CAS 38748-32-2 Triptolide, Tripterygium wilfordii - CAS 38748-32-2

CAT	AP38748322-A
CAS	38748-32-2
Structure
Molecular Weight	360.40

Description	A novel diterpene triepoxide isolated from the Chinese herb Tripterygium wilfordii that acts as a potent immunosuppressant and anti-inflammatory agent.
Solubility	DMSO: 20 mg/mL
Assay	≥95% (HPLC)
Color	off-white
Form	solid; protect from light
Size	1MG, 5MG
Storage Conditions	-20C

Disappearance of Sexual Dimorphism in Triptolide Metabolism in Monosodium Glutamate Treated Neonatal Rats

Li Liu, Zhenzhou Jiang, Xiaofeng Huang, Jing Liu, Juan Zhang, Jingwei Xiao, Qingli Bao, Jing Wen, Shuang Zhang, Dan Zhu, Pinghu Zhang, Luyong Zhang

Arzneimittelforschung. 2011;61(2):98-103.

PMID: 21428244

Effect of Triptolide on Aromatase Activity in Human Placental Microsomes and Human Placental JEG-3 Cells

Juan Zhang, Zhenzhou Jiang, Luyong Zhang

Arzneimittelforschung. 2011;61(12):727-33.

PMID: 22282961

Effect of Triptolide on Progesterone Production From Cultured Rat Granulosa Cells

J Zhang, Z Jiang, X Mu, J Wen, Y Su, L Zhang

Arzneimittelforschung. 2012 Jun;62(6):301-6.

PMID: 22592319

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Case Study

The Impact of Triptolide on Tumors via Autophagy Pathways

Feng, Ke, et al. Heliyon (2024).

Numerous molecular pathways mediate the autophagy modulation by triptolide, with oxidative stress playing a crucial role. In fact, triptolide can alter the regulation of various genes associated with oxidative stress cascades, as demonstrated by genetic code microarray studies.
Triptolide triggers autophagy in glioblastoma cell lines by increasing levels of reactive oxygen species (ROS) and intracellular calcium. The stimulation of autophagy by triptolide in pancreatic cancer cells is associated with elevated intracellular calcium levels. This mechanism is also regulated by sustained endoplasmic reticulum (ER) stress, inhibition of the p70S6K/Akt/mTOR cascade, and activation of the ERK signaling pathway. Triptolide induces ER stress in prostate tumor cells, leading to the release of free calcium into the cytoplasm. Subsequently, calcium activates the β-(CaMKKβ)-AMPK signaling cascade, resulting in the inhibition of mTOR and regulation of the PI3KIII and ULK1 subunits, thereby initiating autophagy.
In podocytes, triptolide increases autophagy and activates the mTOR-ULK1 pathway while downregulating levels of p-mTOR, p-Akt, and p-ULK1. Other processes have also been investigated in the autophagy regulated by triptolide. Activation of ERK protein may be related to the stimulation of autophagy by triptolide in lung cancer cells. Triptolide enhances p53 nuclear localization in Hela cells, leading to an increase in the lysosomal protein DNA damage-regulated autophagy modulator (DRAM) and a decrease in mTOR activity.
In the rat brain, triptolide improves autophagosome function by reducing the elevated expression levels of mTOR caused by ischemic injury. Furthermore, triptolide may have specific mechanisms of action in cardiomyocytes and breast cancer cells within lysosomes. Therefore, triptolide may regulate autophagy by targeting various mechanisms or signaling pathways.

Triptolide Targets and Inhibits the HNF1A/SHH Axis

Li, Ling-bing, et al. Acta Pharmacologica Sinica 45.5 (2024): 1060-1076.

Taxane resistance is associated with poor prognosis in non-small cell lung cancer (NSCLC) patients, and there are currently no promising drugs to treat taxane resistance. This study investigates the molecular mechanisms of chemoresistance in human NSCLC-derived cell lines. Taxane-resistant NSCLC cell lines (A549/PR and H460/PR) were established through prolonged exposure to paclitaxel. It was found that the diterpene epoxide triptolide, isolated from the traditional medicine triptolide Hook F, effectively enhanced the sensitivity of taxane-resistant cells to paclitaxel by reducing the expression of ABCB1 both in vivo and in vitro.
High-throughput sequencing revealed that the SHH-activated Hedgehog signaling pathway plays a significant role in this process. Triptolide was found to directly bind to the SHH transcription factor HNF1A, inhibiting HNF1A/SHH expression and thereby weakening Hedgehog signaling. In NSCLC tumor tissue microarrays and cancer network databases, a positive correlation between HNF1A and SHH expression was identified.
The results reveal a novel molecular mechanism whereby triptolide targets and inhibits HNF1A, blocking the activation of the Hedgehog signaling pathway and reducing ABCB1 expression. This study suggests that triptolide has potential clinical applications and provides a promising outlook for targeting the HNF1A/SHH pathway in the treatment of taxane-resistant NSCLC patients.

Site-Specific Construction of Antibody-Drug Conjugates Based on Triptolide

Wei, Ding, et al. Bioorganic & Medicinal Chemistry 51 (2021): 116497.

Antibody-drug conjugates (ADCs) have emerged as effective agents for targeted delivery of cytotoxic drugs while reducing off-target side effects. Triptolide has gained attention for its potential use in ADC development. In this study, three rationally designed triptolide drug linkers were synthesized for site-specific ADC construction.
To prepare the linker drugs, each component was synthesized separately, including the payload derivative 1, linker-drug fragments 2-4, and the coupling linker BVP. Triptolide was converted into its reactive carbonate analog 1 through a reaction with 4-nitrophenyl carbonyl chloride. Compound 1 reacted with the linker NH₂-CH₂CH₂-(OCH₂CH₂)₃-N₃ to yield linker-drug fragment 2. Compound 1 was treated with N,N'-dimethyl ethylenediamine to obtain carbamate 3a, which further reacted with the linker COOH-CH₂-(OCH₂CH₂)₃-N₃ to produce linker-drug fragment 3. Another linker-drug fragment 4 was also derived from compound 1. The PEG branched carbamate 4a was obtained by reacting compound 1 with t-butyl (2,5,8,11-tetraoxatetradecyl-16-yl)(methyl)carbamate. After removing the Boc protecting group from 4a, it was condensed with COOH-CH₂-(OCH₂CH₂)₃-N₃ to yield compound 4. Subsequently, the BVP-based linker drugs L1-TL, L2-TL, and L3-TL were prepared via azide-alkyne cycloaddition reactions.