{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
Restrict the search for
angiotensin ii
to a specific field?
Status:
Investigational
Source:
NCT01063907: Phase 1/Phase 2 Interventional Completed Multiple Myeloma
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
KW-2478 is a novel and potent non-ansamycin inhibitor of heat shock protein 90 designed to overcome the limitations, including low water solubility and hepatotoxicity, of 17-allylamino-17-demethoxygeldanamycin (17-AAG). KW-2478 exerts a strong antitumor activity against multiple myeloma (MM) cells with various chromosomal translocations. KW-2478 inhibits cell growth and apoptosis associated with Hsp90 client protein degradation. Recent study results have revealed that KW-2478 is able to deplete Hsp90 client Cdk9 and the phosphorylated 4E-BP1, a transcriptional kinase and a transcription inhibitor respectively, leading to reduced expression of FGFR3, c-Maf, and cyclin D1. KW-2478 suppresses tumor growth and induces the degradation of client proteins in tumors in NCI-H929 s.c. inoculated model at doses of 100 mg/kg or more. KW-2478 reduces both serum M protein and MM tumor burden in the bone marrow in OPM-2/GFP i.v. inoculated mouse model at doses of 100 mg/kg.
Status:
Investigational
Source:
NCT03878849: Phase 2 Interventional Active, not recruiting Advanced Ovarian Cancer
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
E7449 also known as 2X-121 (8-(isoindolin-2-ylmethyl)-2,9-dihydro-
3H-pyridazino[3,4,5-de]quinazolin-3-one) is an orally
bioavailable, brain penetrable, small molecule dual Poly(ADP-ribose) polymerase /Tankyrase
inhibitor that is not a substrate for P-glycoprotein. It demonstrates potent antineoplastic potential both in vivo and in vitro. 2X Oncology is developing E7449 for the treatment of solid cancers.
Status:
Investigational
Source:
NCT02294266: Phase 1 Interventional Completed Amphetamine-Related Disorders
(2014)
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Mephedrone (4-methylmethcathinone) is a β-ketoamphetamine belonging to the family of synthetic cathinones, an emerging class of designer drugs known for their hallucinogenic and psychostimulant properties as well as for their abuse potential. Mephedrone is a stimulant of dopamine (DA) release and blocks its reuptake through its interaction with the dopamine transporter. Furthermore, it has some affinity for various 5-hydroxytryptamine (5-HT) receptor subtypes. Neurotoxic effect of mephedrone on 5-HT and DA systems remains controversial. Although some studies in animal models reported no damage to DA nerve endings in the striatum and no significant changes in brain monoamine levels, some others suggested a rapid reduction in 5-HT and DA transporter function. Persistent serotonergic deficits were observed after binge like treatment in a warm environment and in both serotonergic and dopaminergic nerve endings at high ambient temperature. Oxidative stress cytotoxicity and an increase in frontal cortex lipid peroxidation were also reported. Despite the re-classification of mephedrone as a Class B restricted substance by the United Kingdom and restrictive legislation by the United States, international policy regarding mephedrone control is still developing and interest in synthetic amphetamine-like drugs could drive the development of future mephedrone analogues.
Status:
Investigational
Source:
INN:esoxybutynin [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Esoxybutynin is (S)-enantiomer of oxybutynin. Esoxybutynin exerts antimuscarinic properties. Racemic oxybutynin is used clinically to treat urinary incontinence. Sepracor was developing (S)-oxybutynin, a single-isomer version of Alza's Ditropan (racemic oxybutynin), a muscarinic acetylcholine receptor antagonist, as a potential treatment for urinary incontinence.
Status:
Investigational
Source:
NCT00095212: Not Applicable Interventional Completed HIV Infection
(2004)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT01540071: Phase 2 Interventional Completed Castration Resistant Prostate Cancer
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
VTP-194204 (NRX 194204, IRX4204) is a second-generation retinoid X receptor (RXR) agonist that has no cross-reactivity with retinoic acid receptors, farnesoid X receptor, liver X receptors or peroxisome proliferator-activated receptor PPARγ. Rexinoid NRX 194204 selectively binds to and activates RXRs. Because RXRs can form heterodimers with several nuclear receptors (NRs), RXR activation by this agent may result in a broad range of gene expression depending on the effector DNA response elements activated. Rexinoid NRX 194204 may inhibit the tumour-necrosis factor (TNF)-mediated release of nitric oxide (NO) and interleukin 6 (IL6) and may inhibit tumour cell proliferation. This agent appears to be less toxic than RAR-selective ligands. VTP-194204 (IRX-4204) is in phase II clinical trials by Io Therapeutics for the treatment of prostate cancer. It is also in preclinical trials for the treatment of Alzheimer's disease, autoimmune diseases and multiple sclerosis.
