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Restrict the search for
tyrosine
to a specific field?
Status:
Investigational
Source:
NCT02179814: Not Applicable Interventional Suspended Bulimia Nervosa
(2012)
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Racemetirosine is an orally active inhibitor of the enzyme tyrosine 3-monooxygenase, and consequently of the synthesis of catecholamine. At dosages of 600 to 3500mg daily, it is effective in controlling the hypertensive episodes and symptoms of catecholamine excess in phaeochromocytoma during preparation for surgery. Oral Racemetirosine is well absorbed and absorption appears constant in each individual over a wide dosage range. The drug is largely excreted via the kidneys, but extrarenal elimination has not been studied. Case reports on the clinical use of Racemetirosine in phaeochromocytoma indicate that the drug controls hypertension and symptoms of catecholamine excess in most patients during preparation for surgical removal of a tumor. In some cases, the addition of Racemetirosine to phenoxybenzamine plus propranolol has resulted in adequate control of symptoms previously unresponsive to the adrenergic blocking regimen. Drowsiness and sedation have been the most frequently reported side effects of Racemetirosine treatment.
Status:
Investigational
Source:
NCT00003980: Phase 1 Interventional Suspended Unspecified Adult Solid Tumor, Protocol Specific
(1999)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Falnidamol is an epidermal growth factor receptor inhibitor, developed by Boehringer Ingelheim. Falnidamol demonstrated anticancer activity in vitro. The phase I trial was discontinued due to a dose-limiting increase of liver enzymes, low bioavailability of the drug and the detection of a pharmacologically inactive metabolite.
Status:
Investigational
Source:
NCT00908752: Phase 3 Interventional Completed Hepatocellular Carcinoma
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Brivanib is a pyrrolotriazine-based compound and an inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2) with potential antineoplastic activity. It specifically targets and strongly binds to human VEGFR-2, a tyrosine kinase receptor and pro-angiogenic growth factor expressed almost exclusively on vascular endothelial cells. Blockade of VEGFR-2 by this agent may lead to an inhibition of VEGF-stimulated endothelial cell migration and proliferation, thereby inhibiting tumor angiogenesis. Brivanib has a moderate potency compared to VEGFR-2 against VEGFR-1 and FGFR-1 as well. Brivanib is suggested to be efficient in treatment of hepatocellular carcinoma (HCC). As first-line and as second-line therapy brivanib demonstrated promising antitumor activity and a manageable safety profile in patients with advanced, unresectable HCC in phase II clinical trials. On 3 march 2011, orphan designation was granted by the European Commission to Bristol-Myers Squibb for brivanib alaninate for the treatment of hepatocellular carcinoma.[
Status:
Investigational
Source:
Eur J Neurosci. Aug 2015;42(4):2028-35.: Not Applicable Human clinical trial Completed Parkinson Disease/complications
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Status:
Investigational
Source:
NCT03784378: Phase 1 Interventional Completed Non Small Cell Lung Cancer
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
CEP-32496 (RXDX 105) is an orally administered, small molecule, VEGFRsparing, RET, BRAF, EGFR tyrosine kinase inhibitor, for the treatment of solid tumours, including malignant melanoma and colorectal cancer. CEP-32496 was originally discovered by Ambit Biosciences (now Daiichi Sankyo) and Cephalon (now owned by Teva) as part of a research programme to develop orally administered kinase inhibitors. The worldwide rights to the compound were licensed to Teva by Ambit, following the acquisition of Cephalon by Teva. Teva, in March 2015, entered into an asset purchase agreement with Ignyta, pursuant to which, Ignyta has acquired worldwide rights and assets of four oncology development programmes, including CEP-32496. Following the acquisition of the compound by Ignyta, CEP 32496 has been renamed to RXDX 105. Phase I/Ib development of RXDX 105 for the treatment of advanced solid tumours is underway in the US.
