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Restrict the search for
tyrosine
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Status:
Investigational
Source:
NCT00414999: Phase 1 Interventional Completed Macular Degeneration
(2006)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
AGE-RELATED MACULAR DEGENERATION (AMD), PROLIFERATIVE DIABETIC RETINOPATHY (PDR) AND DIABETIC MACULAR EDEMA (DME) are collectively characterized by VEGF mediated retinal leakage, angiogenesis, and an underlying inflammatory process. TargeGen's TG100801 is designed to inhibit a select group of kinases involved in those three processes. Currently approved drug based therapy for macular degeneration requires repeated injection into the eye. TG100801 is the first topically applied, VEGFR)/Src kinase inhibitor to advance into the clinic for the treatment of Age-related macular degeneration, diabetic retinopathy. The formation of new blood vessels (angiogenesis), blood vessel leakage, and inflammation contribute to the progression of the eye disease, which is the leading cause of irreversible, severe loss of vision in people 55 years of age and older in the developed world. In cell based assays, following topical instillation, TG100572, the active drug produced by conversion of TG100801 as it penetrates the eye, was shown to induce apoptosis in proliferating endothelial cells responsible for neovasculariztion and to inhibit inflammatory-mediated processes as measured by endotoxin-induced nitric oxide release in vitro.
Status:
Investigational
Source:
NCT01215799: Phase 2 Interventional Completed Hormone Refractory Prostate Cancer
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Bafetinib (NS-187, INNO-406) is a second-generation tyrosine kinase inhibitor in development by CytRx under license from Nippon Shinyaku for treating Bcr-Abl+ leukemia's, including chronic myelogenous leukemia (CML) and Philadelphia+ acute lymphoblastic leukemia. It is a rationally developed tyrosine kinase inhibitor based on the chemical structure of imatinib, with modifications added to improve binding and potency against Bcr-Abl kinase. Besides Abl, bafetinib targets the Src family kinase Lyn, which has been associated with resistance to imatinib in CML. In preclinical studies, bafetinib was 25- to 55-fold more potent than imatinib in vitro and ≥ 10-fold more potent in vivo. Bafetinibinhibits 12 of the 13 most frequent imatinib-resistant Bcr-Abl point mutations, but not a Thr315Ile mutation. A small fraction of bafetinib crosses the blood-brain barrier, reaching brain concentrations adequate for suppression of Bcr-Abl+ cells. Data from a phase I clinical trial conducted in patients with imatinib-resistant or -intolerant CML have confirmed that bafetinib has clinical activity in this setting, inducing a major cytogenetic response in 19% of those patients in chronic phase. Currently, bafetinib is being developed in two phase II clinical trials for patients with B-cell chronic lymphocytic leukemia and prostate cancer, and a trial is in progress for patients with brain tumors. In 2005, the compound was licensed to Innovive Pharmaceuticals (acquired by CytRx Oncology in 2008) by Nippon Shinyaku on a worldwide basis, with the exception of Japan, for the treatment of CML. Orphan drug designation was assigned to the compound for the treatment of CML in the U.S in 2007 and in the E.U. in 2010. Bafetinib is in phase II for the treatment of hormone-refractory prostate cancer and chronic lymphocytic leukemia.
Status:
Investigational
Source:
NCT00535522: Phase 1 Interventional Completed Cancer
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
TAK-285 is a novel low-molecular weight compound that was designed, synthesized by Takeda Pharmaceutical Company, Osaka, Japan, and has been shown to selectively and potently inhibit HER2 and EGFR kinase activities. Biochemically, TAK-285 inhibits HER2 and EGFR phosphorylation, with 50% inhibition concentrations of 17 and 23 nmol –1, respectively. This drug was in the phase I of clinical trial for the treatment of solid rumors and cancer but was discontinued due to strategic reasons. In addition was investigated that TAK-285 is not Pgp substrates, which is why it may be useful in the development of agents with the potential to treat brain metastases.
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Fosfosal (2-phosphonoxybenzoic acid) is a O-phosphorylated derivative of salicylic acid used in analgesic and anti-inflammatory therapy. Fosfosal showed analgesic effect in the acetic acid-induced writhing and in the hot plate tests in mice, and showed antiinflammatory effect in the xylene induced mice ears swelling and in acetic acid induced increased vascular permeability tests in mice. Both the effects had no significant differences between fosfosal and aspirin, but the former had less stomach irritation.
Status:
Investigational
Source:
NCT02029157: Phase 3 Interventional Completed Liver Cancer
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Tivantinib (ARQ 197) is the first non-ATP-competitive small molecule that selectively targets the c-Met receptor tyrosine kinase. Exposure to Tivantinib resulted in the inhibition of proliferation of c-Met-expressing cancer cell lines as well as the induction of caspase-dependent apoptosis in cell lines with constitutive c-Met activity. ArQule and its collaborators Daiichi Sankyo and Kyowa Hakko Kirin are developing tivantinib as a potential therapy for many cancers. c-Met is overexpressed in many cancers. Tivantinib currently is in phase 3 clinical development for the treatment of hepatocellular carcinoma and non-small cell lung cancer.
