Triptolide (PG490)

Catalog No.S3604 Synonyms: NSC 163062

Triptolide (PG490) Chemical Structure

Molecular Weight(MW): 360.4

Triptolide is a diterpene triepoxide, immunosuppresive agent extracted from the Chinese herb Tripterygium wilfordii. It functions as a NF-κB inhibitor with dual actions by disruption of p65/CBP interaction and by reduction of p65 protein.

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Cited by 10 Publications

5 Customer Reviews

  • Spironolactone (sp.) and triptolide inhibit NER in myeloma cells. RPMI8226 cells were incubated with dimethyl sulfoxide (DMSO), spironolactone (10 μm) or triptolide (1 μm) for 6 h before NER evaluation. The figure represents the persistence of DNA-damage signal 150 min after exposure to UV (AFU: arbitrary fluorescent unit). Figure 4a shows representative merged pictures of DAPI and DDB2 proteo-probe signal (b).

    Leukemia, 2018, 32(1):111-119. Triptolide (PG490) purchased from Selleck.

    Treatment with triptolide selectively induces apoptosis of cultured and primary CD19+ CLL cells. A. Percent apoptosis (Annexin V-FITC and PI staining) in Mec-1, Mec-2 and WAC3-CD5+ cells exposed to the indicated doses of triptolide for 48 hrs; bars indicate standard deviation. B. Percent apoptosis of CD19+ normal and primary CLL (both high and low risk) cells exposed to the indicated doses of triptolide for 48 hrs; bars indicate standard deviation. C. Percent of WaC3-CD5+ and Mec-1 cells in different phases of the cell cycle (G0/G1, S and G2/M) exposed to the indicated doses of triptolide for 24 hrs. D. Immunoblot analyses of HSF1, HSP70, cleaved caspase-3 and β-actin obtained from the cell lysates of CD19+ primary CLL cell samples treated with the indicated doses of triptolide for 24 hrs.

    Oncotarget, 2015, 6(31):31767-79. Triptolide (PG490) purchased from Selleck.

  • Triptolide decreases the levels of XRCC1, PARP1 and RAD51. (A) After treatment with 30 nM triptolide for 24 h, western blot assay shows triptolide decreases the levels of XRCC1, PARP1 and slightly influences the levels of RAD51. The assay was repeated in triplicate. (B) The quantification of western blot assay was analyzed. t-test, ***p < 0.001, **p < 0.01 vs the control group.

    Biomed Pharmacother, 2019, 109:1541-1546. Triptolide (PG490) purchased from Selleck.

    Triptolide inhibited the growth, viability and ACTH secretion of AtT20 cells. (A) AtT20 cells were treated with increasing doses of triptolide. Cell growth was determined by CCK8 assay after 96 h. The data were quantified as% of vehicle (0.01% DMSO). (B) AtT20 cells were treated with increasing doses of triptolide for 96 h. Cells were trypsinized and counted. The data were calculated as% of vehicle control. (C) AtT20 cells were treated with indicated doses of triptolide for 14–21 days. The colonies were visualized by crystal violet staining and quantified in 4 random fields each well. The average number of colonies were calculated and presented as% of vehicle control. (D) AtT20 cells were treated with 100 nM triptolide for 24 h, 48 h, 72 h and 96 h respectively. Cell growth was determined by CCK8 assay. The data were calculated as% of corresponding vehicle control. (E) Cells were treated with indicated doses of triptolide for 24 h. Effects of triptolide on Pomc mRNA expression were assessed by real-time PCR, using β-actin as a control. (F) Cells were treated with indicated doses of triptolide for 24 h. Equal amount of the cell culture supernatants were used for hormone measurement by competitive-ELISA, ACTH secreting levels were calculated according to the standard reference provided by the company. Data were normalized with the number of cells. All Data were presented as means ± SD of three independent experiments each performed with at least quadruplicates. *P < 0.05; **P < 0.01. vs control.

    Biomed Pharmacother, 2017, 95:771-779. Triptolide (PG490) purchased from Selleck.

