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Tubeimoside I


Catalogue Number : BF-T3014
Specification : 98%
CAS number : 102040-03-9
Formula : C63H98O29
Molecular Weight : 1319.43
PUBCHEM ID : 5462420
Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Bolbostemma paniculatum

Structure Type



Standards;Natural Pytochemical;API



TUBEIMOSIDE 1/β-D-Xylopyranosyl-(1->3)-6-deoxy-α-L-mannopyranosyl-(1->2)-1-O-{[(2R,3S,4S,4aR,5aS,8S,9S,9aR,17aR,17bR,19aR,19bS,21aS,25aS,27aR,27bR,29S,29aR,30aR)-3,4,8,9,13,29-hexahydroxy-2-(hydroxymethyl)-1 3,17a,19a,19b,24,24,27b-heptamethyl-11,15-dioxo-3,4,4a,7,8,9,9a,12,13,14,15,17a,18,19,19a,19b,20,21,22,23,24,25,25a,27,27a,27b,28,29,29a,30a-triacontahydro-2H,5aH,11H,17H-piceno[3,4-h]dipyrano[3,2-b:3 ;',2'-e][1,4,7,11]tetraoxacyclohexadecin-21a(/TubeimosideI/TUBELMOSIDEA/TUBEMOSIDE A/TUBEIMOSIDE I (RG)/(1S,4S,7S,8S,9R,11S,13S,14S,18S,22S,25S,27R,28S,29S,30R,32R,34R,35S,37R,38R,41R,42R,46S,53S,54R,55R,56R,57S,58R)-7,8,18,28,29,35,55,56,58-Nonahydroxy-30,54-bis(hydroxymethyl)-13,18,37,41,48,48,53,54-o ;ctamethyl-2,16,20-trioxo-3,5,10,12,15,21,24,26,31,33-decaoxadecacyclo[]octapentacont-44-en-57-yl β-D-xylopyranosideOlean-12-en-28-oicacid,3-[[2-O-[4-O-(4-carboxy-3/α-L-Arabinopyranose, O-β-D-xylopyranosyl-(1->3)-O-6-deoxy-α-L-mannopyranosyl-(1->2)-1-O-[[(2R,3S,4S,4aR,5aS,8S,9S,9aR,17aR,17bR,19aR,19bS,21aS,25aS,27aR,27bR,29S,29aR,30aR)-3,4,4a,5a,8,9,9a ,12,13,14,15,17a,18,19,19a,19b,20,21,22,23,24,25,25a,27,27a,27b,28,29,29a,30a-triacontahydro-3,4,8,9,13,29-hexahydroxy-2-(hydroxymethyl)-13,17a,19a,19b,24,24,27b-heptamethyl-11,15-dioxo-2H,7H,11H,17H- piceno[3,4-h]dipyrano[3,2-b:3',2'-e][1,4,7,1/Lobatoside H/Tubeimoside I



1.5±0.1 g/cm3


Methanol; Water

Flash Point

Boiling Point

Melting Point


InChl Key

WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:102040-03-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Parkinson’s disease (PD), a frequent degenerative disease in the elderly, is characterized by dopaminergic neurodegeneration in the substantia nigra pars compacta (SNpc). Neuroinflammation caused by over-activated microglia plays a crucial role in the pathogenesis of PD. Tubeimoside I (TBMS1) has a broad anti-inflammatory effect in peripheral tissues, but the effect on neuroinflammation has not been reported. Therefore, we explored whether TBMS1 could protect dopaminergic neurons by inhibiting the activation of microglia in lipopolysaccharide (LPS)-induced PD rat model. In addition, then, the effect and mechanism of TBMS1 on neuroinflammation were assessed in LPS-exposed murine microglial BV-2 cells. The results in vivo showed that TBMS1 suppressed microglial activation and dopaminergic neurons’ reduction in LPS-injected PD rat model. In vitro study found that TBMS1 could inhibit LPS-induced inflammatory responses in BV-2 cells, and this effect was mediated by suppressing the phosphorylation of protein kinase B (AKT), nuclear factor-kappa B (NF-κB p65), p38 and extracellular regulated protein kinases (ERK1/2). Taken together, these results demonstrated for the first time that TBMS1 played a role in protecting dopaminergic neurons by inhibiting neuroinflammation mediated by microglia.


MAPKs; NF-κB; Parkinson’s disease; Tubeimoside I; microglia.


