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Restrict the search for
tyrosine
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Status:
Other
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Other
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Butein, a plant polyphenol, has been reported to exhibit several important pharmacological effects, such as anti-inflammatory, anti-cancer, anti-oxidant and anti-angiogenic. It was first found in Toxicodendronvernicifluum, a tree widely used as a local food additive and therapeutic supplement in South East Asia. It can also be isolated from the heartwood of Dalbergiaodorifera, the seed of Cyclopiasubternata and the stems of Semecarpusanacardium, as well as many other plants. Butein was shown to be a specific protein tyrosine kinase inhibitor. This compound inhibited tyrosine-specific protein kinase activities of EGF receptor and p60(c-Src). In preclinical settings, it was shown to improve the treatment outcome of several chronic diseases including inflammation, neurological disorders, neoplasms, atherosclerosis, as well as infectious diseases, and most of these actions were accomplished by the inhibition of the transcription factor NF-κB and its downstream targets.
Status:
Other
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Malonoben is a synthetic inhibitor of protein tyrosine kinase (PTK) that displays characteristics of a potent reversible inhibitor of platelet-derived growth factor (PDGF)-induced mitogenesis via inhibition of tyrosine kinase activity of the PDGFR (PDGF receptor) and other signaling cascades. Malonoben significantly attenuated CCR7-induced Pyk2 tyrosine phosphorylation, activation of cofilin and sequentially abolished F-actin rearrangement, diminished the chemotaxis and migration ability of squamous cell carcinoma of the head and neck. Malonoben treatment resulted in the formation of fragmented mitochondria filament. Treatment of malonoben also evoked mitochondrial fragmentation in other cells including the neuroblastomas. Malonoben induces Drp1-mediated mitochondrial fission and apoptotic cell death.
Status:
Other
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, SAL) is a tetrahydroisoquinoline derivative, detected in humans. Salsolinol can be formed in the mammalian brain by three different mechanisms: (1) via the nonenzymatic Pictet–Spengler condensation of dopamine and aldehydes producing salsolinol as two racemic isomers (R or S). (2) By the nonenzymatic condensation of dopamine and pyruvate yielding 1-carboxyl-tetrahydroisoquinoline, followed by decarboxylation and reduction, which produces (R)-salsolinol. (3) By selective synthesis of (R)-salsolinol from dopamine and acetaldehyde, the level of which is increased after ethanol intake. Apart from that salsolinol has also been detected in certain beverages and foodstuff, including soy sauce, cheese. Only the (R) enantiomer of Salsolinol and occur in the human brain, cerebrospinal fluid (CSF) and intraventricular fluid (IVF), and the (S) enantiomer was not detected. Salsolinol was also found to be involved in neurotoxicity processes altering the normal function and survival of dopamine neurons. It has been proposed, that salsolinol participated in the etiopathogenesis of Parkinson’s disease. Salsolinol could inhibit various enzymes, for example, monoamine oxidase and tyrosine hydroxylase and recently was revealed, that (R)-SAL and (S)-SAL were agonists of the μ-opioid receptor. (S)-SAL is a more potent agonist than the (R)-SAL stereoisomer, it was suggested that an opioid action of SAL or its enantiomers is involved in the rewarding effects of ethanol.