  • TtT/GF and AtT20 cells were treated with triptolide at 0, 50, 100 nM for 48 h. Transwell invasion assay was employed to detect the invasion ability (200×). All data were shown as means ± SD of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 vs. NC (negative control) group.

    Life Sci, 2018, 194:150-156. Triptolide (PG490) purchased from Selleck.

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Biological Activity

Description Triptolide is a diterpene triepoxide, immunosuppresive agent extracted from the Chinese herb Tripterygium wilfordii. It functions as a NF-κB inhibitor with dual actions by disruption of p65/CBP interaction and by reduction of p65 protein.
In vitro

Triptolide is a diterpene triepoxide with potent immunosuppressive and antiinflammatory properties. Triptolide is shown to inhibit the expression of IL-2 in activated T cells at the level of purine-box/nuclear factor and NF-κB mediated transcription activation. [1] Triptolide inhibits the proliferation and colony formation of tumor cells at extremely low concentrations (2–10 ng/mL). Triptolide has an inhibitory activity on breast, stomach and leukemia cell line HL-60 cells. Triptolide induces apoptosis in tumor cells by blocking NF-κB activation and sensitizing tumor cells for TNF-&alpha induced programmed cell death. [2]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human HT-29 cells M1zQ[mN6fG:2b4jpZ:Kh[XO|YYm= NUTaeJZvS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUFRvMkmgZ4VtdHNuIFnDOVA:Oi5zIH7N Mm\ENlE1PzB6NkS=
human SKOV3 cells M3jFN2N6fG:2b4jpZ:Kh[XO|YYm= NWXMU4NbPzJiaB?= NH;3cldEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBUU0:YMzDj[YxteyCjZoTldkA4OiCqcoOgZpkhe3WuZn;ybI9l[W2rbnWgRkBie3OjeTygTWM2OD1yLkCwOkDPxE1? MoC1NlQ{Pzh5MEm=
human KBM5 cells NX;QbmdwS3m2b4TvfIlkyqCjc4PhfS=> M1n6bVczKGh? M4W1bGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGmvYYTpcoljNXKnc3nzeIFvfCCqdX3hckBMSk13IHPlcIx{KGijcnLvdolv\yCEY4KtRYJtKFR|MUXJJI12fGGwdDDh[pRmeiB5MjDodpMh[nliTWTTJIF{e2G7LDDJR|UxRTBwMEC4N{DPxE1? MWmyNFE1QTZ4NR?=
human HCT116 cells NGXlR3pEgXSxdH;4bYPDqGG|c3H5 NXmxcFl{PzJiaB?= M3nWbGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGhEXDFzNjDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVAvODFizszN NGDHdZAyQTZ|N{i3OC=>
MDA-MB-468 cells MmXTR5l1d3SxeHnjxsBie3OjeR?= NFrkTWxEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOTEFvTVKtOFY5KGOnbHzzJIJ6KFOUQjDhd5NigSxiSVO1NF0xNjBzIN88US=> MVWxPVY{Pzh5NB?=
human A549 cells NIrlc41HfW6ldHnvckBie3OjeR?= NV7GT|RySW62YXfvcol{fCCjY4Tpeol1gSCjdDDoeY1idiCSQWKyJIV5eHKnc4Pl[EBqdiCqdX3hckBCPTR7IHPlcIx{KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4YhOmZvTFnHVmxQNU6KMj3pcoR2[2WmIF7Gb4FxeGGEIHHjeIl3[XSrb36gZpkhdHWlaX\ldoF{\SC{ZYDvdpRmeiCpZX7lJIF{e2G7LDDJR|UxRTBwMEG0JO69VQ>? MW[yN|g6PTR7Mh?=
human Rh30 cells NWfDPGFES3m2b4TvfIlkyqCjc4PhfS=> MX63NkBp NYWxfJJzS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hWmh|MDDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVAvODF2IN88US=> NVq3Z3ZmOTl4M{e4O|Q>
human SGC7901 cells MlGwR5l1d3SxeHnjxsBie3OjeR?= MVi3NkBp MoLyR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gV2dEPzlyMTDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F697zOIFnDOVA:OC5yMUWg{txO NE\nT4gyQTZ|N{i3OC=>
human MOLT4 cells NUXWeoRLS3m2b4TvfIlkyqCjc4PhfS=> NY\4Opo4PzJiaB?= NVewSVd{S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVU:OVESgZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KE2WVDDhd5NigSxiSVO1NF0xNjBzNzFOwG0> NETwT3cyQTZ|N{i3OC=>
human SMMC7721 cells MoPjR5l1d3SxeHnjxsBie3OjeR?= NUfSWnIyPzJiaB?= NWDiUI4zS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hW02PQ{e3NlEh[2WubIOgZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3OjeTygTWM2OD1yLkCxPEDPxE1? NX6xb|djOTl4M{e4O|Q>
