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Restrict the search for
m momelotinib
to a specific field?
Status:
Investigational
Source:
NCT03397134: Phase 3 Interventional Completed Negative Symptoms of Schizophrenia
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
CYR-101 (MIN-101) is a cyclic amide derivative that has high equipotent affinities for 5-HT2A and sigma-2 receptors (Ki of 7.53 nM and 8.19 nM for 5-HT2A and sigma-2, respectively). MIN-101 also shows binding affinity for a1-adrenergic receptors but low or no affinity for muscarinic, cholinergic, and
histaminergic receptors. MIN-101 demonstrated statistically significant efficacy in reducing negative symptoms and good tolerability in stable schizophrenia patients. The drug is in phase II clinical trials for the treatment of Schizophrenia.
Status:
Investigational
Source:
NCT00005835: Phase 1 Interventional Completed Neuroblastoma
(2001)
Source URL:
Class (Stereo):
CHEMICAL (MIXED)
Buthionine sulfoximine (BSO) is a selective inhibitor of γ-glutamylcysteine synthetase (γ-GCS), the rate-limiting enzyme in glutathione (GSH) synthesis. In cancer cells, glutathione depletion significantly increased cytotoxicity via oxidative stress. In addition, in neuroblastoma cells susceptible to Buthionine sulfoximine treatment, DNA damage and cell apoptosis occurred via ROS production. Buthionine sulfoximine plus melphalan was effective in treatment for patients with recurrent/refractory neuroblastoma. Buthionine sulfoximine may also be used to increase the sensitivity of parasites to oxidative antiparasitic drugs. Buthionine sulfoximine has been shown to increase the efficacy of nifurtimox against T. cruzi and has also been shown to be an effective modulator of GSH-mediated chemoresistance by increasing the in vitro cytotoxicity of alkylating agents and radiation. Buthionine sulfoximine has been tested in animal studies and in human phase I trials for adults with solid tumors, with documented clinical responses in patients with melanoma, ovarian carcinoma and small cell carcinoma of the lung treated with the combination of Buthionine sulfoximine and melphalan.
Status:
Investigational
Source:
NCT03750786: Phase 3 Interventional Completed Colo-rectal Cancer
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
METHYLENETETRAHYDROFOLIC ACID, L-(+), an endogenous biomodulator that was developed under the brand name modufolin or arfolitixorin by the Isofol Medical. Arfolitixorin is developed to increase the efficacy of standard of care chemotherapy for advanced colorectal cancer. This drug is currently being studied in a global phase 3 clinical trial. Besides, the drug successfully completed phase II as rescue therapy for osteosarcoma. 21 May 2019 Isofol Medical has received clinical patent protection for the arfolitixorinin USA. It relates to a method of increasing blood concentration of deoxyuridine, a blood biomarker for inhibition of tumor growth in human cancer treatment.
Status:
Investigational
Source:
NCT00436852: Phase 2 Interventional Completed Disseminated Neuroblastoma
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
ABT-751 is an orally bioavailable antimitotic sulfonamide, which binds to the colchicine-binding site on beta-tubulin and inhibits the polymerization of microtubules, leads to a block in the cell cycle at the G2M phase, resulting in cellular apoptosis. ABT-751 had been in phase Ⅱ clinical studies for the treatment of breast cancer; colorectal cancer; non-small cell lung cancer; renal cancer, prostate cancer, but these researches have been discontinued.
Status:
Investigational
Source:
NCT01677780: Phase 1 Interventional Completed Myelogenous Leukemia, Chronic, Neoplasms, Myelogenous Leukemia, Acute
(2012)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
RO-5045337 (RG7112) is a small molecule that binds to a MDM2, a negative regulator of tumor-supressor protein p53. It was discovered by Roche and investigated in clinical trials against solid tumors, leukemias and sarcomas.
Status:
Investigational
Source:
NCT01472939: Phase 2 Interventional Completed Gastroesophageal Reflux Disease
(2012)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Revexepride is a selective 5-hydroxytryptamine receptor 4 agonist and member of a class of prokinetic agents that stimulate gastric emptying. Revexepride is thought to stimulate the release of acetylcholine at the myenteric plexus, leading to increased gastrointestinal contractions. This drug has been evaluated for potential use in treatment of gastroesophageal reflux disease. Phase I studies in healthy volunteers have shown no serious adverse events after administration of revexepride. However, a phase II study reported respiratory, thoracic and mediastinal disorders and pulmonary hypertension in 1 patient (0.85%). Furthermore, a European clinical trial showed that four weeks of treatment did not improve symptoms or gastric emptying in patients with symptoms suggestive of gastroparesis compared to placebo.
