Kukoamine B mesylate
Based on 1 publication(s) in Google Scholar
Kukoamine B, a spermine alkaloid, is a potent dual LPS and CpG DNA inhibitor with Kd values of 1.23 µM and 0.66 µM, respectively. Kukoamine B exerts anti-inflammatory, anti-diabetic, anti-oxidant, anti-osteoporotic and neuroprotective effects. Kukoamine B has the potential for the study of sepsis. .
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- CAS No.: 1375179-86-4
- Formula: C29H46N4O9S
- Molecular Weight:626.76
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Publications Citing Use of MedChemExpress (MCE) Kukoamine B mesylate
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Biological Activity
Kukoamine B (5-20 μM, 2 h) increases cell viability, and prevents plasma membrane from damaging in SH-SY5Y cells[2].
Kukoamine B (5-20 μM, 2 h) attenuates H2O2-induced Apoptosis and mitochondria membrane potential (MMP) loss in SH-SY5Y cells[2].
Kukoamine B (5-20 μM, 2 h) demonstrates anti-oxidative stress effects by modulating the MAPKs and PI3K-AKT signaling pathways in SH-SY5Y cells[2].
Kukoamine B (10-20 μM, 3 days) increases osteoblast differentiation and the mineralized nodule formation of preosteoblastic MC3T3-E1 cells[3].
Kukoamine B (50-200 μM, 12 h) is a dual inhibitor of LPS- and CpG DNA-induced TNF-a and IL-6 release from RAW 264.7 cells and murine peritoneal macrophages[4].
Kukoamine B (50-200 μM, 12 h) down-regulates two receptors (TLR4 and TLR9) and two important enzymes (iNOS and COX-2) mRNA expressions upregulated by LPS and CpG DNA in RAW 264.7cells[4].
Kukoamine B (0-200 μM, 30min-2 h) inhibits IkB-a and p38 phosphorylation and NF-kB activation induced by LPS and CpG DNA in RAW 264.7cells [4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:SH-SY5Y cells
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Concentration:5, 10, 20 μM (H2O2, 100 μM, for another 12 h)
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Incubation Time:2 h
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Result:Prevented cell death and improved cell viability dose-dependently.
Lowered the LDH release.
Increased the activity of CAT, SOD, and GSH-Px, and reduced the MDA production
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Cell Line:SH-SY5Y cells
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Concentration:5, 10, 20 μM (H2O2, 100 μM, for another 12 h)
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Incubation Time:2 h
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Result:Decreased total apoptotic cells and late apoptotic cells.
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Cell Line:SH-SY5Y cells
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Concentration:5, 10, 20 μM (H2O2, 100 μM, for another 12 h)
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Incubation Time:2 h
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Result:Increased the fluorescence intensity of Rho (Rhodamine) 123.
Decreased the ROS production.
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Cell Line:SH-SY5Y cells
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Concentration:5, 10, 20 μM (H2O2, 100 μM, for another 12 h)
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Incubation Time:2 h
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Result:Restored the mitochondria function via inhibiting the ratio of Bcl-2/Bax.
Decreased cytochromec, caspase-3, caspase-9, p-p38, p-ERK and p-JNK expression.
Increased p-AKT expression.
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Cell Line:RAW 264.7 cells
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Concentration:0, 100, 200 μM
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Incubation Time:12 h
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Result:Down-regulated the mRNA expression of two receptors (TLR4 and TLR9) and two important enzymes (iNOS and COX-2).
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Cell Line:RAW 264.7 cells
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Concentration:0, 100, 200 μM
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Incubation Time:30 min-2 h
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Result:Suppressed the IkB-a and p38 phosphorylation as well as the degradation of IkB-a.
Kukoamine B (2, 5 mg/kg, p.o., daily, 12 weeks) demonstrates the anti-osteoporotic effects in ovariectomized (OVX) mice[3].
Kukoamine B (1.25-60 mg/kg, i.v., only one injection or very 8 h for 3 days) protects mice challenged with E. coli and reduces the circulatory levels of LPS and TNF-a in sepsis model mice[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male, 4-week old db/db mice (BKS.Cgm+/+Leprdb/J) and wildtype (WT) mice (C57BLKS/J-m+/+ db). A spontaneous type 2 diabetic animal model[1].
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Dosage:20, 50 mg/kg
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Administration:i.g., daily, 9 weeks
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Result:Successfully controlled the augment of blood glucose with age increase.
Reduced levels of 29 inflammatory markers such as IL-2, IL-3, IL-4, IL-5, IL-6, IL-7 and IL8.
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Animal Model:Seven-week-old female ddy mice underwent either an ovariectomy or sham-operated surgery[3].
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Dosage:2, 5 mg/kg
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Administration:p.o., daily, 12 weeks
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Result:Inhibited the OVX-induced BMD loss in the right femur bone and restored the impaired bone structural properties of BV/TV, Tb.Th, Tb.N, and Tb.Sp.
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Animal Model:Kunming (KM) mice, 4–6 weeks old, 18–20 g, male and female in equal number. Mice were injected with heat-killed E. coli (EC, 1.0 * 1011 CFU•kg-1) in order to establish the sepsis model.[4].
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Dosage:1.25, 2.5, 5, 10, 15, 30, 60 mg/kg
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Administration:80 mice (15, 30, 60 mg/kg), i.v., only one injection; 100 mice (1.25, 2.5, 5 mg/kg), i.v., every 8 h for 3 days; 96 mice, (60 mg/kg), i.v., once at 0, 2, 4, 6, 8 h after injection of EC.
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Result:Significantly decreased the mortality rate from 87.5% to 62.5%, 62.5%, or 37.5% (15, 30, 60 mg/kg).
Decreased the mortality rate from 95% to 65%, 60% and 45% (1.25, 2.5 and 5 mg/kg).
Decreased the circulatory LPS and TNF-a levels in a time-dependent manner.
Chemical Information
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CAS No. 1375179-86-4
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Molecular Weight 626.76
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Formula C29H46N4O9S
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SMILES
O=C(CCC1=CC=C(C(O)=C1)O)NCCCNCCCCN(CCCN)C(CCC2=CC=C(C(O)=C2)O)=O.O=S(O)(C)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (1)
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Journal Impact Factor
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Most Recent
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Adv Sci (Weinh)
TrxR2 Lactylation Facilitates Mitochondrial Protection and Endothelial Ferroptosis Resistance in Diabetic Cardiomyopathy. [Abstract]2026 Apr;13(22):e21997. PMID: 41704008
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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