White crystalline powder
Aconitum carmichaelii / Radix; Aconitum carmichaeli Debx/Alkaloid from Root of Aconitum flavum and Aconitum pendulum (Ranunculaceae)
(1α,3α,6α,14α,15α,16β)-3,8-Diacetoxy-20-ethyl-13,15-dihydroxy-1,6,16-trimethoxy-4-(methoxymethyl)aconitan-14-yl benzoate/3-acetylaconitine/Aconitane-3,8,13,14,15-pentol, 20-ethyl-1,6,16-trimethoxy-4-(methoxymethyl)-, 3,8-diacetate 14-benzoate, (1α,3α,6α,14α,15α,16β)-/Flaconitine
Flaconitine is isolated from the ammonium hydroxide wetted root of A.szechenyianum Gay. Flaconitine is considered to be a NF-κB inhibitor.
715.9±60.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:77181-26-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
To study the processing principles of different processed products of Aconitum pendulum.
Using high performance liquid chromatography and acute toxicity test to compare the changes in chemical composition and toxicity of the roots and processed products of A. pendulum.
The main toxic components of the roots of A. pendulum were aconitine, deoxyaconitine and 3-acetylaconitine. The contents of these three alkaloids were significantly reduced in processed products, while benzoylaconitine significantly increased. In addition, processed products emerged aconine, polyschistine-D, beyzoyldeoxyaconine, 16-epi-pyroaconitine and 16-epi-pyrodeoxyaconitine. From the structural analysis, these new emerged compounds transformed from the aconitine, deoxyaconitine and 3-acetylaconitine.
Different processing methods can reduce the toxicity of the roots of A. pendulum. Processing principle is ester hydrolysis and high-temperature pyrolysis.
[Study on processing principle of Aconitum pendulum].
Wang Y1, Zhang J, Tian H, Zeng C, Yao Z, Zhang Y.
The effect of the Aconitum alkaloids aconitine, 3-acetylaconitine, lappaconitine, and N-desacetyllappaconitine to inhibit [3H]noradrenaline uptake was investigated in rat hippocampal synaptosomes. Aconitine and 3-acetylaconitine, which are known to activate sodium channels, had comparable inhibitory potencies and yielded Ki (inhibitor constant) values of 230 +/- 66 nM and 316 +/- 96 nM, respectively. In contrast, lappaconitine and N-desacetyllappaconitine failed to inhibit [3H]noradrenaline uptake. When either lappaconitine or N-desacetyllappaconitine was applied in combination with aconitine, [3H]noradrenaline uptake was not affected. The sodium channel blocker tetrodotoxin enhanced [3H]noradrenaline uptake, whereas uptake was completely blocked in sodium-free incubation medium. The inhibitory action of aconitine and 3-acetylaconitine on [3H]noradrenaline uptake was blocked by addition of tetrodotoxin. Patch clamp studies performed on cultured rat hippocampal neurons revealed an inhibitory action of lappaconitine and N-desacetyllappaconitine on whole cell sodium currents. It is concluded that the blockade of [3H]noradrenaline uptake evoked by aconitine and 3-acetylaconitine is mediated indirectly by an increased sodium concentration in the synaptosomes.
Different effects on [3H]noradrenaline uptake of the Aconitum alkaloids aconitine, 3-acetylaconitine, lappaconitine, and N-desacetyllappaconitine in rat hippocampus.
Seitz U1, Ameri A.
1998 Mar 15
The effects of the Aconitum alkaloid 3-acetylaconitine on neuronal activity were investigated in the slice preparation and on cultivated neurons of rat hippocampus by extracellular and patch-clamp recordings, respectively. 3-Acetylaconitine (0.01-1 microM) diminished the orthodromic and antidromic population spike in a concentration-dependent manner. The inhibitory action of the drug was preceded by a transiently enhanced excitability. The latency of onset of the inhibition was accelerated by increased stimulation frequency, whereas recovery during washout of the alkaloid was accelerated by decreased stimulation frequency. Moreover, the inhibitory effect of 3-acetylaconitine was evaluated in two different models of epileptiform activity induced either by blockade of GABA receptors by bicuculline (10 microM) or by a nominal Mg(2+)-free bathing medium. In accordance with the activity-dependent mode of action, this compound abolished the synaptically evoked population spikes in the presence of bicuculline or nominal Mg(2+)-free bathing medium, respectively. Whole-cell patch-clamp recordings revealed an interaction of 3-acetylaconitine with the voltage-dependent sodium channel. At a concentration of 1 microM, 3-acetylaconitine did not affect the peak amplitude of the sodium current, but shifted the current-voltage relationship in the hyperpolarized direction such that sodium currents were already activated at the resting potential.
Inhibition of rat hippocampal excitability by the plant alkaloid 3-acetylaconitine mediated by interaction with voltage-dependent sodium channels.