human MCF7 cells Mn\WR5l1d3SxeHnjxsBie3OjeR?= M4nsSFczKGh? M1SyVGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1ETjdiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2wMlAyQSEQvF2= MV2xPVY{Pzh5NB?=
A549 cells MV7DfZRwfG:6aXRCpIF{e2G7 M3LjWWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGE2PDliY3XscJMtKEmFNUC9NE4xOTlizszN MYKyNVQ4ODh4NB?=
human PC3 cells M2fMXHBzd2yrZnXyZZRqd25iYYPzZZk> NVzs[HlEPzJiaB?= Mn7uRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCSQ{OgZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KFOUQjDhd5NigSxiSVO1NF0xNjB{IN88US=> NHixd5MzODh|M{W0Ny=>
human Bel7402 cells NUixNmZIS3m2b4TvfIlkyqCjc4PhfS=> NH3zbIo4OiCq NEPQelZEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBD\Wx5NECyJINmdGy|IHHmeIVzKDd{IHjyd{BjgSCPVGSgZZN{[XluIFnDOVA:OC5yMjFOwG0> NVTKOol2OTl4M{e4O|Q>
human 786-O cells NGS5OZREgXSxdH;4bYPDqGG|c3H5 M4npOFczKGh? MUfDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjC3PFYuVyClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBKSzVyPUCuNFIzKM7:TR?= Mnq0NVk3Ozd6N{S=
human DU145 cells NX\heXdnS3m2b4TvfIlkyqCjc4PhfS=> NIC3e2s4OiCq NFTtT2JEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBFXTF2NTDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVAvODJ2IN88US=> MX2xPVY{Pzh5NB?=
human MDA-MB-231 cells M361XGN6fG:2b4jpZ:Kh[XO|YYm= NHHPd4g4OiCq NEnCdVNEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOTEFvTVKtNlMyKGOnbHzzJIFnfGW{IEeyJIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;MD6wNlQh|ryP NVLUS41FOTl4M{e4O|Q>
human HO8910 cells MnftR5l1d3SxeHnjxsBie3OjeR?= MYS3NkBp M2TDVGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGhQQDlzMDDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVAvODJ6IN88US=> NFfvVmkyQTZ|N{i3OC=>
human HCT15 cells MW\DfZRwfG:6aXRCpIF{e2G7 MlXvO|IhcA>? M4\r[mN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGhEXDF3IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9NE4xOjlizszN NEjacJEyQTZ|N{i3OC=>
human U251 cells M2LHdmN6fG:2b4jpZ:Kh[XO|YYm= NVLRToxKS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hXTJ3MTDj[YxteyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKGOnbHygdJJwdGmoZYLheIlwdiCkeTDzeYxnd3Kqb3ThcYlv\SCEIHHzd4F6NCCLQ{WwQVAvODN|IN88US=> NIXt[o8zPTR4N{G1PC=>
mouse 32D cells NYr5eoNWS3m2b4TvfIlkyqCjc4PhfS=> M3H2[|czKGh? NUKwbHhvS3m2b4TvfIlkcXS7IHHnZYlve3RibX;1d4UhOzKGIHPlcIx{KGijcnLvdolv\yC5aXzkJJR6eGViQnPyMWFjdCCjZoTldkA4OiCqcoOgZpkhVVSVIHHzd4F6NCCLQ{WwQVAvODN{IN88US=> MXuyNFE1QTZ4NR?=
human KB cells MUHDfZRwfG:6aXRCpIF{e2G7 M17RflczKGh? Ml\rR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gT2Ih[2WubIOgZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3Ojef-8kEBKSzVyPUCuNFQ{KM7:TR?= NUfBNYJmOTl4M{e4O|Q>
human HeLa cells M4j1PGN6fG:2b4jpZ:Kh[XO|YYm= NW\he3loPzJiaB?= NWPKWWJMS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUGWOYTDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVAvODR5IN88US=> MVexPVY{Pzh5NB?=
human K562 cells M4jyRmN6fG:2b4jpZ:Kh[XO|YYm= NH7EZ4g4OiCq NV3tZW5oS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUzV4MjDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVAvODVizszN M3PpO|E6PjN5OEe0
human SW1116 cells NG\LV5lEgXSxdH;4bYPDqGG|c3H5 NIm2XJg4OiCq NVr0OHhkS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hW1dzMUG2JINmdGy|IHHmeIVzKDd{IHjyd{BjgSCPVGSgZZN{[XluIFnDOVA:OC5yNUKg{txO NVPVRoRFOTl4M{e4O|Q>
human A549 cells NFTPOXNEgXSxdH;4bYPDqGG|c3H5 MWW3NkBp M1LKOWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGE2PDliY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2wMlA2QSEQvF2= NYTXPVZZOTl4M{e4O|Q>
human MKN28 cells NHfybY9EgXSxdH;4bYPDqGG|c3H5 MYe3NkBp M4XjcmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1MVjJ6IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9NE4zKM7:TR?= Mn7INVk3Ozd6N{S=
MEF NWXwPGI6S3m2b4TvfIlkyqCjc4PhfS=> MYe3NkBp M4XDRmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KE2HRjDh[pRmeiB5MjDodpMh[nliTWTTJIF{e2G7LDDJR|U:QS5{IN88US=> M{TK[FIxOTR7Nk[1

