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Réf. Catalogue: S4735
Structure chimique
| Cibles apparentées | HDAC JAK BET Histone Methyltransferase PKC PARP HIF PRMT EZH2 AMPK |
|---|---|
| Autre Sirtuin Inhibiteurs | SRT 1720 Hydrochloride Selisistat (EX-527) Sirtinol Fisetin 3-TYP AGK2 SRT2104 (GSK2245840) OSS_128167 SirReal2 SRT2183 |
| Poids moléculaire | 718.61 | Formule | C36H30O16 |
Stockage (À compter de la date de réception) | 3 years -20°C powder (seal) |
|---|---|---|---|---|---|
| N° CAS | 121521-90-2 | Télécharger le SDF | Stockage des solutions mères | Les solutions sont instables. Préparer des solutions fraîches ou acheter des formats petits et préemballés. Reconditionner dès réception. | |
| Synonymes | Sal B, Lithospermate B, Lithospermic acid B | Smiles | C1=CC(=C(C=C1CC(C(=O)O)OC(=O)C=CC2=C3C(C(OC3=C(C=C2)O)C4=CC(=C(C=C4)O)O)C(=O)OC(CC5=CC(=C(C=C5)O)O)C(=O)O)O)O | ||
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In vitro |
DMSO
: 100 mg/mL
(139.15 mM)
Water : 100 mg/mL Ethanol : 100 mg/mL |
|
In vivo |
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Étape 1 : Saisir les informations ci-dessous (Recommandé : Un animal supplémentaire pour tenir compte des pertes pendant l'expérience)
Étape 2 : Saisir la formulation in vivo (Ceci est seulement le calculateur, pas la formulation. Veuillez nous contacter d'abord s'il n'y a pas de formulation in vivo dans la section Solubilité.)
Résultats du calcul :
Concentration de travail : mg/ml;
Méthode de préparation du liquide maître DMSO : mg médicament prédissous dans μL DMSO ( Concentration du liquide maître mg/mL, Veuillez nous contacter d'abord si la concentration dépasse la solubilité du DMSO du lot de médicament. )
Méthode de préparation de la formulation in vivo : Prendre μL DMSO liquide maître, puis ajouterμL PEG300, mélanger et clarifier, puis ajouterμL Tween 80, mélanger et clarifier, puis ajouter μL ddH2O, mélanger et clarifier.
Méthode de préparation de la formulation in vivo : Prendre μL DMSO liquide maître, puis ajouter μL Huile de maïs, mélanger et clarifier.
Note : 1. Veuillez vous assurer que le liquide est clair avant d'ajouter le solvant suivant.
2. Assurez-vous d'ajouter le(s) solvant(s) dans l'ordre. Vous devez vous assurer que la solution obtenue, lors de l'ajout précédent, est une solution claire avant de procéder à l'ajout du solvant suivant. Des méthodes physiques telles que le vortex, les ultrasons ou le bain-marie chaud peuvent être utilisées pour faciliter la dissolution.
| Targets/IC50/Ki |
SIRT
|
|---|---|
| In vitro |
Salvianolic acid B, also known as satanic acid B or lithospermic acid B, is a new generation of the natural antioxidants. It can influence Ca2+ aggregation and endothelial cell NO release of hypoxia/ reoxygenation-induced cell. When this compound concentration is 2.5, 5, and 10 mg/l, cell viability and superoxide dismutase (SOD) activity are enhanced, and the formation of malondialdehyde (MDA) in human umbilical vein endothelial cells (ECV304) is inhibited. SalB inhibits HG-induced oxidative stress and reduces the generation of ROS and 8-hydroxy-2-deoxyguanosine (8-OHDG) and mitochondrial depolarization and apoptosis in a dose-dependent manner. It can downregulate the expression of Bax and AIF nuclear translocation and cytochrome c release mediated by HG, but upregulate the expression of Bcl-2 induced by HG. Besides, this chemical attenuates HG-induced caspase of the enzyme 3, 9 and minimize PARP cleavage of Schwann cells (SCs). It inhibits angiotensin II or H2O2 and TNF-α-induced gelatinolytic activity in human aortic smooth muscle cells (HASMCs) in a concentration-dependent manner. This compound can inhibit platelet aggregation and adhesion. It can promote cardiac angiogenesis effect. SalB can enhance cell activity and reduce the number of sub-G1 and apoptotic nuclei of ischemic cell model in order to show its antiapoptotic effects. It inhibits ischemia and hypoxia of myocardial injury. This chemical inhibits the synthesis of type I collagen of non-TGF-1 stimulated human hepatic stellate cell line (LX-2). SalB activates mammalian sirtuins 1 (SIRT1), an NAD-dependent class III histone deacetylase (HDAC) that plays important roles in several physiological processes, including gene transcription, senescence, energy metabolism, oxidative stress and inflammation. (HG:High glucose)
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| In vivo |
Salvianolic acid B can significantly reduce the myocardial infarct size and blood lactate dehydrogenase level of model rat with acute myocardial infarction, improve cardiac function and myocardial tissue structure, thus inhibiting ischemia and hypoxia of myocardial injury. This compound can improve blood hemorheology, reduce oxidative damage, improve the vascular endothelial cell function, and prevent the development of coronary artery disease. It could selectively inhibit the activity of MMP-9 in a rat model of myocardial infarction. This chemical can also effectively increase the thickness of the left ventricular wall in the myocardial infarction rats to improve the contraction of the heart, and reduce cardiac fibrosis. SalB treatment ameliorates ethanol-induced hepatic inflammation by decreasing the levels of hepatotoxic cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). It has beneficial effects against hepatic fibrosis in animal models and has been shown to possess cardioprotective and neuroprotective activity via anti-oxidative and anti-inflammatory actions.
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Références |
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(données du https://clinicaltrials.gov, mis à jour le 2024-05-22)
| Numéro NCT | Recrutement | Conditions | Promoteur/Collaborateurs | Date de début | Phases |
|---|---|---|---|---|---|
| NCT02694848 | Unknown status | Angina |
China Academy of Chinese Medical Sciences|Xiyuan Hospital of China Academy of Chinese Medical Sciences|Guang''anmen Hospital of China Academy of Chinese Medical Sciences|General Hospital of Beijing PLA Military Region|Guangdong Provincial Hospital of Traditional Chinese Medicine |
2016-02 | Phase 4 |