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  • Brand : BIOFRON

  • Catalogue Number : BF-T2004

  • Specification : 98%

  • CAS number : 38647-11-9

  • Formula : C20H22O6

  • Molecular Weight : 358.39

  • PUBCHEM ID : 65411

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Yellow crystalline powder

Botanical Source

Tripterygium wilfordii

Structure Type



Standards;Natural Pytochemical;API




l-triptonide/Triptolide,14-deoxy-14-oxo/Triptonide/(3bS,4aS,5aS,6aS,7aS,7bS,8aS,8bS)-6a-Isopropyl-8b-methyl-3b,4,4a,7a,7b,8b,9,10-octahydrotrisoxireno[6,7:8a,9:4b,5]phenanthro[1,2-c]furan-1,6(3H,6aH)-dione/Trisoxireno[6,7:8a,9:4b,5]phenanthro[1,2-c]furan-1,6(3H,6aH)-dione, 3b,4,4a,7a,7b,8b,9,10-octahydro-8b-methyl-6a-(1-methylethyl)-, (3bS,4aS,5aS,6aS,7aS,7bS,8aS,8bS)-/14-Deoxy-14-oxotriptolide/(3bS,4aS,5aS,6aS,7aS,7bS,8aS,8bS)-8b-methyl-6a-(propan-2-yl)-3b,4,4a,7a,7b,8b,9,10-octahydrotrisoxireno[6,7:8a,9:4b,5]phenanthro[1,2-c]furan-1,6(3H,6aH)-dione




1.5±0.1 g/cm3


Methanol; Dichloromethane

Flash Point

257.8±30.2 °C

Boiling Point

581.1±50.0 °C at 760 mmHg

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#:38647-11-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




The increasing incidence of prostate cancer (PCa) indicates an urgent need for the development of new effective drugs in PCa therapy. Triptonide has been reported to have a strong inhibition activity in cancers through screening of Chinese herbal medicine. This study aims to investigate the effects of triptonide on anti-PCa activity and its mechanisms.

Three human advanced PCa cell lines PC3, DU145, and LNCap, and a human normal prostate epithelial cell line RWPE were treated with a range (0, 1.25, 2.5, 5, 10, 20, 40, 80, 160, and 320 nM) of triptonide concentrations for 72 hours respectively. Then, cell viability was assessed by cell counting kit-8. PCa cells were treated with different doses (0-20 nM) of triptonide for 72 hours. Cell cycle and apoptosis were assessed by flow cytometry assays. Nude mice bearing human PCa xenografts were intraperitoneally injected daily with either triptonide (10 mg/kg/d) or phosphate-buffered saline as a control for 35 days. RNA-sequencing (RNA-seq) was performed by an Illumina Hiseq Sequencing platform and confirmed by a real-time polymerase chain reaction. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes pathway analysis, and ingenuity pathway analysis were used to analyze RNA-seq results.

Triptonide effectively inhibits the proliferation of human PCa cells PC3, DU145, and LNCap in vitro with their IC50 values as 11.961, 10.259, and 12.012 nM, respectively. Triptonide (10 mg/kg) potently inhibits the growth of PCa cell xenografts in vivo at an inhibition rate of over 97.95%. Treatment with triptonide (5 nM) significantly promotes cell apoptosis and retaining cell-cycle arrest in the G2/M phase. RNA-seq data revealed that total of 936 genes were upregulated or downregulated in triptonide treated. Moreover, the phosphorylation of mechanistic target of rapamycin (mTOR) and the downstream protein p70S6K were both inhibited, most obviously in PCa cells.

Our findings suggest that triptonide can efficaciously suppress PCa growth in vitro and in vivo via inhibiting the phosphorylation of mTOR and the activities of related downstream signaling pathways.

© 2019 Wiley Periodicals, Inc


RNA-seq; mechanistic target of rapamycin; proliferation; prostate cancer; triptonide


Triptonide acts as a novel antiprostate cancer agent mainly through inhibition of mTOR signaling pathway.


Dong F1,2, Yang P3, Wang R1,2, Sun W4, Zhang Y1,2, Wang A1,2, Chen M1,2, Chen L1,2, Zhang C1,2, Jiang M1,2.

