Usenamine A
Usenamine A is an orally active natural dibenzofuran compound with multiple biological activities such as anti-inflammatory and anticancer effects. Usenamine A inhibits the AKT/mTOR/STAT3/ID1 signaling axis and induces ubiquitin-proteasome degradation of ID1. Usenamine A targets the TNF-TNFR2 complex, inhibits RGS2, and interferes with Myosin-9/actin cytoskeleton remodeling. Usenamine A induces apoptosis, autophagy and ROS-mediated endoplasmic reticulum stress in cancer cells, inhibits cancer cell proliferation and invasion, and reduces the production of pro-inflammatory cytokines. Usenamine A alleviates arthritis-related symptoms. Usenamine A can be used in studies related to liver cancer, non-small cell lung cancer, rheumatoid arthritis and ankylosing spondylitis.
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- CAS No.: 1428417-60-0
- Formule: C18H17NO6
- Masse moléculaire:343.33
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Stockage:
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Activité biologique
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Chemical Information
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Activité biologique
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STAT3 |
mTOR |
Akt |
TNF-α |
IL-17A |
Usenamine A (0-10 µM; 12-48 h) inhibits the proliferation of human HepG2 and SK-HEP-1 hepatocellular carcinoma cells in a dose- and time-dependent manner[1].
Usenamine A (0-4 µM) inhibits the invasive ability of human HepG2 and SK-HEP-1 hepatocellular carcinoma (HCC) cells, and this effect is partially dependent on the expression of ID1 and STAT3[1].
Usenamine A (8 µM; 24 h) downregulates the expression of ID1 in human HepG2 hepatocellular carcinoma cells, as detected by gene expression profiling analysis[1].
Usenamine A (0-8 µM; 6-24 h) downregulates ID1 protein expression, inhibits STAT3 activity via reducing its phosphorylation, and suppresses the AKT/mTOR signaling pathway in human HepG2 and SK-HEP-1 hepatocellular carcinoma cells by decreasing the phosphorylation levels of AKT and mTOR. All the above effects are dose- and time-dependent[1].
Usenamine A (UD32-3) (1-80 μM; 48 h) potently inhibits the viability of H1299 and H520 non-small cell lung cancer (NSCLC) cells, with IC50 values of 15.15 μM and 15.08 μM, respectively, while showing low cytotoxicity against normal BEAS-2B and MIHA cells[4].
Usenamine A (2.5-15 μM; 48 h) inhibits colony formation of H1299 and H520 non-small cell lung cancer (NSCLC) cells in a dose-dependent manner, with the maximum inhibitory effect observed at 15 μM[4].
Usenamine A (1-7.5 μM for 48 h in H1299 cells; 0.5-5 μM for 48 h in H520 cells) inhibits the migration of H1299 and H520 non-small cell lung cancer (NSCLC) cells in a dose-dependent manner[4].
Usenamine A (5 μM) exerts synergistic anti-non-small cell lung cancer (NSCLC) activity with Gemcitabine (HY-17026) in H1299 and H520 cells[4].
Usenamine A (compound 1) (incubated for 48 h) potently inhibits the growth of human hepatoma HepG2 cells, with an IC50 value of 6.0 μM[5].
Usenamine A (8 µM; 24 h) significantly downregulates the expression of ID1 mRNA in human HepG2 and SK-HEP-1 hepatocellular carcinoma cells[1].
Usenamine A (8 µM; 24 h) inhibits the binding of STAT3 to the ID1 gene promoter and reduces STAT3-mediated ID1 transcription in human HepG2 and SK-HEP-1 hepatocellular carcinoma cells[1].
Usenamine A (8 µM; 2-8 h) increases the degradation rate of ID1 protein in human HepG2 and SK-HEP-1 hepatocellular carcinoma cells, and its down-regulation of ID1 protein levels in these cells is dependent on the proteasome pathway[1].
Usenamine A (8 μM; 12-24 h) disrupts the distribution of actin filaments, impairs the interaction between myosin-9 and actin, and interferes with cytoskeleton remodeling in human hepatocellular carcinoma HepG2 and SK-HEP-1 cells[2].
Usenamine A (20 μM; 2 h) directly binds to RGS2 in RGS2-overexpressing HEK-293T cells, enhances the thermal stability of RGS2 protein and protects it from pronase E-mediated degradation[4].
Usenamine A (15 μM; 3-9 h for mRNA; 6-18 h for protein) downregulates the mRNA and protein expression of RGS2 in H1299 and H520 non-small cell lung cancer cells in a time-dependent manner[4].
Usenamine A inhibits the production of proinflammatory cytokines (IFN-γ, IL-17A, GM-CSF, TNF-α) in CD3/CD28-stimulated peripheral blood mononuclear cells (PBMCs) from patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS)[3].
Usenamine A (15 μM; 1-8 h) induces time-dependent endoplasmic reticulum (ER) stress in H1299 and H520 non-small cell lung cancer (NSCLC) cells via ROS generation, as evidenced by increased protein expression levels of ATF4 and CHOP[4].