Status:
Investigational
Source:
NCT00056459: Phase 3 Interventional Completed Colorectal Neoplasms
(2003)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Vatalanib a potent oral tyrosine kinase inhibitor with a selective range of molecular targets, has been extensively investigated and has shown promising results in patients with solid tumors in early trials. Vatalanib selectively inhibits the tyrosine kinase domains of vascular endothelial growth factor (VEGF) receptor tyrosine kinases (important enzymes in the formation of new blood vessels that contribute to tumor growth and metastasis), platelet-derived growth factor (PDGF) receptor, and c-KIT. The adverse effects of vatalanib appear similar to those of other VEGF inhibitors. In the CONFIRM trials, the most common side effects were high blood pressure, gastrointestinal upset (diarrhea, nausea, and vomiting), fatigue, and dizziness.
Status:
Investigational
Source:
NCT03887169: Phase 1/Phase 2 Interventional Completed Pulmonary Alveolar Proteinosis
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Homocysteine, an amino acid synthesized intracellularly by removal of the N-methyl group from the essential amino acid methionine. High plasma level of homocysteine is called hyperhomocysteinemia is a clinical biomarker for increased risk of cardiovascular disease, thromboembolic diseases, and myocardial infarction. It was shown, that hyperhomocysteinemia could be an independent risk factor for dementia and Alzheimer's disease. The falling of homocysteine concentrations in response to increasing B-group-vitamin status, have the hope that mental decline, or Alzheimer's disease, could be prevented by dietary modification or food fortification. Besides, homocysteine can behave as an anti-oxidant agent by increasing the antioxidant capacity of the tumor and endothelial cells.
Status:
Investigational
Source:
USAN:IOTYROSINE I 131 [USAN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Ioxabrolic Acid is triiodobenzoic acid derivative and iodine-containing radiopharmaceutical
Status:
Investigational
Source:
NCT00779480: Phase 1 Interventional Terminated Acute Myelogenous Leukemia (AML)
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
KW-2449, a multikinase inhibitor of FLT3, ABL, ABL-T315I, and Aurora kinase, is under investigation to treat leukaemia patients. KW-2449 is a multikinase inhibitor of FLT3, ABL, ABL-T315I, and Aurora kinase with IC50 values of 6.6nM, 14nM, 4nM and 48nM, respectively. KW-2449 has potent growth inhibitory activity against various types of leukaemia by several mechanisms of action. Kyowa Hakko Kirin Pharma Inc. (a US subsidiary of Kyowa Hakko Kirin Co) was developing KW-2449 for the treatment of acute lymphoblastic leukaemia; acute myeloid leukaemia; chronic myeloid leukaemia; myelodysplastic syndromes, but later these studies were discontinued.
Status:
Investigational
Source:
NCT01071928: Phase 2 Interventional Withdrawn Urothelial Carcinoma
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Vadimezan (5,6-dimethyl(xanthenone-4-acetic acid), ASA404, DMXAA) is a fused tricyclic analogue of flavone acetic acid with potential antineoplastic activity. In pre-clinical mouse tumour models it was demonstrated that administration of Vadimezan rapidly leads to disruption of the existing vasculature in the tumour and consequent haemorrhagic necrosis of the tumour. This was consistent with the finding that a single dose of Vadimezan induced a prolonged reduction in the growth of xenografted tumours in animal models. The ability to disrupt the vasculature in these pre-clinical models has been attributed to a rapid induction of cytokines, particularly TNFα (tumour necrosis factor α), serotonin and nitric oxide, resulting in hemorrhagic necrosis and a decrease in angiogenesis. Despite the fact that the molecular targets for the drug remained unknown, the promising pre-clinical results led to Vadimezan being selected for clinical development. Results of Phase I trials showed some restriction of tumour blood flow within 24 h of treatment, although this was not as dramatic as seen in pre-clinical models. Unlike the animal models, there was also very little evidence for the rapid death of blood vessels or for increases in TNFα levels in human tumors. No difference in antitumour activity, cytokine induction or toxicity was observed between two parallel Phase I trials, one dosed weekly and the other dosed every 3 weeks. Therefore the drug proceeded to Phase II clinical trials, dosed every 21 days in combination with chemotherapeutic agents. These trials indicated the drug had small benefits in the treatment of non-small-cell lung cancer and prostate cancer. However, a subsequent Phase III clinical trial was not able to reproduce this response and clinical development was halted.