Publish date

2019 Aug




Lung cancer is a leading lethal disease with a 5-year survival rate of only 16%. Inadequate potent anti-cancer drugs appear to be a bottleneck in the treatment of lung cancer; hence, how to develop effective anti-lung cancer therapeutics is an urgent problem. In this study, we aim to explore a novel compound with potent anti-lung cancer effect and study its anti-cancer mechanisms. We found that triptonide at very low concentrations of 5-10 nM caused a marked suppression of cell proliferation and colony formation of lung cancer cells. More interestingly, triptonide also robustly inhibited the lung cancer cell formation of tumor spheres, and reduced the stemness and tumorigenicity of the sphere-forming cells. In vivo studies showed that administration of triptonide significantly inhibited the tumor growth with low toxicity. Molecular mechanistic studies revealed that triptonide significantly decreased expression of the Gli1 at both mRNA and protein levels by repressing Gli1 gene promoter activity. Additionally, triptonide reduced the levels of cancer stem cell key signaling protein sonic hedgehog (Shh), but increased the amount of Ptch1, a protein binding to SMO to diminish the Shh signal transduction, thus inhibition of the Shh-Gli1 signaling pathway. Together, our findings show that triptonide effectively inhibits lung cancer cell growth, stemness, and tumorigenicity, and support the notion that triptonide is a new Shh-Gli1 signaling inhibitor and a novel anti-lung cancer drug candidate for further developing effective lung cancer therapeutics.

Copyright © 2019 Elsevier Inc. All rights reserved.


Cancer therapy; Gli1; Lung cancer; Shh; Signaling pathway; Triptonide


Triptonide inhibits lung cancer cell tumorigenicity by selectively attenuating the Shh-Gli1 signaling pathway.


Zhang M1, Tan S1, Yu D2, Zhao Z1, Zhang B1, Zhang P1, Lv C1, Zhou Q3, Cao Z4.

Publish date

2019 Feb 15




Advanced stage nasopharyngeal carcinoma (NPC) has a poor prognosis. Triptonide (“TN”) is a small molecule monomer extract from the ancient Chinese herb Tripterygium wilfordii Hook. We show that TN, at nanomolar concentrations, potently inhibited survival and proliferation of multiple established and primary human NPC cells. TN induced NPC cell cycle arrest and apoptosis activation. NPC cell migration and invasion were also inhibited by TN. Importantly, TN was non-cytotoxic to nasopharyngeal epithelial cells. TN treatment in NPC cells disrupted LncRNA THOR (“Lnc-THOR”)-IGF2BP1 association, causing depletion of Lnc-THOR and downregulation of IGF2BP1 mRNA targets (Myc, IGF2 and Gli1). Lnc-THOR or IGF2BP1 knockout by CRISPR/Cas9 gene-editing methods mimicked and abolished TN’s actions in NPC cells. Conversely, ectopic Lnc-THOR overexpression inhibited TN-induced cytotoxicity in NPC cells. Significantly, Lnc-THOR, IGF2BP1 and its mRNA targets are elevated in human NPC tissues and cells, but almost undetectable in nasopharyngeal epithelial tissues and cells. In vivo, intraperitoneal TN administration significantly inhibited subcutaneous NPC xenograft growth in mice. Similarly, Lnc-THOR-knockout HONE-1 xenografts grew significantly slower than control tumors. Thus, TN inhibits human NPC cell growth in vitro and in vivo via disrupting Lnc-THOR-IGF2BP1 signaling.

Copyright © 2018 Elsevier B.V. All rights reserved.


IGF2BP1; LncRNA THOR; Molecularly-targeted therapy; Nasopharyngeal carcinoma; Triptonide


Triptonide inhibits human nasopharyngeal carcinoma cell growth via disrupting Lnc-RNA THOR-IGF2BP1 signaling.


Wang SS1, Lv Y2, Xu XC2, Zuo Y3, Song Y3, Wu GP4, Lu PH5, Zhang ZQ6, Chen MB7.

Publish date

2019 Feb 28

Description :

Triptonide(NSC 165677; PG 492), extracted from Tripterygium wilfordii Hook, inhibited the proliferation of mouse splenocytes induced by suboptimal concentration of concanavalin A or lipopolysaccharide at concentrations of 0.02, 0.1, and 0.5 mg/ml.