Acteoside

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Cat Number

PIPE61276173

CAS Number

61276-17-3

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CAS Number

61276-17-3

EINECS

604-604-1

Storage

Cool and dry place

Synonyms

Verbascoside; kusagin

Molecular Formula

C29H36O15

Molecular Weight

624.59

Smiles

C[C@H]1[C@@H]([C@H]([C@H]([C@@H](O1)O[C@@H]2[C@H]([C@@H](O[C@@H]([C@H]2OC(=O)/C=C/C3=CC(=C(C=C3)O)O)CO)OCCC4=CC(=C(C=C4)O)O)O)O)O)O

Appearance

White to pale yellow solid

Melting Point

232 ℃

Boiling Point

908.8±65.0 °C

Relative Density

1.60±0.1

General Description

In spite of the fact that acteoside(a biologically active natural product) was first isolated from Verbascum, it is also present in Cistanche and Forsythia. Its stability is not an issue under acid conditions, but the degradation in non‑acidic media could be significantly inhibited by adding ascorbic acid. Its potential for drug discovery and development in the future has been considered significant owing to several important pharmacological features-anti‑inflammatory, antioxidant, anticancer and neuroprotective, which have been reported over the years.

Mechanism of Action

Acteoside displays a wide range of biological effects, such as anti‑inflammatory, antibacterial, antiviral, antioxidant, antidiabetic, neuroprotective, cardioprotective, anticancer, and wound‑healing activities. Acteoside exerts its pharmacological effects, such as anti-inflammatory and anti-cancer activities, by modulating various signaling pathways (e.g., NF-κB, PI3K/AKT) or regulating enzyme activities (e.g., α-amylase, phosphatase).

Application

Acteoside exerts an effect by decreasing TGF-β1 expression to suppress mesangial cell proliferation and delay the progress of glomerulosclerosis. Acteoside has been combined with benazepril (a common kidney disease drug) and shown to seemingly improve the therapeutic effect ( acteoside being the key active component in this combination). Acteoside has been seen to have a greater effect when compared with benazepril alone for reducing proteinuria.

The anti‑inflammatory action of acteoside works by blocking the NF‑κB pathway. It prevents IκB‑α phosphorylation and degradation, and stops NF‑κB p65 from moving into the nucleus. As a result, key pro‑inflammatory genes (TNF‑α, IL‑1β, IL‑6, COX‑2, iNOS) are down-regulated.
To counter oxidative damage, it both reduces ROS generation and enhances cellular defenses—by scavenging radicals, chelating metal ions, and increasing GST activity.
Against cancer cells, acteoside employs varied mechanisms across different signaling pathways, inhibiting growth or triggering apoptosis depending on the context. These are summarized in Fig.1.

Fig. 1 Acteoside's neuroprotective effects. (Mohammed RA.; et al. 2023)

References

Mohammed RA, et al. Acteoside as a multifunctional natural glycoside: therapeutic potential across various diseases.Inflammopharmacology, 2025 Jun 23.

Renal fibrosis represents the ultimate pathological alteration in kidney diseases and is also recognized as a critical factor in the progression of diabetic nephropathy (DN) to renal failure. In their study investigating the protective effects of acteoside against renal interstitial fibrosis—induced in DN rats through intraperitoneal injection of streptozotocin (STZ) combined with unilateral nephrectomy—and its underlying mechanisms, Zhou et al. discovered that acteoside could regulate reactive oxygen species (ROS), autophagic flux and lysosomal function in diabetic nephropathy mice. This could reduce oxidative tubular injury and delay renal interstitial fibrosis in DN mice, which was related to the antioxidant activity of acteoside and its regulation of the autophagy-lysosome pathway.

Fig. 2 The mechanism underlying the inhibitory effect of acteoside on fibrosis progression in diabetic nephropathy. (Zhou M.; et al. 2024)

References

Zhou M, et al. Acteoside delays the fibrosis process of diabetic nephropathy by anti-oxidation and regulating the autophagy-lysosome pathway. Eur J Pharmacol, 2024 Sep 5;978:176715.