Cancer cells in which GST expression levels were increased by transfection with the GST P1-1 gene, were more sensitive to the cytotoxic effects of canfosfamide than the parental cell lines Canfosfamide in combination with pegylated liposomal doxorubicin is well tolerated and active in platinum and paclitaxel refractory or resistant ovarian cancer.
Status:
Investigational
Source:
NCT01482221: Phase 2 Interventional Completed Major Depressive Disorder
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Lanicemine is a low-trapping NMDA channel blocker, which was developed by Fisons Pharmaceuticals and later by AstraZeneca for the treatment of the major depressive disorder. The development was terminated in phase II as the drug did not meet the primary endpoint.
Status:
Investigational
Source:
NCT00280631: Phase 1/Phase 2 Interventional Completed Myelodysplastic Syndrome (MDS)
(2006)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Ezatiostat (TLK199) [γ-glutamyl-S-(benzyl)cysteinyl-R-phenyl glycine diethyl ester] is an inhibitor of Glutathione S-transferase P1–1 (GSTπ). The drug is a peptidomimetic of GSH (glutathione), esterified to enhance cellular uptake and designed to bind to the “G-site” of GSTP1–1. Independent of catalysis inhibition, TLK199 also disrupts the protein:protein interaction site(s) between GSTP1–1 and JNK1. Telik Inc was developing TLK-199 for the potential prevention of myelosuppression in blood diseases, namely myelodysplastic syndrome.
Class (Stereo):
CHEMICAL (ACHIRAL)
Glicetanile is a derivative of sulphonamides (antibacterial sulfa drugs). It has antihyperglycemic activity. The compound is metabolized and eliminated by the body rapidly after both oral and intravenous administration, and therefore prevents adverse hypoglycemic effects.
Status:
Investigational
Source:
NCT01188967: Phase 2 Interventional Completed Nicotine Dependence
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02249949: Phase 2 Interventional Completed Liposarcoma
(2015)
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Efatutazone (CS-7017 or RS-5444) is a peroxisome proliferator-activated receptor gamma (PPAR-gamma) agonist with antineoplastic properties. Mediated through activation of PPAR-gamma, this agent is capable of inducing cell differentiation and apoptosis, thereby leading to a reduction in cellular proliferation. Efatutazone was in clinical trials for the treatment of solid tumors however; its development has been discontinued.