Status:
Investigational
Source:
NCT03042013: Phase 2 Interventional Withdrawn Subjects With NSCLC With an EGFR Activating Mutation
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Naquotinib (ASP8273) is an orally available, irreversible, mutant-selective, epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Naquotinib was found by mass spectrometry to covalently bind to a mutant EGFR (L858R/ T790M) via cysteine residue 797 in the kinase domain of EGFR with long-lasting inhibition of EGFR phosphorylation for 24 h. In the NSCLC cell lines harboring the above EGFR mutations, Naquotinib had IC50 values of 8-33 nM toward EGFR mutants, more potently than that of WT EGFR (IC50 value of 230 nM). In mouse xenograft models, Naquotinib induced complete regression of the tumors after 14 days of treatment. ASP8273 even showed activity in mutant EGFR cell line which is resistant to other EGFR TKIs. Naquotinib is in phase III clinical trials for the oral treatment of EGFR mutated non-small cell lung cancer (NSCLC).
Status:
Investigational
Source:
NCT01038804: Phase 2 Interventional Completed Breast Cancer
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Sepantronium bromide (YM155) is a selective survivin suppressant that exhibits potent antitumor activities by inducing apoptosis and autophagy in various types of cancer. Sepantronium bromide inhibited the growth of various human cancer cell lines in vitro with GI50 values in the low nM range. Sepantronium bromide blocked the growth of 119 human cancer cell lines, with the greatest inhibition in lines derived from non-Hodgkin's lymphoma, hormone-refractory prostate cancer, ovarian cancer, sarcoma, non-small-cell lung cancer, breast cancer, leukemia, and melanoma, with an average GI50 of 15 nM. Sepantronium bromide inhibited the growth of tumor cell lines regardless of their p53 status and demonstrated significant antitumor activity in 5 mice xenograft models. It also caused tumor regressions in vivo, possibly by its effects in reducing intratumoral survivin expression levels and increasing apoptosis. Sepantronium Bromide had been in phase II clinical trials by Astellas for the treatment of prostate cancer, melanoma, non-Hodgkin's lymphoma, breast cancer, diffuse large B cell lymphoma, non-small cell lung cancer (NSCLC) and other solid tumors. This compound had also been in clinical trials by National Cancer Institute (NCI) for the treatment of solid tumors (phase I) and advanced non-small cell lung cancer (NSCLC) (phase II). However, all these researches about this compound for all indications were discontinued.
Status:
Investigational
Source:
NCT01048255: Phase 2 Interventional Completed Partial Epilepsy
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Belnacasan (VX-765), and its active metabolite VRT- 043198, is a novel and irreversible IL-converting enzyme/ caspase-1 inhibitor. VRT-043198 exhibits 100- to 10,000-fold selectivity against other caspase-3, -6 and -9. It exhibited potent inhibition against ICE/caspase-1 and caspase-4 with Ki of 0.8 nM and less than 0.6 nM, respectively. And VRT-043198 also inhibits IL-1β release from both PBMCs and whole blood with IC50 of 0.67 uM and 1.9 uM, respectively. Belnacasan inhibits the release of IL-1, IL-18 and IL-33. Belnacasan has shown to inhibit acute partial seizures in preclinical models and has shown activity in preclinical models of chronic partial epilepsy that do not respond to currently available compounds for epilepsy. In addition, it seems to reduce disease severity and the expression of inflammatory mediators in models of rheumatoid arthritis and skin inflammation. Belnacasan had been in phase II clinical trials by Vertex for the treatment of epilepsy. However, this study has been terminated later.
Status:
Investigational
Source:
NCT02586155: Phase 3 Interventional Completed Diabetes Mellitus, Type 2
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Apabetalone (RVX-208) is a small molecule BET bromodomain inhibitor selective for BRD4-BD2 undergoing clinical development as a potential therapy to enhance ApoA-I production and treat atherosclerosis and prevent cardiovascular disease events. Apabetalone increases apolipoprotein A-I and high-density lipoprotein cholesterol (HDL-Cholesterol) in vitro and in vivo which is believed to provide a new approach to treating atherosclerosis through the stimulation of reverse cholesterol transport. RVX-208 increased the Tm of all BET bromodomains, indicative of binding. RVX-208 competes for acetylated histone H4 peptide binding to both bromodomains of BRD4, similar to JQ-1, but with a preference for BD2 over BD1. RVX-208 also binds to the bromodomains of BRDs 2 and 3 with a similar preference for BD2 (Kd~5–30 nM) over BD1 (Kd~2–3 uM). Treatment of humans for 1 week with oral RVX-208 increased apoA-I, pre-beta-HDL, and HDL functionality. Resverlogix Corp. has commenced a Phase 3 clinical trial in cardiovascular disease patients with type 2 diabetes mellitus with a primary endpoint of time to first occurrence of Major Adverse Cardiac Events (MACE).