Status:
Investigational
Source:
NCT00806338: Phase 1 Interventional Completed Diabetes Mellitus
(2008)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Trodusquemine (MSI-1436) is a "first-in-class" highly selective non-competitive, allosteric inhibitor of PTP1B that can cross the blood-brain barrier to suppress feeding and promote insulin sensitivity and glycemic control. Trodusquemine is a naturally occurring cholestane that can be purified from the liver of the dogfish shark, Squalus acanthias, but it can also be manufactured synthetically by a fairly laborious process that requires several weeks. Trodusquemine has potential hypoglycemic, anti-diabetic, anti-obesity, and antineoplastic activities. Upon administration, trodusquemine selectively targets and inhibits PTP1B, thereby preventing PTP1B-mediated signaling. This prevents the dephosphorylation of the insulin receptor, which improves insulin signaling and insulin sensitivity, and decreases blood glucose levels. In susceptible cancer cells, inhibition of PTP1B causes a reduction of tumor cell proliferation.
Status:
Investigational
Source:
NCT00116376: Phase 1/Phase 2 Interventional Completed Glioblastoma Multiforme
(2004)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
AEE-788 is an orally available anticancer agent that was being developed by Novartis. AEE-788 is a dual family epidermal growth factor receptor/ErbB2 and vascular endothelial growth factor receptor tyrosine kinase inhibitor with antitumor and antiangiogenic activity. At the enzyme level, AEE-788 inhibited EGFR and VEGF receptor tyrosine kinases in the nm range (IC(50)s: EGFR 2 nm, ErbB2 6 nm, KDR 77 nm, and Flt-1 59 nm). In cells, growth factor-induced EGFR and ErbB2 phosphorylation was also efficiently inhibited (IC(50)s: 11 and 220 nm, respectively). AEE-788 demonstrated antiproliferative activity against a range of EGFR and ErbB2-overexpressing cell lines (including EGFRvIII-dependent lines) and inhibited the proliferation of epidermal growth factor- and VEGF-stimulated human umbilical vein endothelial cells. These properties, combined with a favorable pharmacokinetic profile, were associated with a potent antitumor activity in a number of animal models of cancer, including tumors that overexpress EGFR and or ErbB2. Oral administration of AEE-788 to tumor-bearing mice resulted in high and persistent compound levels in tumor tissue. Moreover, AEE-788 efficiently inhibited growth factor-induced EGFR and ErbB2 phosphorylation in tumors for >72 h, a phenomenon correlating with the antitumor efficacy of intermittent treatment schedules. AEE-788 has potential as an anticancer agent targeting deregulated tumor cell proliferation as well as angiogenic parameters. AEE-788 had been in phase Ⅱ clinical trials by Novartis for the treatment of glioblastoma multiforme. However, this research has been discontinued.
Status:
Investigational
Source:
USAN:DIOTYROSINE I 131 [USAN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Diotyrosine I 131 is the diagnostic aid manufactured by Abbott.
Status:
Investigational
Source:
NCT03130790: Phase 2/Phase 3 Interventional Completed Gastric Cancer
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Varlitinib (Alternative Names: ARRY-334543; ARRY-543; ASLAN-001; Varlitinib tosylate) is a small molecule based reversible pan-HER inhibitor of EGFR, HER2 and HER4. In response to the binding of various ligands, these kinases undergo heterodimerisation and homodimerization, resulting in activation of numerous growth factor signaling pathways, by inhibiting the activation of the HER receptors via drug, effects such as shrinkage of the tumor and longer survival can be anticipated. In a large variety of cancers, the overexpression and/or constitutive activation of EGFR and HER2 are often observed and frequently correlate with poor clinical prognosis. Licensed from Array BioPharma with global rights for all indications, varlitinib is being developed as first-in-class drug for cholangiocarcinoma, gastric and colorectal cancer, and as best-in-class drug for breast cancer.
Status:
Investigational
Source:
NCT00034281: Phase 1 Interventional Completed Breast Neoplasm
(2002)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
TAK-165 is a new potent inhibitor of human epidermal growth factor receptor 2 (HER2) tyrosine kinase. Mubritinib displays > 4000-fold selectivity over other tyrosine kinases, such as EGFR, FGFR, PDGFR, Jak1, Src and Blk. A Phase I study to investigate a safe dose of Mubritinib, once daily (QD), in patients with tumors known to express HER2 (Breast Neoplasm, Pancreatic Neoplasm, Lung Neoplasm, Ovarian Neoplasm, Renal Neoplasm) has been completed, but appears to have been discontinued, as no new information on the drug has surfaced since December 2008.
