research use only
Cat.No.S3814
| Related Targets | Bcl-2 Caspase PD-1/PD-L1 Ferroptosis p53 Synthetic Lethality STAT TNF-alpha Ras KRas |
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| Other Apoptosis related Inhibitors | Importazole Genipin Pitstop 2 Plumbagin 6-Gingerol Crocin Colcemid Euphorbia factor L3 Sophoridine Pomolic acid |
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In vitro |
DMSO
: 100 mg/mL
(75.79 mM)
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In vivo |
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Working concentration: mg/ml;
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.
Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
Note: 1. Please make sure the liquid is clear before adding the next solvent.
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| Molecular Weight | 1319.43 | Formula | C63H98O29 |
Storage (From the date of receipt) | |
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| CAS No. | 102040-03-9 | -- | Storage of Stock Solutions |
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| Synonyms | Lobatoside H | Smiles | CC1C(C(C(C(O1)OC2C(C(COC2OC(=O)C34CCC(CC3C5=CCC6C(C5(CC4)C)(CCC7C6(CC(C8C7(COC(=O)CC(CC(=O)OC9C(C(COC9OC1C(C(C(OC1O8)CO)O)O)O)O)(C)O)C)O)C)C)(C)C)O)O)O)OC1C(C(C(CO1)O)O)O)O | ||
| In vitro |
TBMS I inhibits the proliferation of both HepG2 and L-02 cells in a dose- and time-dependent manner, but HepG2 cells appear more sensitive to the agent. When exposed to TBMS I for 24, 48 and 72 h, IC50 for HepG2 cells versus L-02 cells are 15.5 vs. 23.1, 11.7 vs. 16.2, 9.2 vs. 13.1 (μM, p<0.01), respectively. TBMS I induces cell shrinkage, nuclear condensation and fragmentation, cell cycle arrest at the G2/M phase, mitochondrial membrane disruption, release of cytochrome c from the mitochondria, activation of caspase 3 and 9, and shifting Bax/Bcl-2 ratio from being anti-apoptotic to pro-apoptotic, all indicative of initiation and progression of apoptosis involving mitochondrial dysfunction.
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| In vivo |
TBMS1 significantly inhibits the production of the pro-inflammatory cytokines, TNF-α, IL-6 and IL-1β in vitro and in vivo. Pretreatment with TBMS1 markedly attenuates the development of pulmonary edema, histological severities and inflammatory cells infiltration in mice with acute lung injury (ALI). TBMS1 exerts an anti-inflammatory effect in vivo model of ALI through suppression of IkB activation and p38/extracellular signal-regulated kinase mitogen-activated protein kinases signaling in a dose-dependent manner. TBMS1 could be a potent anti-tumor agent by inducing apoptosis in a variety of cancer types via the mitochondrial-related signaling pathway.
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References |
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