1. Anti-infection Neuronal Signaling Metabolic Enzyme/Protease Apoptosis
  2. Bacterial Cholinesterase (ChE) MMP TNF Receptor
  3. Thunberginol C

Thunberginol C is an orally active, selective, and non-competitive inhibitor of AChE and BChE, with IC50 values of 41.96 and 42.36 μM, respectively. Thunberginol C exerts cytoprotective, pro-collagen type I restorative, MMP-1 inhibitory, hyaluronic acid restorative, anti-photoaging effects in skin cells. Thunberginol C exerts neuroprotective, anxiolytic, TNF-α inhibitory, neuroinflammation inhibitory, and oxidative stress inhibitory effects. Thunberginol C can be used for the research of Alzheimer’s disease, UVB-induced skin photoaging, allergic reactions, oral bacterial infections, and stress-induced anxiety.

For research use only. We do not sell to patients.

Thunberginol C

Thunberginol C Chemical Structure

CAS No. : 147517-06-4

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Description

Thunberginol C is an orally active, selective, and non-competitive inhibitor of AChE and BChE, with IC50 values of 41.96 and 42.36 μM, respectively. Thunberginol C exerts cytoprotective, pro-collagen type I restorative, MMP-1 inhibitory, hyaluronic acid restorative, anti-photoaging effects in skin cells. Thunberginol C exerts neuroprotective, anxiolytic, TNF-α inhibitory, neuroinflammation inhibitory, and oxidative stress inhibitory effects. Thunberginol C can be used for the research of Alzheimer’s disease, UVB-induced skin photoaging, allergic reactions, oral bacterial infections, and stress-induced anxiety[1][2][3][4].

IC50 & Target[1][2]

AChE

41.96 μM (IC50)

BChE

42.36 μM (IC50)

MMP-1

 

In Vitro

Thunberginol C non-competitively inhibits acetylcholinesterase (AChE) with an IC50 of 41.96 μM and a Ki of 45.6 μM via van der Waals interactions at the enzyme's peripheral anionic site[1].
Thunberginol C non-competitively inhibits butyrylcholinesterase (BChE) with an IC50 of 42.36 μM and a Ki of 49.2 μM via a hydrogen bond and hydrophobic interactions at the enzyme's peripheral anionic site[1].
Thunberginol C (1 μM; 24 h) significantly increases cell viability, type I procollagen and hyaluronic acid production and inhibits MMP-1 production in UVB-irradiated Hs68 human foreskin fibroblast[2].
Thunberginol C (10 ppm) inhibits the growth of Bacteroides melaninogenicus and Fusobacterium nucleatum oral bacteria, with an MIC of 10 ppm for both species[3].
Thunberginol C inhibits antigen-induced contraction of tracheal chain isolated from sensitized guinea pig, while showing little inhibition for histamine-induced contraction[3].
Thunberginol C (1-30 μM; 24 h) protects primary cortical neurons against Corticosterone (HY-B1618)-induced cell death[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

ELISA Assay[2]

Cell Line: UVB-irradiated Hs68 human foreskin fibroblasts
Concentration: 1 μM
Incubation Time: 24 h
Result: Restored type I procollagen production to 76.80% of non-irradiated control levels from UVB-induced 63.38%.\nReduced UVB-induced MMP-1 production to 108.97% of non-irradiated control levels from 396.10%.\n
Increased hyaluronic acid production to 80.54% of non-irradiated control levels from UVB-induced 58.29%, with no statistical significance.

Cell Viability Assay[4]

Cell Line: Neuronal cells
Concentration: 1; 3; 10; 30 μM
Incubation Time: 24 h
Result: Protected primary cortical neurons against Corticosterone-induced cell death.
In Vivo

Thunberginol C (2-20 mg/kg; p.o.; daily; 14 days) dose-dependently attenuates chronic restraint stress-induced anxiety, neuroinflammation, and oxidative stress in male CD-1 mice[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male CD-1 mice (chronic restraint stress model)[4]
Dosage: 2; 20 mg/kg
Administration: p.o.; daily; 14 days
Result: Significantly improved the restraint stress-induced decrease in percentage of time spent in open arms and percentage of open arm entries, without affecting total arm entries at both 2 mg/kg and 20 mg/kg.
Significantly inhibited the restraint stress-induced increase in plasma TNF-α concentration at 20 mg/kg, but did not affect plasma corticosterone concentration.
Dose-dependently reduced the restraint stress-induced increase in Iba-1-labeled area in the hippocampus at both 2 mg/kg and 20 mg/kg.
Significantly reduced the restraint stress-induced increase in hippocampal TBARS levels, and significantly increased the activities of hippocampal superoxide dismutase, glutathione peroxidase, and glutathione reductase that were decreased by restraint stress at 20 mg/kg.
Molecular Weight

272.25

Formula

C15H12O5

CAS No.
SMILES

O=C1C2=C(O)C=C(O)C=C2CC(C3=CC=C(O)C=C3)O1

Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation
References
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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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