Status:
Investigational
Source:
NCT04090736: Phase 3 Interventional Active, not recruiting Leukemia, Myeloid, Acute
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Pevonedistat (MLN4924), discovered by Millennium, is a small molecule inhibitor of the NEDD8-Activating Enzyme (NAE), a key component of the protein homeostasis pathway. MLN4924 is a mechanism-based inhibitor of NAE and creates a covalent NEDD8-MLN4924 adduct catalyzed by the enzyme. The NEDD8-MLN4924 adduct resembles NEDD8 adenylate, the first intermediate in the NAE reaction cycle, but cannot be further utilized in subsequent intraenzyme reactions. The stability of the NEDD8-MLN4924 adduct within the NAE active site blocks enzyme activity, thereby accounting for the potent inhibition of the NEDD8 pathway by MLN4924. This drug is in phase II clinical trial for the treatment acute myeloid leukemia, chronic myelomonocytic leukemia and myelodysplastic syndromes. In addition in phase I for treatment acute lymphoblastic leukemia. The ability of MLN4924 to cross the blood-brain barrier, its low toxicity, and clinical efficacy in other cancers suggests that this drug is an attractive treatment against glioblastomas.
Status:
Investigational
Source:
NCT01740336: Phase 2 Interventional Completed Breast Cancer
(2013)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Pictilisib is an oral potent inhibitor of class I PI3K with nanomolar activities against p110alpha, p110beta, p110delta, and p110gamma. The drug was developed for the treatment of solid tumors and reached phase II in patients with breast cancer and lung carcinoma, however its development was terminated.
Status:
Investigational
Source:
NCT00456053: Phase 2 Interventional Completed Renal Anemia
(2005)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
FG 2216 is an erythropoietic small molecule prolyl hydroxylase inhibitor, originally developed by FibroGen, that is undergoing development for the treatment of anemia. PDH inhibitor FG-2216 was orally bioavailable and induced significant and reversible EPO induction in vivo. Chronic oral dosing in male rhesus macaques was well tolerated, significantly increased erythropoiesis, and prevented anemia induced by weekly phlebotomy. Furthermore, modest increases in HbF-containing red cells and reticulocytes were demonstrated by flow cytometry. FG 2216 had been in phase II clinical trials for the treatment of anemia, however, all researchers on this drug candidate were discontinued.
Status:
Investigational
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Lorediplon is a novel non-benzodiazepine, the hypnotic drug acting as a GABAA receptor modulator, differentially active at the alpha1-subunit, associated with promoting sleep. As compared with other selective benzodiazepine receptor agonists, lorediplon has demonstrated in pre-clinical studies a potent hypnotic profile with potential advantages in sleep maintenance and sleep architecture preservation associated with a good safety profile, that is, no induction of tolerance, lack of next-day hangover effect, weak effect on muscular tone, and weak interaction with ethanol. Lorediplon demonstrated a minimum of 10-fold and the 6-fold increase in potency (respectively) in the spontaneous motor activation studies, compared with the currently marketed hypnotics (zolpidem and zaleplon). Additionally, when the electroencephalogram (EEG) effects of lorediplon and zolpidem were compared in the sleep-wake cycle in the mouse, lorediplon demonstrated a 10-fold increase in potency compared with zolpidem in the sleep-wake cycle and 13% greater possibility of fewer wake episodes than zolpidem. At concentrations of 1.2mg/kg, lorediplon demonstrated a 57%increased effect on Slow Wave Sleep (SWS), when compared with a placebo. In clinical trials, the clinical safety and tolerability were excellent for all doses tested. In pharmacokinetic studies, after oral administration, lorediplon is rapidly absorbed from the gastrointestinal tract reaching maximum plasma concentrations at approximately 2 h. Lorediplon demonstrated a dose-dependent improvement in sleep, whereas zolpidem showed a more sustained wake after sleep onset effect. No next-day hangover effects were observed. These sleep effects are also consistent with the pharmacokinetic profile of lorediplon.