Usenamine A (15 μM; 2 h) induces autophagy in H1299 and H520 non-small cell lung cancer (NSCLC) cells, a process essential for its antitumor activity, as demonstrated by rescue experiments with 3-MA[4].
Usenamine A (15 μM; 4-12 h) upregulates LC3II and downregulates Cleaved-Notch1 in H1299 and H520 non-small cell lung cancer (NSCLC) cells, and autophagy induction and Notch1 inhibition occur via independent pathways[4].
Usenamine A (0-15 μM; 48 h) induces dose-dependent apoptosis in human hepatocellular carcinoma HepG2 cells, and the apoptosis rate at the concentration of 15 μM increases by approximately 5-fold compared with untreated cells[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human hepatocellular carcinoma (HCC) HepG2 and SK-HEP-1 cells
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Concentration:2, 4, 6, 8, 10 µM
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Incubation Time:12 h; 24 h; 48 h
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Result:Significantly suppressed the proliferation of HepG2 and SK-HEP-1 cells in a dose- and time-dependent manner.
Exhibited 48-h IC50 values < 10 µM in both cell lines.
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Cell Line:human hepatocellular carcinoma (HCC) HepG2 and SK-HEP-1 cells
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Concentration:8 µM
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Incubation Time:24 h
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Result:Downregulated ID1 mRNA expression in human HepG2 and SK-HEP-1 HCC cells.
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Cell Line:human hepatocellular carcinoma (HCC) HepG2 and SK-HEP-1 cells
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Concentration:0, 4, 6, 8 µM (ID1, p-AKT, p-mTOR, p-STAT3 dose-dependent analysis)
8 µM (ID1, p-STAT3 time-dependent analysis) -
Incubation Time:24 h (dose-dependent analysis)
6, 18, 24 h (time-dependent ID1, p-STAT3 analysis) -
Result:Decreased ID1 protein levels in both cell lines in a dose- and time-dependent manner.
Reduced p-STAT3 levels in a dose- and time-dependent manner with total STAT3 levels unchanged.
Decreased p-AKT and p-mTOR levels in a dose-dependent manner with total AKT and mTOR levels unchanged.
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Cell Line:human hepatocellular carcinoma (HCC) HepG2 and SK-HEP-1 cells
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Concentration:8 µM (co-incubated with 50 µM CHX)
8 µM (in the presence of 20 µM MG-132 (HY-13259)) -
Incubation Time:2 h; 4 h; 8 h
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Result:Accelerated the downregulation of ID1 protein levels in the presence of CHX in both cell lines.
Had its inhibitory effect on ID1 protein levels attenuated in both cell lines when treated with MG-132.
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Cell Line:human NSCLC cell lines (H1299, H520), normal human cell lines (BEAS-2B, MIHA)
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Concentration:0, 1, 2.5,
5, 10, 20, 40, 60, 80 μM (H1299, BEAS-2B, MIHA)
0, 1, 5, 10, 15,
20, 40, 60 μM (H520) -
Incubation Time:48 h
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Result:Inhibited viability of H1299 and H520 NSCLC cells in a concentration-dependent manner, with IC50 values of 15.15 μM and 15.08 μM, respectively.
Showed significantly lower cytotoxicity against normal BEAS-2B lung epithelial cells and MIHA liver cells.
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Cell Line:human NSCLC cell lines (H1299, H520)
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Concentration:0, 5, 5, 7.5, 15 μM
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Incubation Time:48 h
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Result:Inhibited the colony-forming ability of H1299 and H520 cells in a dose-dependent manner.
Nearly eliminated colony formation in both cell lines at 15 μM.
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Cell Line:human NSCLC cell lines (H1299, H520)
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Concentration:0, 1, 2.5, 5, 7.5 μM for
H1299 and 0, 0.5, 1, 2.5, 5 μM for H520 -
Incubation Time:48 h
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Result:Inhibited the migratory ability of H1299 and H520 cells, as measured by reduced wound closure compared to untreated controls.
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Cell Line:human NSCLC cell lines (H1299, H520)
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Concentration:15 μM
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Incubation Time:0, 1, 2, 4, 8 h
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Result:Increased protein expression levels of ER stress markers ATF4 and CHOP in H1299 and H520 cells in a time-dependent manner.
Pretreatment with ROS scavenger NAC (5 mM) attenuated both the increase in ATF4/CHOP expression and cell death.
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Cell Line:human NSCLC cell lines (H1299, H520)
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Concentration:15 μM
15 μM (with 5 mM 3-MA (HY-19312) pretreatment) -
Incubation Time:2 h
2 h (with 5 mM 3-MA pretreatment for 2 h) -
Result:Increased MDC fluorescence intensity in H1299 and H520 cells, indicating enhanced autophagy flux.
This effect was reversed by pretreatment with autophagy inhibitor 3-MA, which also attenuated Usenamine A-induced cell death.
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Cell Line:human NSCLC cell lines (H1299, H520)
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Concentration:15 μM
15 μM (with 5 mM 3-MA pretreatment) -
Incubation Time:4, 8, 12 h
9 h (with 5 mM 3-MA pretreatment for 2 h) -
Result:Upregulated autophagy marker LC3II and downregulated Cleaved-Notch1 protein levels in H1299 and H520 cells in a time-dependent manner.
