| Identification | Back Directory | [Name]
KukoaMine B | [CAS]
164991-67-7 | [Synonyms]
KukoaMine B
Benzenepropanamide,N-(3-aminopropyl)-N-[4-[[3-[[3-(3,4-dihydroxyphenyl)-1-oxopropyl]amino]propyl]amino]butyl]-3,4-dihydroxy- | [Molecular Formula]
C28H42N4O6 | [MDL Number]
MFCD29904539 | [MOL File]
164991-67-7.mol | [Molecular Weight]
530.66 |
| Chemical Properties | Back Directory | [Boiling point ]
844.3±65.0 °C(Predicted) | [density ]
1.232±0.06 g/cm3 (20 ºC 760 Torr) | [storage temp. ]
-20°C | [solubility ]
DMF:30.0(Max Conc. mg/mL);56.53(Max Conc. mM)
DMSO:30.0(Max Conc. mg/mL);56.53(Max Conc. mM)
Ethanol:30.0(Max Conc. mg/mL);56.53(Max Conc. mM)
PBS (pH 7.2):10.0(Max Conc. mg/mL);18.84(Max Conc. mM)
Water:62.5(Max Conc. mg/mL);117.78(Max Conc. mM) | [form ]
A crystalline solid | [pka]
9.78±0.10(Predicted) | [color ]
White to off-white | [Major Application]
food and beverages | [InChIKey]
IWRAOCFRRTWUDF-UHFFFAOYSA-N | [SMILES]
C1(CCC(N(CCCN)CCCCNCCCNC(=O)CCC2=CC=C(O)C(O)=C2)=O)=CC=C(O)C(O)=C1 |
| Hazard Information | Back Directory | [Chemical Properties]
White crystalline powder, soluble in organic solvents such as methanol, ethanol, DMSO, etc., derived from the bark of Lycium bark. | [Uses]
Kukoamine B is an amide alkaloiad used in the protection against NMDA-induced neurotoxicity and potential harmful mechanisms. In addition it is seen to inhibit the inflammatory response in the livers of septic mice. | [Definition]
ChEBI: Kukoamine B is an amine. | [in vivo]
Kukoamine B (20, 50 mg/kg, i.g., daily, 9 weeks) reduces inflammation and blood glucose without body weight gain or liver mass increase[1].
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].
| 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]. | | Dosage: | 20, 50 mg/kg | | Administration: | i.g., daily, 9 weeks | | 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]. | | Dosage: | 2, 5 mg/kg | | Administration: | p.o., daily, 12 weeks | | 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]. | | Dosage: | 1.25, 2.5, 5, 10, 15, 30, 60 mg/kg | | 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. | | 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.
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