Triptophenolide is a colorless crystalline plate isolated from ethyl acetate extracts of Tripterygium wilfordii. IC50 value:Target:In vitro: Triptophenolide can remarkably inhibit the delayed type hypersensitivity (DTH) reaction induced by DNCB and BSA; and diminished the peripheral blood ANAE+lymphocytes in rats and micc. Moreover, triptophenolide can dramatically increase the amount of total serum complement and significautly decrcase the serum antibody products (1gG ) of rats and mice. The phagocytosis of perioneal exudate macrophages in mice present double effects in vitro [1].In vivo:
Paclitaxel is a potent anticancer medication which can promote microtubule (MT) assembly, inhibit MT depolymerization, and change MT dynamics required for mitosis and cell proliferation.
Cynaropicrin is a sesquiterpene lactone which can inhibit tumor necrosis factor (TNF-α) release with IC50s of 8.24 and 3.18 μM for murine and human macrophage cells, respectively. Cynaropicrin also inhibits the increase of cartilage degradation factor (MMP13) and suppresses NF-κB signaling.
alpha-Boswellic acid is a natural product.
20-Deoxyingenol is a natural compound.
Ginsenoside Rg3 is the main component of Red ginseng. Ginsenoside Rg3 inhibits Na+ and hKv1.4 channel with IC50s of 32.2±4.5 and 32.6±2.2 μM, respectively. Ginsenoside Rg3 also inhibits Aβ levels, NF-κB activity, and COX-2 expression.
Picrotoxin is a noncompetitive antagonist of GABAA receptor.
Curdione, one of the major sesquiterpene compounds from Rhizoma Curcumae, has been shown to exhibit multiple bioactive properties.IC50 value: 60–80 μMTarget:In vitro: The study of the influence of curdione on the hemorheological changes in blood stasis model rats and thrombolysis in vitro showed that curdione only possessed thrombolytic effect in dose of 0.235 g·L-1 and 2.35 g·L-1, but has not the notable activity of thrombolysis [1]. The effects of curdione on human platelet aggregation induced by thrombin (0.3 U/ml) were tested in vitro. Curdione preferentially inhibited PAF- and thrombin- induced platelet aggregation in a concentration-dependent manner (IC50: 60–80 μM), whereas much higher concentrations of curdione were required to inhibit platelet aggregation induced by ADP and AA. Curdione also inhibited P-selectin expression in PAF-activated platelets. Moreover, curdione caused an increase in cAMP levels and attenuated intracellular Ca2+ mobilization in PAF-activated platelets. In vivo: Curdione showed significant antithrombotic activity [2].
Alisol C 23-acetate, a natural product extracted from Alisma orientale, can significantly and strongly inhibit DTH response after oral administration.
Dodecanoic acid ingenol ester is a natural compound.
Pristimerin is a potent and reversible monoacylglycerol lipase (MGL) inhibitor with an IC50 of 93 nM.
Oleanolic acid is a triterpenoid, inhibits infection by HIV-1 in in vitro infected PBMC, naturally infected PBMC and monocyte/macrophages with EC50 of 22.7 mM, 24.6 mM and 57.4 mM, respectively. Besides,it has IC50 of 17μM for the production of leukotriene B4 from rat peritoneal leukocytes.IC50:17μM(The production of leukotriene B4 from rat peritoneal leukocytes)[1]IC50:22.7 mM, 24.6 mM and 57.4 mM(in vitro infected PBMC, naturally infected PBMC and monocyte/macrophages by HIV-1, respectively.[2]In vitro: The highest of the four tested doses (100 μM), showed only a slight inhibition approximately, 30%. In contrast, the more powerful effect of oleanonic acid in this system, suggests that it acts through a mechanism related to the inhibition of 5-lipoxygenase, either directly or interfering with some of the mechanisms that participate in the complex activation of this enzyme. Oleanonic acid also acts by reducing prostaglandin synthesis.[1]Oleanolic acid inhibits the HIV-1 replication in all the cellular systems used (EC50 values: 22.7 microM, 24.6 microM and 57.4 microM for in vitro infected PBMC, naturally infected PBMC and M/M, respectively). As regards the mechanism of action, oleanolic acid inhibits in vitro the HIV-1 protease activity.