Pretreatment with 3-MA reversed the increase in LC3II but did not alter the reduction in Cleaved-Notch1, indicating Notch1 is not downstream of autophagy.
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Cell Line:human NSCLC cell lines (H1299, H520)
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Concentration:15 μM
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Incubation Time:6, 12, 18 h
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Result:Downregulated RGS2 protein expression in a time-dependent manner in H1299 and H520 NSCLC cells.
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Cell Line:human NSCLC cell lines (H1299, H520)
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Concentration:15 μM
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Incubation Time:3, 6, 9 h
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Result:Downregulated RGS2 protein expression in a time-dependent manner in H1299 and H520 NSCLC cells.
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Cell Line:human hepatoma HepG2 cells
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Concentration:0, 8, 15 μM
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Incubation Time:48 h
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Result:Increased the rate of apoptosis (early and late apoptotic cells combined) in a dose-dependent manner: ~8% at 0 μM, ~12% at 8 μM, and ~40% at 15 μM, with significant differences between the 15 μM group and the 0 μM/8 μM groups.
Usenamine A (15-30 mg/kg; i.p.; daily) exhibits potent in vivo anti-hepatocellular carcinoma activity. It significantly inhibits tumor proliferation, induces tumor cell apoptosis, upregulates autophagy levels, and causes no observable organ toxicity[2].
Usenamine A (UA) (0.5 mg/kg; p.o.; daily administration) significantly reduces clinical arthritis scores, enthesitis and enteritis symptoms in female SKG mice with curdlan-induced arthritis[3].
Usenamine A (UD32-3) (2 mg/kg; i.p.; once every two days; 7 doses total) exerts anti-non-small cell lung cancer (NSCLC) activity by inhibiting tumor growth, reducing tumor cell proliferation, inducing endoplasmic reticulum (ER) stress, and activating Notch1-mediated autophagy, while overexpression of RGS2 attenuates these effects[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude mice (4-5 weeks old, 9 mice per cohort)[2]
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Dosage:15 mg/kg; 30 mg/kg
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Administration:i.p.; once daily; 24 days
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Result:Attenuated HepG2 tumor growth dose-dependently, restricting tumor expansion to 14-fold (15 mg/kg) and 10-fold (30 mg/kg) vs control’s 22-fold.
Cut Ki-67 positive cell proportion to 40% of control.
Raised tumor apoptosis rate to 900% and LC3 staining density to 600% relative to control.
Retained mouse body weight and produced no visible organ toxicity in heart, liver, spleen, lung and kidney.
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Animal Model:SKG mice (female, 8 weeks old, BALB/c background, curdlan-induced rheumatoid arthritis)[3]
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Dosage:0.5 mg/kg
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Administration:p.o.; daily
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Result:Suppressed arthritis clinical scores from week 3 to week 7, and alleviated ankle enthesitis as well as intestinal enteritis scores versus disease controls.
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Animal Model:BALB/C nude mice (female, 5 weeks old, subcutaneous xenograft model injected with control or RGS2-overexpressing H1299 cells)[4]
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Dosage:2 mg/kg
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Administration:i.p.; once every two days; 7 doses
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Result:Suppressed volume and weight of control xenograft tumors, while RGS2 overexpression weakened such inhibition.
Lowered Ki-67 positive cell counts in control xenografts, an effect blunted by RGS2 overexpression.
Modulated tumor protein levels: elevated ATF4, CHOP and LC3II, reduced cleaved-Notch1; RGS2 overexpression reversed all above alterations.
Exerted no obvious impact on mouse body weight.
Chemical Information
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CAS No. 1428417-60-0
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Masse moléculaire 343.33
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Formule C18H17NO6
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SMILES
C[C@@]12C3=C(O)C(C)=C(O)C(C(C)=O)=C3OC1=CC(/C(C2=O)=C(N)/C)=O
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Structure Classification
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Initial Source
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
[1]. Yang A, et al. Interfering with the AKT/mTOR/STAT3/ID1 signaling axis with usenamine A restrains the proliferative and invasive potential of human hepatocellular carcinoma cells. Chinese medicine. 2024 Jan 05;19(1):4. [Content Brief]
[2]. Yang A, et al. Usenamine A induces apoptosis and autophagic cell death of human hepatoma cells via interference with the Myosin-9/actin-dependent cytoskeleton remodeling. Phytomedicine : international journal of phytotherapy and phytopharmacology. 2023 Jul 25;116:154895. [Content Brief]
[3]. Lee YJ, et al. Usenamine A: a potential therapeutic agent for rheumatoid arthritis and ankylosing spondylitis through its anti-inflammatory activity. Frontiers in pharmacology. 2024;15:1456216. [Content Brief]
[4]. Cheng L, et al. Usenamine A, an RGS2 inhibitor, exerts anti-NSCLC activity and enhances cytotoxicity of gemcitabine by inducing ER stress and Notch1-mediated autophagy. Bioorganic chemistry. 2025 Oct;165:109010. [Content Brief]
Calculators
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Usenamine A Related Classifications
HY-N20711 Related Classifications
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