TMV/Tobacco mosaic virus (IC50 = 5.5 μM)
Yadanziolide A modulates cellular signaling pathways to exert its effects. It induces apoptosis in tumor cells, which is a key mechanism for its antitumor activity. The compound's antiviral activity is demonstrated by its ability to inhibit the tobacco mosaic virus (TMV). While its precise molecular targets are not fully elucidated, its effects are thought to be mediated through the modulation of various signaling pathways involved in cell survival, proliferation, and viral replication. The compound is a quassinoid, a class of compounds known for their potent biological activities.

Yadanziolide A is a natural product found in Brucea mollis and Brucea javanica. Yadanziolide A inhibited the replication of Tobacco Mosaic Virus (TMV) with an IC50 of 5.5μM and an inhibition rate of 83.4% at 20 μM.[1]
In vitro, Yadanziolide A has demonstrated potent antiviral activity against the tobacco mosaic virus (TMV), with an IC50 of 5.5 μM. This indicates that it is a highly effective inhibitor of this plant virus. It also shows significant antitumor effects. Studies have shown that compounds from Brucea javanica, including Yadanziolide A, can be used to treat glioblastoma, one of the most aggressive forms of brain cancer. The compound's in vitro activity is typically assessed using antiviral and anticancer cell-based assays.

The inhibitory activities of compounds 1−17 (compound # 9 is yadanziolide A))against TMV replication were tested using two approaches. First, the half-leaf method was used to test the antiviral activity in the local lesion host N. glutinosa in vivo. Then, the leaf-disk method was used to evaluate the antiviral activity of each compound in the systemic infection host N. tabacum cv. K326. Ningnanmycin, a commercial product for plant disease in China, was used as a positive control.[1]
The antiviral inhibition rates of compounds 1−17 at the concentration of 20 μM tested by the half-leaf method were listed in Table 2. The results showed that all the compounds exhibited inhibition activities against TMV replication with inhibition rates ranging from 24.1% to 94.6%. Except compound 11 (bruceoside A, 24.1%), all the other compounds showed higher inhibition rates than that of the positive control, ningnanmycin (25.3%). Among the 17 quassinoids, brusatol (3) and bruceine B (4), sharing a diosphenol (3-hydroxy-3-en-2-one) unit in ring A, exhibited the best activity, with the inhibition rates 94% and 94.6%, respectively. Replacement with β-glucose at 3-OH (5−7) or a hydrogenation at 3-OH (8−9) gave a slight decrease of activity (Table 2). The saturation of the 3,4-double bond resulted in great loss of the antiviral activity from 94% (3) to 52% (1). The lost of the carbonyl at C-2 can also led to great lost in antiviral activity; the inhibition rate decreased from 84.7% (8) to 31.1% (13) and 30.6% (15) and from 83.4% (9) to 24.1% (14) with the carbonyl at C-2 in 8−9 substituted by the hydrogen (13−14) or β-glucose (15), which indicated the C-2 carbonyl was essential for the antiviral activity. Compared with compounds 1−17, nigakilactone B (a quassinoid from Picrasma quassioides), without an epoxymethano bridge from C-8 to C-13, showed no anti-TMV activity, indicating the epoxymethano bridge moiety might be essential for anti-TMV activity.[1]
In vivo, the antitumor effects of Yadanziolide A observed in vitro suggest it has therapeutic potential for treating cancer. Its antiviral activity also suggests potential applications in treating viral infections. However, specific in vivo efficacy data for Yadanziolide A are not extensively documented in the public literature. The compound is primarily used as a research tool to study its antiviral and anticancer mechanisms. Further studies, including animal models, are required to confirm its therapeutic potential and characterize its pharmacokinetics.

For in vitro antiviral assays, Yadanziolide A is evaluated for its activity against the tobacco mosaic virus (TMV). The compound's ability to inhibit viral replication is measured by infecting plant cells or tissues with TMV in the presence of varying concentrations of the compound. The reduction in viral load or the number of lesions is quantified to determine the IC50. For antitumor assays, cancer cell lines are treated with the compound, and cell viability is measured using MTT or CCK-8 assays.