[2]In vivo: Oleanonic acid exerted no activity on the oedema induced by application of ethyl phenylpropiolate after a pre-treatment of 16 h. In the TPA ear oedema test, it showed a non-significant 28% inhibition. However, when assayed on the ear oedema induced by DPP, oleanonic acid reduced the swelling by 40%, an effect similar to that of the standard carbamazepine. In the mouse model of delayed hypersensitivity induced by dinitrofluorobenzene, oleanonic acid was ineffective at both 24 and 96 h, while oleanolic acid reduced non-significantly the oedema at 96 h by 32%.In the TPA model of chronic inflammation induced by multiple applications, oleanonic acid showed a significant effect, with 45% inhibition. In contrast, oleanolic acid was inactive. Both inhibited the neutrophil infiltration measured as myeloperoxidase activity by 84% and 67%, respectively. The inhibition observed for dexamethasone on the swelling and myeloperoxidase activity was around 90%. The histological study of ears treated only with repeated doses of TPA showed an extensive diffusive inflammatory lesion with microabscesses affecting dermis and epidermis. The main infiltrating cells in the skin were neutrophils and epithelial thickness was 6.6±1.0 cells. In the tissues treated only with the solvent acetone, epithelial thickness was 2.1±0.5 and no signs of lesion or leukocyte infiltration were detectable. The multidose treatment with oleanonic acid reduced both the intensity and extension of the damage produced by TPA, as this was localized in the dermis, where the main infiltrating cells were lymphocytes, and where fibrosis was observed. In this case, epithelium thickness was 4.4±0.7 cells. The ears treated with dexamethasone showed minimal inflammatory lesions and sometimes none at all, and the epithelium thickness was 4.3±0.7 cells.The paw oedema induced by bradykinin was significantly reduced (61%) by oleanonic acid, whereas isoprenaline had a slightly lower effect (52%). Both oleanolic and oleanonic acid also reduced the paw oedema induced by phospholipase A2; the latter showing its strongest effect at 60 min, with an 84% inhibition, and maintaining activity at 90 min. Oleanolic acid also had its maximum effect at 60 min, vanishing at 90 min, while the activity of cyproheptadine was uniform along the experiment, ranging 80–90% inhibition .[1]
Betulinaldehyde(Betunal) belongs to pentacyclic triterpenoids and was reported to exhibit antimicrobial activities against bacteria and fungi, including S. aureus.IC50 value:Target: Betulinaldehyde(Betunal) belongs to pentacyclic triterpenoids that are based on a 30-carbon skeleton comprising four six-membered rings and one five-membered ring. Betulinaldehyde regulates multiple desirable targets which could be further explored in the development of therapeutic agents for the treatment of S. aureus infections [1]. Study compounds α-amyrin [3β-hydroxy-urs-12-en-3-ol (AM)], betulinic acid [3β-hydroxy-20(29)-lupaene-28-oic acid (BA)] and betulinaldehyde [3β-hydroxy-20(29)-lupen-28-al (BE)] belong to pentacyclic triterpenoids and were reported to exhibit antimicrobial activities against bacteria and fungi, including S. aureus. The MIC values of these compounds against a reference strain of methicillin-resistant S. aureus (MRSA) (ATCC 43300) ranged from 64 μg/ml to 512 μg/ml. However, the response mechanisms of S. aureus to these compounds are still poorly understood [2].
Alisol B 23-acetate, a natural triterpenoid, produces protective effects against EE-induced cholestasis, due to FXR-mediated gene regulation.IC50 Value:Target: Anti-hepatotoxic natural product. In vitro: Alisol-B 23-acetate has an effect on FXR activation in a dose-dependent manner using luciferase reporter assay in HepG2 cells [3].In vivo: In alisol B 23-acetate-treated mice, the changes in transporters and enzymes, as well as ameliorative liver histology were abrogated by FXR antagonist guggulsterone [1]. Alisol B 23-acetate treatment in a dose-dependent manner resulted in protection against hepatotoxicity induced by CCl4via FXR activation. Through FXR activation, alisol B 23-acetate promoted hepatocyte proliferation via an induction in hepatic levels of FoxM1b, Cyclin D1 and Cyclin B1. Alisol B 23-acetate also reduced hepatic bile acids through a decrease in hepatic uptake transporter Ntcp, bile acid synthetic enzymes Cyp7a1, Cyp8b1, and an increase in efflux transporter Bsep, Mrp2 expression. In addition, alisol B 23-acetate induced the expression of STAT3 phosphorylation, and STAT3 target genes Bcl-xl and SOCS3, resulting in decreased hepatocyte apoptosis [2].
Hederacoside C is a principal bioactive pharmaceutical ingredient of Hedera helix leaf that can treat respiratory disorders, because of its expectorant, bronchodilator, antibacterial, and bronchospasmolytic effects.
Alantolactone is a selective STAT3 inhibitor, with potent anticancer activity.
8-O-Acetyl shanzhiside methyl ester (ND01) is an iridoid glucoside isolated from the leaves of Lamiophlomis rotata Kudo, a Chinese folk medicinal plant in Xi-zang. 8-O-Acetyl shanzhiside methyl ester could inhibt NF-κB.
