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Restrict the search for
dimethyl fumarate
to a specific field?
Status:
Investigational
Source:
NCT03653546: Phase 2/Phase 3 Interventional Completed Non-small Cell Lung Cancer
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
AZD-3759 is an oral inhibitor of both wild-type and mutant EGFR with IC50 values in nanomolar range. The drug was discovered by AstraZeneca for the treatment of non-small-cell lung cancer with CNS metastases. AZD-3759 can penetrate the blood-brain barrier and was confirmed to be effective in vitro with NSCLC cell lines as well as in mouse model of brain metastases. AZD-3759 is currently in Phase 1 clinical trial.
Status:
Investigational
Source:
NCT02521844: Phase 1 Interventional Active, not recruiting Solid Tumors
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
ETC-159 (ETC-1922159) is an inhibitor of membrane-bound O-acyltransferase porcupine. Porcupine palmitoleates Wnt and this modification is essential for binding to chaperone WLS and Frizzled receptors and is therefore required for the activity of all Wnts. ETC-159 exerts antineoplastic properties both in vitro and in vivo due to inhibition of Wnt pathway. ETC-159 development has progressed to phase I clinical trial.
Status:
Investigational
Source:
NCT00751803: Phase 2 Interventional Completed Migraine Disorders
(2008)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
BI 44370 was developed as a calcitonin gene-related peptide receptor antagonist for the treatment of acute migraine attacks. In spite of the positive results from the phase II clinical trials, the BI-44370 study has been discontinued.
Status:
Investigational
Source:
NCT01971554: Phase 1 Interventional Completed Type 2 Diabetes Mellitus
(2013)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT03813160: Phase 3 Interventional Completed Dermatomyositis
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Ajulemic acid, designated as Resunab™, is being developed by Corbus Pharmaceuticals, for the treatment of cystic fibrosis, systemic sclerosis, systemic lupus erythematosus.Ajulemic acid (AJA) is a first-in-class, synthetic, orally active, cannabinoid-derived drug that preferentially binds to the CB2 receptor and is nonpsychoactive. In preclinical studies, and in Phase 1 and 2 clinical trials, AJA showed a favorable safety, tolerability, and pharmacokinetic profile. It also demonstrated significant efficacy in preclinical models of inflammation and fibrosis. It suppresses tissue scarring and stimulates endogenous eicosanoids that resolve chronic inflammation and fibrosis without causing immunosuppression. AJA is currently being developed for use in 4 separate but related indications including systemic sclerosis (SSc), cystic fibrosis, dermatomyositis (DM), and systemic lupus erythematosus. Phase 2 clinical trials in the first 3 targets demonstrated that it is safe, is a potential treatment for these orphan diseases and appears to be a potent inflammation-resolving drug with a unique mechanism of action, distinct from the nonsteroidal anti-inflammatory drug (NSAID), and will be useful for treating a wide range of chronic inflammatory diseases.
Status:
Investigational
Source:
NCT00357357: Phase 2 Interventional Completed Alzheimer's Disease
(2006)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Class (Stereo):
CHEMICAL (RACEMIC)
Pranolium (UM-272) is propranolol derivative. It can reduce the extent of myocardial injury sustained during severe ischemia. UM-272 lacks significant beta-adrenergic blocking activity but retains the negative chronotropic, negative inotropic and antiarrhythmic effects common to both d- and l-propranolol. The protective effects of UM-272 during myocardial ischemia cannot be due to metabolic effects of the beta-adrenergic blockade but may be due to effects on oxygen consumption or to effects on myocardial membrane properties that are related to its antiarrhythmic and myocardial depressant activity. The ability of UM-272 to enhance blood flow to subendocardial myocardium may also play a role in its beneficial effects during ischemia. UM-272 may protect the ischemic heart through direct effects on myocardial Ca++ regulating mechanisms. UM-272 has kinetically similar use-dependent inhibitory action of the fast sodium channels of cardiac muscles as other Class Ia antiarrhythmic drugs like quinidine or procainamide. Pranolium was investigated as an antiarrhythmic agent.
Status:
Investigational
Source:
NCT01984294: Phase 2 Interventional Completed Chronic HCV Infection
(2013)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Radalbuvir (also known as GS-9669 ) is a Hepatitis C virus NS 5 protein inhibitor for the treatment of hepatitis C virus (HCV) infection developed by Gilead Sciences. Radalbuvir is a highly optimized thumb site II nonnucleoside inhibitor, with a binding affinity of 1.35 nM for the genotype (GT) 1b protein. It is a selective inhibitor of HCV RNA replication, with a mean 50% effective concentration of ≤ 11 nM in genotype 1 and 5 replicon assays, but lacks useful activity against genotypes 2 to 4. In preclinical Radalbuvir exhibited at least additive activity in combination with agents encompassing four other direct modes of action (NS3 protease, NS5A, NS5B via an alternative allosteric binding site, and NS5B nucleotide) as well as with alpha interferon or ribavirin in replicon assays. It exhibited high metabolic stability in vitro human liver microsomal assays, which, in combination with its pharmacokinetic profiles in rat, dog, and two monkey species, is predictive of good human pharmacokinetics. In clinical trials, Radalbuvir shows highly effective inhibition of wild-type HCV.
Status:
Investigational
Source:
NCT04542499: Phase 3 Interventional Completed Parkinson Disease
(2020)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Stercuronium is a conessine derivative patented by Koninklijke Nederlandsche Gist-en Spiritusfabriek N. V. as a competitive neuromuscular blocking agent with antimuscarinic activity. In preclinical models, Stercuronium produced significantly greater inhibition (P < 0.05) of the bradycardia than of the vasodepressor response produced by carbachol. In guinea-pig atria, the negative chronotropic response to carbachol was inhibited to a similar degree to the negative inotropic response by Stercuronium, whereas in bladder and ileum Stercuronium was 17 fold less active as an antimuscarinic drug. The affinity of Stercuronium for the prejunctional muscarinic receptor on sympathetic nerve endings in the rabbit ear artery was similar to that for the muscarinic receptor mediating negative inotropic responses to carbachol in the rabbit left atrium. Unfortunately, in clinical trials Stercuronium producing marked tachycardia in some patients when used as a muscle relaxant.