To assess whether these quassinoids inhibit TMV replication in systemic infection host N. tabacum cv. K326, the leaf-disk method along with Western blot analysis of TMV coat protein (CP) in the presence of 20 μM compound was carried out (Figure 2). The bands of CP were not detected, when treated with compounds 3−9 (Figure 2A and B); while treated with compounds with moderate activity (16, 17) or low activity (10−15), weak or strong bands were detected (Figure 2B). This result was in accordance with their inhibition rates in Table 2. However, nigakilactone B, a quassinoid from Picrasma quassioides Benn., showed no activity with a strong CP band as that of negative control (Figure 2B). Western-blot analysis further confirmed quassinoids from Brucea javanica could inhibit the accumulation of TMV CP in vitro. The quantity of TMV CP decreased with increasing concentrations of compounds in a dose-dependent manner (e.g., Figure 2C, compound 3).[1]
For in vitro cell-based assays, the anticancer activity of Yadanziolide A is evaluated using various cancer cell lines, including glioblastoma cells. Cells are treated with the compound, and apoptosis is assessed by Annexin V staining, caspase activity assays, or DNA fragmentation analysis. Cell cycle distribution is analyzed by flow cytometry. The compound's effects on cell signaling pathways are studied using Western blotting to identify the molecular mechanisms of its action.

For in vivo animal studies, Yadanziolide A is typically administered orally or intraperitoneally in rodent models of cancer or viral infection. To evaluate its antitumor efficacy, xenograft models of glioblastoma or other cancers can be used. Tumor-bearing mice are treated with the compound, and tumor growth is monitored. To evaluate its antiviral efficacy, animal models of viral infections can be used. However, specific published studies on Yadanziolide A in animal models are limited.

Pharmacokinetic properties of Yadanziolide A: The compound has a molecular weight of 426.41 and a molecular formula of C20H26O10. It is a natural product isolated from Brucea javanica. As a quassinoid, it is expected to have poor oral bioavailability. Detailed pharmacokinetic parameters, such as half-life and tissue distribution, are not publicly available.

Specific toxicity data for Yadanziolide A are limited. As a natural compound, its safety profile is not well characterized. Comprehensive toxicological studies have not been published. The compound is used for research purposes only and is not intended for human use. Standard laboratory safety precautions should be observed.

[1].Yan XH, et al. Anti-tobacco mosaic virus (TMV) Quassinoids from Brucea javanica (L.) Merr. J Agric Food Chem. 2010 Feb 10;58(3):1572-7.

[2].Liu JQ, et al. One new pregnane glycoside from the seeds of cultivated Brucea javanica. Arch Pharm Res. 2011 Aug;34(8):1297-300.

According to reports, A. yadanziolide has been found in both the hairy sea anemone (Brucea mollis) and the Javan sea anemone (Brucea javanica), and relevant data are available for reference.
Yadanziolide A is a research compound with no clinical trial or regulatory approval status. It is a natural product isolated from Brucea javanica with strong antiviral and antitumor activities. It is commercially available from chemical suppliers for research purposes only. The compound is of interest in cancer research and antiviral drug discovery.

C20H26O10

426.4144

426.153

95258-14-3

10320238

Typically exists as White to off-white solids

1.68±0.1 g/cm3

285-287 ºC

Brucea javanica

-2.9

6

10

1

30

872

11

O[C@]12[C@@]3(OC[C@@]41[C@H](OC([C@@H]2O)=O)C[C@H]1C(=CC([C@H]([C@]1(C)[C@H]4[C@H]([C@@H]3O)O)O)=O)C)CO

QXKKRGMRXXMDDP-JVDXBALSSA-N

InChI=1S/C20H26O10/c1-7-3-9(22)13(24)17(2)8(7)4-10-18-6-29-19(5-21,14(25)11(23)12(17)18)20(18,28)15(26)16(27)30-10/h3,8,10-15,21,23-26,28H,4-6H2,1-2H3/t8-,10+,11+,12+,13+,14-,15-,17-,18+,19+,20-/m0/s1

(1R,2R,3R,6R,8S,12S,13S,14R,15R,16S,17R)-2,3,12,15,16-pentahydroxy-17-(hydroxymethyl)-9,13-dimethyl-5,18-dioxapentacyclo[12.5.0.01,6.02,17.08,13]nonadec-9-ene-4,11-dione

yadanziolide A; 95258-14-3; (1R,2R,3R,6R,8S,12S,13S,14R,15R,16S,17R)-2,3,12,15,16-Pentahydroxy-17-(hydroxymethyl)-9,13-dimethyl-5,18-dioxapentacyclo[12.5.0.01,6.02,17.08,13]nonadec-9-ene-4,11-dione; CHEMBL2037039;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~234.52 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (5.86 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

---

Solubility in Formulation 2: ≥ 2.5 mg/mL (5.86 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

---

View More

Solubility in Formulation 3: ≥ 2.5 mg/mL (5.86 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

---

 (Please use freshly prepared in vivo formulations for optimal results.)