Atractyloside A(126054-77-1) is a natural TCM reference compound.
Astragaloside I is a natural product isolated from Astragalus.
Alpha-cyperone is associated with the down-regulation of COX-2,IL-6,Nck-2,Cdc42 and Rac1, resulting in reduction of inflammation. which would be highly beneficial for treatment of inflammatory diseases such as AD.In vitro: The anti-inflammatory activity of alpha-cyperone is associated with the down-regulation of COX-2 and IL-6 via the negative regulation of the NFκB pathway in LPS-stimulated RAW 264.7 cells.[1]Alpha-Cyperone binds and interacts with tubulin and is capable of distinctly destabilizing microtubule polymerization. The effect of this interaction could result in reduction of inflammation which would be highly beneficial for treatment of inflammatory diseases such as AD. One microliter of alpha-Cyperone was dissolved in DMSO (1:1 v/v) and it was further diluted in double distilled water (ddH2O) to a final volume of 20 microliter. [2]
Ginsenoside Rg6 is the component isolated from notoginseng. Ginsenoside Rg6 inhibits TNF-α-induced NF-κB transcriptional activity with an IC50 of 29.34±2.22 μM in HepG2 cells. Ginsenoside Rg6 also exhibits apoptosis-inducing effect.
20-O-Acetylingenol-3-angelate is a natural compound.
Asiaticoside, a trisaccaride triterpene from Centella asiatica, suppresses TGF-β/Smad signaling through inducing Smad7 and inhibiting TGF-βRI and TGF-βRII in keloid fibroblasts; Asiaticoside shows antioxidant, anti-inflammatory, and anti-ulcer properties.
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.
Chikusetsusaponin IVa a major active ingredient of triterpenoid saponins, exerts antithrombotic effects, including minor hemorrhagic events. This appears to be important for the development of new therapeutic agents. a novel AMPK activator that is capable of bypassing defective insulin signalling and could be useful for the treatment of T2DM or other metabolic disorders.IC50 Value: 199.4 ± 9.1 μM (inhibiting thrombin-induced fibrinogen clotting) Target: In vitro: Using biochemical and pharmacological methods, it proves that chikusetsusaponin IVa prolongs the recalcification time, prothrombin time, activated partial thromboplastin time, and thrombin time of normal human plasma in a dose-dependent manner; inhibits the amidolytic activity of thrombin and factor Xa upon synthetic substrates S2238 and S2222; inhibits thrombin-induced fibrinogen clotting (50% inhibition concentration, 199.4 ± 9.1 μM); inhibits thrombin- and collagen-induced platelet aggregation. Chikusetsusaponin IVa can also preferentially inhibits thrombin in a competitive manner (K(i)=219.6 μM) [1]. Chikusetsusaponin IVa suppresses the production of iNOS, COX-2, IL-1β, IL-6, and TNF-α in LPS-stimulated THP-1 cells likely by inhibiting NF-κB activation and ERK, JNK, and p38 signal pathway phosphorylation [2].In vivo: Studies were performed on type 2 diabetic mellitus (T2DM) rats given CHS for 28 days to test the antihyperglycemic activity. Oral administration of CHS dose-dependently increased the level of serum insulin and decreased the rise in blood glucose level [3].
alpha-hederin is a water-soluble pentacyclic triterpenoid saponin, possessing several biological properties such as antispasmodic, moliscicidic, anthelmithic and inhibiting cell proliferation，In vitro: a-hederin is cytotoxic and inhibits proliferation in bothcel lines at rather low concentrations. , a-hederin reduces themitotic activity in treated cels.[1]In vivo: alpha-hederin had preventive effect on sensitized rats like thymoquinone. It may intervene in miRNA-126 expression, which consequently could interfere with IL-13 secretion pathway leading to a reduction in inflammatory responses. [2]
Ginkgolide A is an extract from in Ginkgo biloba and a g-aminobutyric acid (GABA) antagonist.Target: GABA ReceptorGinkgolide A is a highly active PAF antagonist cage molecule that is isolated from the leaves of the Ginkgo biloba tree. Shows potential in a wide variety of inflammatory and immunological disorders. Ginkgolide A significantly shortened the sleeping time induced by anesthetics in mice [1]. Ginkgolide A failed to affect apoptotic damage neither in serum-deprived nor in staurosporine-treated neurons [2].
Methyl deacetylasperulosidate is an iridoid isolated from Borreria and Spermacoce species.
Tripterin (Celastrol) is a proteasome inhibitor which potently and preferentially inhibits the chymotrypsin-like activity of a purified 20S proteasome with IC50 of 2.5 μM.