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Tubeimoside I CAS: 102040-03-9

Category: Inhibitors
Product Name: Tubeimoside I
Cat No: I000147
CAS No: 102040-03-9
Synonyms: Tubeimoside;Tubeimoside A
Molecular Formula: C63H98O29
Molecular Weight: 1319.4
SMILES: CC1(C)CC[C@]23CC[C@@]4(C)[C@]5(C)CC[C@@]6([H])[C@@](CO)(C)[C@](O[C@@H]7O[C@H](CO)[C@@H](O)[C@H](O)[C@H]7O[C@]8([H])OC[C@H](OC(C[C@@](O)(C)CC(O[C@@H]9[C@@H](O[C@@]%10([H])[C@H](O)[C@@H](O)[C@H](O)CO%10)[C@@H](O)[C@H](O[C@@]%11([H])[C@H](OC3=O)OC[C@H](O)[C@
InChIKey: MCPFEAJYKIXPQF-DXZAWUHFSA-N
Solubility: 10 mM in DMSO
Target: Anticancer natural compound
Storage: -20°C
CAS 102040-03-9,Tubeimoside I
  • Description

Tubeimoside I(Lobatoside-H) is an extract from Chinese herbal medicine Bolbostemma paniculatum (MAXIM.) FRANQUET (Cucurbitaceae) has been shown as a potent anti-tumor agent for a variety of human cancers.
IC50 value:
Target: Anticancer natural compound
in vitro: TBMS I inhibited the proliferation of both HepG2 and L-02 cells in a dose- and time-dependent manner, but HepG2 cells appeared more sensitive to the agent. When exposed to TBMS I for 24, 48 and 72 h, IC50 for HepG2 cells versus L-02 cells were 15.5 vs. 23.1, 11.7 vs. 16.2, 9.2 vs. 13.1 (μM, p<0.01), respectively. TBMS I induced 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 [1]. TBMS1-induced molecular events were related to mitochondria-induced intrinsic apoptosis and P21-cyclin B1/cdc2 complex-related G2/M cell cycle arrest [2]. TBMS1 combined with CDDP promoted cell apoptosis, decreased proliferation activity and increased cytosolic Ca2+ levels. Bcl-2 protein expression was down-regulated but Bax was up-regulated. Moreover, GST-π mRNA and protein expression were decreased. TBMS1 reduced the resistance of the cells to CDDP-induced cytotoxicity [4]. Treatment with TBMS1 resulted in dose- and time-dependent inhibition of proliferation, led to arrest in phase G2/M of the cell cycle and increased the levels of intracellular Ca2. Furthermore, TBMS1 up-regulated the levels of the glucose-regulated protein 78/immunoglobuin heavy chain binding protein (GRP78/Bip), C/EBP homologous protein (CHOP), Bax, and cleaved caspase-3 and down-regulated the levels of Bcl-2 [5].
in vivo: TBMS1 significantly inhibited the production of the pro-inflammatory cytokines, TNF-α, IL-6 and IL-1β in vitro and in vivo. Pretreatment with TBMS1 markedly attenuated the development of pulmonary edema, histological severities and inflammatory cells infiltration in mice with ALI [3].

  • Spec

Appearance: Powder
Purity: 98.0%

  • References


[1]. Wang Y, et al. Natural plant extract tubeimoside I promotes apoptosis-mediated cell death in cultured human hepatoma (HepG2) cells. Biol Pharm Bull. 2011;34(6):831-8.
[2]. Xu Y, et al. Intrinsic apoptotic pathway and G2/M cell cycle arrest involved in tubeimoside I-induced EC109 cell death. Chin J Cancer Res. 2013 Jun;25(3):312-21.
[3]. Wu Q, et al. Tubeimoside-1 attenuates LPS-induced inflammation in RAW 264.7 macrophages and mouse models. Immunopharmacol Immunotoxicol. 2013 Aug;35(4):514-23.
[4]. Liu HZ, et al. Tubeimoside I sensitizes cisplatin in cisplatin-resistant human ovarian cancer cells (A2780/DDP) through down-regulation of ERK and up-regulation of p38 signaling pathways. Mol Med Rep. 2011 Sep-Oct;4(5):985-92.
[5]. Chen WJ, et al. Tubeimoside-1 induces G2/M phase arrest and apoptosis in SKOV-3 cells through increase of intracellular Ca2+ and caspase-dependent signaling pathways. Int J Oncol. 2012 Feb;40(2):535-43.


price inquiry for CAS:102040-03-9, Product:Tubeimoside I