Tubeimoside I Protects Dopaminergic Neurons Against Inflammation-Mediated Damage in Lipopolysaccharide (LPS)-Evoked Model of Parkinson's Disease in Rats


Dewei He 1 , Bingxu Huang 2 , Shoupeng Fu 3 , Yuhang Li 4 , Xin Ran 5 , Yandan Liu 6 , Guangxin Chen 7 , Juxiong Liu 8 , Dianfeng Liu 9

Publish date

2018 Jul 31




In the present study, the effects of tubeimoside I (TBMS1) on particulate matter <2.5 µm in diameter (PM2.5)-induced pulmonary injury and its mechanisms of action were investigated. Male BALB/c mice were randomly assigned into five groups (n=10/group): Control, PM2.5, PM2.5 + TBMS1 45 mg/kg, PM2.5 + TBMS1 90 mg/kg and PM2.5 + TBMS1 180 mg/kg. The dose of the PM2.5 suspension administered to the mice was 40 mg/kg via nasal instillation. The PM2.5 + TBMS1 groups received TBMS1 daily orally for 21 consecutive days, while the mice in the control and PM2.5 groups received equivalent volumes of PBS. Subsequently, lactic dehydrogenase, acid phosphatase, alkaline phosphatase, albumin, tumor necrosis factor-α and interleukin-6 protein levels in bronchoalveolar lavage fluid were determined. Oxidative stress was evaluated by detecting the protein levels of malondialdehyde, superoxide dismutase and inducible nitric oxide synthase, and the level of nitric oxide in lung tissue. Lastly, histopathological images of lung sections were obtained to observe changes in the lung tissue with treatment. The results indicated that exposure to PM2.5 induced pathological pulmonary changes, and biofilm and parenchymal cell damage, and promoted inflammation and oxidative stress. Treatment with TBMS1 attenuated the development of PM2.5-induced pulmonary injury. Its mechanisms of action were associated with reducing cytotoxic effects, levels of inflammatory mediators and oxidative damage. In conclusion, the results of the present study indicate that TBMS1 is a potential therapeutic drug for treating PM2.5-induced pulmonary injury.


inflammation; oxidative damage; particle matter <2.5 µm in diameter; pulmonary injury; tubeimoside I.


Tubeimoside I Attenuates Inflammation and Oxidative Damage in a Mice Model of PM 2.5-induced Pulmonary Injury


Jin-Bo Zhang 1 , Lei Zhang 2 , Shi-Qing Li 3 , Ai-Hua Hou 4 , Wei-Chao Liu 1 , Ling-Ling Dai 4

Publish date

2018 Feb




Cervical cancer is one of the most aggressive human cancers with poor prognosis due to constant chemoresistance and repeated relapse. Tubeimoside I (TBM) has been identified as a potent antitumor agent that inhibits cancer cell proliferation by triggering apoptosis and inducing cell cycle arrest. Nevertheless, the detailed mechanism remains unclear and needs to be further elucidated, especially in cervical cancer. In this study, we found that TBM could induce proliferation inhibition and cell death in cervical cancer cells both in vitro and in vivo. Further results demonstrated that treatment with TBM could induce autophagosome accumulation, which was important to TBM against cervical cancer cells. Mechanism studies showed that TBM increased autophagosome by two pathways: First, TBM could initiate autophagy by activating AMPK that would lead to stabilization of the Beclin1-Vps34 complex via dissociating Bcl-2 from Beclin1; Second, TBM could impair lysosomal cathepsin activity and block autophagic flux, leading to accumulation of impaired autophagolysosomes. In line with this, inhibition of autophagy initiation attenuated TBM-induced cell death, whereas autophagic flux inhibition could exacerbated the cytotoxic activity of TBM in cervical cancer cells. Strikingly, as a novel lethal impaired autophagolysosome inducer, TBM might enhance the therapeutic effects of chemotherapeutic drugs towards cervical cancer, such as cisplatin and paclitaxel. Together, our study provides new insights into the molecular mechanisms of TBM in the antitumor therapy, and establishes potential applications of TBM for cervical cancer treatment in clinic.


Tubeimoside I Induces Accumulation of Impaired Autophagolysosome Against Cervical Cancer Cells by Both Initiating Autophagy and Inhibiting Lysosomal Function


Xuping Feng 1 2 , Jing Zhou 2 , Jingyi Li 3 , Xueyan Hou 4 , Longhao Li 1 5 , Yongmin Chen 6 , Shuyue Fu 2 , Li Zhou 2 , Changlong Li 7 , Yunlong Lei 8

Publish date

2018 Nov 2