... Click to View More Cell Line Experimental Data

In vivo Triptolide synergizes with cyclosporin A in promoting graft survival in animal models and in suppression of graft versus host disease in allogeneic bone marrow transplants. In addition, it induces apoptosis in tumor cells and potentiates tumor necrosis factor (TNF-α) induction of apoptosis in part through the suppression of c-IAP2 and c-IAP1 induction. [1] [3] Triptolide treatment for 2–3 weeks inhibits the growth of xenografts formed by four different tumor cell lines (B16 melanoma, MDA-435 breast cancer, TSU bladder cancer, and MGC80-3 gastric carcinoma), indicating that TPL has a broad spectrum of activity against tumors that contain both wild-type and mutant forms of p53. In addition, Triptolide inhibits experimental metastasis of B16F10 cells to the lungs and spleens of mice. [2] Triptolide has in vitro and in vivo activities against mouse models of polycystic kidney disease. [4] LD50: Mice 0.83mg/kg (i.v.). [5]

Protocol

Solubility (25°C)

In vitro DMSO 72 mg/mL warmed (199.77 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing.
3mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 360.4
Formula

C20H24O6

CAS No. 38748-32-2
Storage powder
in solvent
Synonyms NSC 163062

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03403569 Not yet recruiting HIV-infection/AIDS Peking Union Medical College Hospital August 1 2018 Phase 3
NCT03403569 Not yet recruiting HIV-infection/AIDS Peking Union Medical College Hospital August 1 2018 Phase 3
NCT02115659 Unknown status Autosomal Dominant Polycystic Kidney Disease (ADPKD) Shanghai Changzheng Hospital April 2014 Phase 3
NCT02115659 Unknown status Autosomal Dominant Polycystic Kidney Disease (ADPKD) Shanghai Changzheng Hospital April 2014 Phase 3
NCT01817283 Unknown status HIV LI Taisheng|Peking Union Medical College January 2013 Phase 1|Phase 2
NCT01817283 Unknown status HIV LI Taisheng|Peking Union Medical College January 2013 Phase 1|Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID