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 15 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 MXvDfZRwfG:6aXRCpIF{e2G7 NVnZRZBxS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUFRvMkmgZ4VtdHNuIFnDOVA:Oi5zIH7N NVziSXJSOjF2N{C4OlQ>
human SKOV3 cells M3rTW2N6fG:2b4jpZ:Kh[XO|YYm= NGLafXA4OiCq M4OxdmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJHNMV1Z|IHPlcIx{KGGodHXyJFczKGi{czDifUB{fWyob4Loc4RidWmwZTDCJIF{e2G7LDDJR|UxRTBwMEC2JO69VQ>? MmPCNlQ{Pzh5MEm=
human KBM5 cells M3nhO2N6fG:2b4jpZ:Kh[XO|YYm= NXHSNIdUPzJiaB?= M{nXXWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGmvYYTpcoljNXKnc3nzeIFvfCCqdX3hckBMSk13IHPlcIx{KGijcnLvdolv\yCEY4KtRYJtKFR|MUXJJI12fGGwdDDh[pRmeiB5MjDodpMh[nliTWTTJIF{e2G7LDDJR|UxRTBwMEC4N{DPxE1? NUn6OoZqOjBzNEm2OlU>
human HCT116 cells MWTDfZRwfG:6aXRCpIF{e2G7 NVfEXlNYPzJiaB?= MXHDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIR3QyOTZiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2wMlAyKM7:TR?= MUCxPVY{Pzh5NB?=
MDA-MB-468 cells NV7hTWxHS3m2b4TvfIlkyqCjc4PhfS=> M3;2SWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1FSS2PQj20Olgh[2WubIOgZpkhW1KEIHHzd4F6NCCLQ{WwQVAvODFizszN M3;MU|E6PjN5OEe0
human A549 cells MY\GeY5kfGmxbjDhd5NigQ>? MmX3RY51[WexbnnzeEBi[3Srdnn0fUBifCCqdX3hckBRSVJ{IHX4dJJme3OnZDDpckBpfW2jbjDBOVQ6KGOnbHzzJIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[gNoYuVEmJUlzPMW5JOi2rbnT1Z4VlKE6Ia3HwdIFDKGGldHn2ZZRqd25iYomgcJVkcW[ncnHz[UBz\XCxcoTldkBo\W6nIHHzd4F6NCCLQ{WwQVAvODF2IN88US=> MkL4NlM5QTV2OUK=
human Rh30 cells MXnDfZRwfG:6aXRCpIF{e2G7 MUG3NkBp M2LISWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJHJpOzBiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2wMlAyPCEQvF2= NWXVd4llOTl4M{e4O|Q>
human SGC7901 cells MXfDfZRwfG:6aXRCpIF{e2G7 NFnFeIU4OiCq Mn[2R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gV2dEPzlyMTDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F697zOIFnDOVA:OC5yMUWg{txO NH3JbVUyQTZ|N{i3OC=>
human MOLT4 cells NWHEZY15S3m2b4TvfIlkyqCjc4PhfS=> MnuxO|IhcA>? MXTDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDNU2xVPCClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBKSzVyPUCuNFE4KM7:TR?= MYKxPVY{Pzh5NB?=
human SMMC7721 cells MnnmR5l1d3SxeHnjxsBie3OjeR?= NXjWdIc5PzJiaB?= NVvGfJl[S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hW02PQ{e3NlEh[2WubIOgZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3OjeTygTWM2OD1yLkCxPEDPxE1? MUmxPVY{Pzh5NB?=
human MCF7 cells NIH3WFNEgXSxdH;4bYPDqGG|c3H5 M{nKb|czKGh? MkXpR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUWNHPyClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBKSzVyPUCuNFE6KM7:TR?= MU[xPVY{Pzh5NB?=
A549 cells M1jwZ2N6fG:2b4jpZ:Kh[XO|YYm= MXvDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDBOVQ6KGOnbHzzMEBKSzVyPUCuNFE6KM7:TR?= NFHCWo4zOTR5MEi2OC=>
human PC3 cells NInEeHlRem:uaX\ldoF1cW:wIHHzd4F6 M4rvelczKGh? Ml;yRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCSQ{OgZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KFOUQjDhd5NigSxiSVO1NF0xNjB{IN88US=> MkLzNlA5OzN3NEO=
human Bel7402 cells NX\jbIpWS3m2b4TvfIlkyqCjc4PhfS=> NUfaSXdPPzJiaB?= MXLDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDC[Yw4PDB{IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9NE4xOiEQvF2= NF73UIgyQTZ|N{i3OC=>
human 786-O cells M3;P[WN6fG:2b4jpZ:Kh[XO|YYm= NYS1VZNZPzJiaB?= M3PsO2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJFc5Pi2RIHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9NE4xOjJizszN NFTGTZQyQTZ|N{i3OC=>
human DU145 cells M1f1ZWN6fG:2b4jpZ:Kh[XO|YYm= M2jvO|czKGh? M33FNGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGRWOTR3IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9NE4xOjRizszN NFLlNFEyQTZ|N{i3OC=>
human MDA-MB-231 cells MkTnR5l1d3SxeHnjxsBie3OjeR?= NEGwXWQ4OiCq MorWR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUWRCNU2ELUKzNUBk\WyuczDh[pRmeiB5MjDodpMh[nliTWTUJIF{e2G7LDDJR|UxRTBwMEK0JO69VQ>? M4jqcVE6PjN5OEe0
human HO8910 cells MmXlR5l1d3SxeHnjxsBie3OjeR?= NWnKUplDPzJiaB?= MmnHR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gTG85QTFyIHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9NE4xOjhizszN NIHMSmkyQTZ|N{i3OC=>
human HCT15 cells MWfDfZRwfG:6aXRCpIF{e2G7 NGKwRpI4OiCq M4HtcWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGhEXDF3IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9NE4xOjlizszN NGLxXVkyQTZ|N{i3OC=>
human U251 cells MnS3R5l1d3SxeHnjxsBie3OjeR?= MkPNR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gWVI2OSClZXzsd{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJINmdGxicILvcIln\XKjdHnvckBjgSC|dXzmc5Jpd2SjbXnu[UBDKGG|c3H5MEBKSzVyPUCuNFM{KM7:TR?= NGXkOWszPTR4N{G1PC=>
mouse 32D cells MnfmR5l1d3SxeHnjxsBie3OjeR?= NXLTPG5OPzJiaB?= M1PWcGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KG2xdYPlJFMzTCClZXzsd{Bp[XKkb4Lpcochf2muZDD0fZBmKEKlcj3BZowh[W[2ZYKgO|IhcHK|IHL5JG1VWyCjc4PhfUwhUUN3ME2wMlA{OiEQvF2= M1;oOlIxOTR7Nk[1
human KB cells Mnm4R5l1d3SxeHnjxsBie3OjeR?= NHu2e3Q4OiCq NXPYdXViS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hU0JiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4Phfg+9lCCLQ{WwQVAvODR|IN88US=> MX[xPVY{Pzh5NB?=
human HeLa cells MUDDfZRwfG:6aXRCpIF{e2G7 MWm3NkBp MWfDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDI[WxiKGOnbHzzJIFnfGW{IEeyJIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;MD6wOFch|ryP MV2xPVY{Pzh5NB?=
human K562 cells NXTnWIpNS3m2b4TvfIlkyqCjc4PhfS=> NHjMcFg4OiCq M3fXUGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGs2PjJiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2wMlA2KM7:TR?= NETVWJMyQTZ|N{i3OC=>
human SW1116 cells NHnGSGVEgXSxdH;4bYPDqGG|c3H5 NYXY[5VKPzJiaB?= NGPSZppEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBUXzFzMU[gZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KE2WVDDhd5NigSxiSVO1NF0xNjB3MjFOwG0> NWPGWo9NOTl4M{e4O|Q>
human A549 cells MVTDfZRwfG:6aXRCpIF{e2G7 NXrXWnY6PzJiaB?= M2fL[WN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGE2PDliY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2wMlA2QSEQvF2= MnfYNVk3Ozd6N{S=
human MKN28 cells NV;FUnJYS3m2b4TvfIlkyqCjc4PhfS=> M{n3cFczKGh? NHHjSVhEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOU05{ODDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVAvOiEQvF2= NFfEe4IyQTZ|N{i3OC=>
MEF M4ny[WN6fG:2b4jpZ:Kh[XO|YYm= MknnO|IhcA>? NGfKNoNEgXSxdH;4bYNqfHliYXfhbY5{fCCPRV[gZYZ1\XJiN{KgbJJ{KGK7IF3UV{Bie3OjeTygTWM2RTlwMjFOwG0> Mnu4NlAyPDl4NkW=

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
c-Jun; 

PubMed: 22666381     


(C) and (D) Triptolide decreased c-Jun protein level in LNCaP (C) and PC-3 (D) cells in a dose-dependent manner. Cells were treated with indicated dose of Triptolide or Celastrol for 24 h before Western blot analysis. α-tubulin was used as a loading control. 

MDM2; 

PubMed: 27004407     


Western blot assays showing the dose-response and time-course of MDM2 inhibition by triptolide. GAPDH served as an internal control for equal protein loading.

p-AKT / AKT / p-Foxo3a / Foxo3a / p53 ; 

PubMed: 27004407     


Western blot assays showing the inhibitory effect of triptolide on Akt activity. MCF-7 and MDA-MB-468 cells were treated with 50 nM triptolide for different times. Cell extracts were tested by Western blot assay for the expression of MDM2, p53, p21, PUMA, Akt, phosphorylated Akt (S473), Foxo3a and phosphorylated Foxo3a. Phosphorylated Akt and phosphorylated Foxo3a were dramatically decreased following treatment with triptolide. The quantification results are shown on the graphs to the right. 

p-PI3K / PI3K / p85 / p110 ; 

PubMed: 27004407     


Triptolide up-regulates p85 expression. MDA-MB-468 cells were treated with 50 nM triptolide for different times. Cell extracts were tested by Western blot assay for the expression of PI3K, phosphorylated PI3K, p85, p110 and REST.

22666381 27004407
Growth inhibition assay
Cell viability; 

PubMed: 22666381     


(C) Effect of Triptolide on LNCaP cells. (E) Effect of Triptolide on PC-3 cells.

22666381
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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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID