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CAS No.:38748-32-2

Catalogue No.: BP1411
Formula: C20H24O6
Mol Weight: 360.406
Botanical Source: Tripterygium wilfordii Hook.f.
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Product Name: Triptolide

Synonym name:
Catalogue No.: BP1411
Cas No.: 38748-32-2
Formula: C20H24O6
Mol Weight: 360.406
Botanical Source: Leigongteng, Tripterygium wilfordii, Tripterygium regelii and Tripterygium forrestii

Purity: >99%
Analysis Method: HPLC-DAD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
Can be supplied from milligrams to grams, up to kilograms.

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Typical COA:

Triptolide is a diterpenoid epoxide which is endogenously produced by the thunder god vine, Tripterygium wilfordii. It has in vitro and in vivo activities against mouse models of polycystic kidney disease and pancreatic cancer, but its physical properties limit its therapeutic potential.Consequently, a synthetic prodrug, minnelide, is being studied clinically instead.Due to its low solubility in water, several water-soluble analogs have been formulated, including Minnelide, which is currently in Phase I clinical trials.

1,Triptolide and chemotherapy cooperate in tumor cell apoptosis. A role for the p53 pathway.
 J Biol Chem. 2001 Jan 19;276(3):2221-7. Epub 2000 Oct 26.

2,Triptolide, an active compound identified in a traditional Chinese herb, induces apoptosis of rheumatoid synovial fibroblasts. BMC Pharmacology 2004, 4:2

3,Triptolide, a constituent of immunosuppressive Chinese herbal medicine, is a potent suppressor of dendritic-cell maturation and trafficking. Blood, 1 October 2005, Vol. 106, No. 7, pp. 2409-2416.

4,Triptolide: A Potential Drug For Polycystic Kidney Disease ScienceDaily  Mar. 12, 20

5, Triptolide is an inhibitor of RNA polymerase I and II-dependent transcription leading predominantly to down-regulation of short-lived mRNA.

Abstract: Triptolide, a natural product extracted from the Chinese plant Tripterygium wilfordii, possesses antitumor properties. Despite numerous reports showing the proapoptotic capacity and the inhibition of NF-kappaB-mediated transcription by triptolide, the identity of its cellular target is still unknown. To clarify its mechanism of action, we further investigated the effect of triptolide on RNA synthesis in the human non-small cell lung cancer cell line A549. Triptolide inhibited both total RNA and mRNA de novo synthesis, with the primary action being on the latter pool. We used 44K human pan-genomic DNA microarrays and identified the genes primarily affected by a short treatment with triptolide. Among the modulated genes, up to 98% are down-regulated, encompassing a large array of oncogenes including transcription factors and cell cycle regulators. We next observed that triptolide induced a rapid depletion of RPB1, the RNA polymerase II main subunit that is considered a hallmark of a transcription elongation blockage. However, we also show that triptolide does not directly interact with the RNA polymerase II complex nor does it damage DNA. We thus conclude that triptolide is an original pharmacologic inhibitor of RNA polymerase activity, affecting indirectly the transcription machinery, leading to a rapid depletion of short-lived mRNA, including transcription factors, cell cycle regulators such as CDC25A, and the oncogenes MYC and Src. Overall, the data shed light on the effect of triptolide on transcription, along with its novel potential applications in cancers, including acute myeloid leukemia, which is in part driven by the aforementioned oncogenic factors.


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