302-27-2 Usage
Chemical Properties
Off-White Solid
Physical properties
Appearance: solid. Solubility: barely soluble in water and soluble in organic solvents such as chloroform or diethyl ether. Its solubility in water and ethanol are
0.3?mg/mL and 35?mg/mL, respectively. Melting point: 203–204?°C (397–399?°F;
476–477?K). Optical rotation:D+17.3°
History
Preparations of Aconitum roots are employed in Chinese medicine for analgesic,
antirheumatic, and neurological indications. In the Ming Dynasty, Chinese people
had extracted the aconitine from the Aconitum plants. Aconitine is synthesized by
the Aconitum plants via the terpenoid biosynthesis pathway (MEP chloroplast
pathway)
Uses
Different sources of media describe the Uses of 302-27-2 differently. You can refer to the following data:
1. Aconitine occurs to the extent of 0.4–0.8%in dried tuberous roots of aconite or monkshood (Aconitum napellus L. and Ranunculaceae) found in India, North America,and Europe. It is used to produce heartarrhythmia in experimental animals and asan antipyretic agent.
2. anesthetic (gastric), antipyretic, and cardiotoxin
3. Neurotoxin. Activates tetrodotoxin-sensitive Na+ channels, inducing presynaptic depolarization, thus blocking the nerve action potential which, in turn, blocks the release of neurotransmitters and dec
reases the end plate potential at the neuromuscular junction. Aconitine also blocks norepinephrine reuptake. In the heart, aconitine induces ventricular tachycardia after intracoronary injection. In c
ultured ventricular myocytes, aconitine increases the duration of the action potential and induces the appearance of early after depolarization.
Used in producing heart arrhythmia in experimental anim
als.
Definition
ChEBI: A diterpenoid that is 20-ethyl-3alpha,13,15alpha-trihydroxy-1alpha,6alpha,16beta-trimethoxy-4-(methoxymethyl)aconitane-8,14alpha-diol having acetate and b
nzoate groups at the 8- and 14-positions respectively.
Indications
Aconitine was previously used as an antipyretic and analgesic. However, the clinical
application of aconitine is limited by its high toxicity. Its lethal dose 50% (LD50) for
mice is 1.8?mg/kg (orally) and 0.308?mg/kg (intraperitoneally).
Health Hazard
Aconitine is among the most toxic alkaloidsknown. Toxic doses are close to therapeuticdoses, and in humans as little as 2 mgmay cause death (Ferry and Vigneau 1983).An oral lethal dose of 28 mg/kg has alsobeen recorded (NIOSH 1986). The toxicsymptoms at low doses may be excitement,drowsiness, and hypermotility. The first signof poisoning from ingestion is a tingling,burning feeling on the lips, mouth, gums,and throat (Hodgson et al. 1988). This isfollowed by nervous disorders, anesthesia,loss of coordination, vertigo, hypersalivation,nausea, vomiting, and diarrhea. Toxic actionsof aconitine are very rapid. The crystallineform of this compound is much more toxicthan the amorphous aconitine. At a lethaldose, death may result from cardiorespiratoryfailure. Procaine may be an effective antidoteagainst aconitine poisoning.
Pharmacology
Aconitum was found to have neurotoxin. It could activate tetrodotoxin-sensitive Na+
channels, inducing presynaptic depolarization and blocking the nerve action potential and, in turn, blocking the release of neurotransmitters and decreasing the end
plate potential at the neuromuscular junction. Aconitine was also found to block
norepinephrine reuptakeIn the heart, aconitine could induce ventricular tachycardia. In cultured ventricular myocytes, aconitine could induce the appearance of early after depolarization by
increasing the duration of the action potential.Research with mouse nerve-hemidiaphragm muscle preparation found that aconitine at low concentrations (<0.1?μM) could increase the electrically evoked acetylcholine release causing an induced muscle tension. Action potentials were
generated more often at this concentration. While at higher concentrations
(0.3–3?μM), aconitine could decrease the electrically evoked acetylcholine release,
resulting in a decrease in muscle tension. Under the circumstance with high
concentration (0.3–3?μM) of aconitine, the sodium-ion channels were constantly
activated, and transmission of action potentials was suppressed, leading to the formation of non-excitable target cells or paralysis.
Clinical Use
In clinic, it can be used for treating and alleviating the symptoms caused by arthritis,
lumbocrural pain, and herpes zoster; however, it is utilized infrequently in clinical
practice due to its obvious side effectsAccording to a review of different reports of aconite poisoning in human beings,
the following clinical features such as neurological, cardiovascular, and gastrointestinal features were observed. The first symptom of aconitine poisoning appeared
approximately 20?min–2?h after oral intake, and they were paresthesia, sweating,
and nausea, which led to severe vomiting, colicky diarrhea, intense pain, and then
paralysis of the skeletal muscles. Following the onset of life-threatening arrhythmia,
including ventricular tachycardia and ventricular fibrillation, death finally occurred
as a result of respiratory paralysis or cardiac arrest.
Purification Methods
Crystallise it from EtOH, CHCl3 or toluene. [Beilstein 21/6 V 310.]
Check Digit Verification of cas no
The CAS Registry Mumber 302-27-2 includes 6 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 3 digits, 3,0 and 2 respectively; the second part has 2 digits, 2 and 7 respectively.
Calculate Digit Verification of CAS Registry Number 302-27:
(5*3)+(4*0)+(3*2)+(2*2)+(1*7)=32
32 % 10 = 2
So 302-27-2 is a valid CAS Registry Number.
InChI:InChI=1/C34H47NO11/c1-7-35-15-31(16-41-3)20(37)13-21(42-4)33-19-14-32(40)28(45-30(39)18-11-9-8-10-12-18)22(19)34(46-17(2)36,27(38)29(32)44-6)23(26(33)35)24(43-5)25(31)33/h8-12,19-29,37-38,40H,7,13-16H2,1-6H3/t19?,20?,21?,22?,23?,24?,25?,26-,27+,28-,29?,31?,32-,33+,34-/m1/s1
302-27-2Relevant articles and documents
Studies on the relative reactivity of three hydroxyl groups in aconitine
She, Xue-Ke,Jian, Xi-Xian,Chen, Dong-Lin,Chen, Qiao-Hong,Wang, Feng-Peng
experimental part, p. 665 - 677 (2012/10/08)
The relative reactivity of three hydroxyl groups in aconitine toward acetylation, chlorination, sulfonylation, and oxidation has been studied in this paper. The reduction of C-3 ketone and C-15 ketone derivatives of aconitine was also investigated. It was found that (1) the relative reactivity of three hydroxyl groups toward acetylation, chlorination, and sulfonylation is 3-OH>13-OH>>15-OH; (2) 3-OH is much more reactive than 15-OH toward oxidation; and (3) reduction of the carbonyl group at C-3 with NaBH4 generated a pair of C-3 epimers, while the reduction products of the carbonyl group at C-15 depend largely on the specific reducing agent and the absolute configuration of 16-OCH3. When the substrate has 16-OCH3, its carbonyl group at C-15 can be reduced with NaBH4 to yield exclusively the 15-OH-containing product. Upon replacement of reducing agent NaBH4 with LiAlH4, the C-15 carbonyl group can be reduced to yield a pair of C-15 epimers. On the other hand, when the substrate has 16-OCH3, C-15 carbonyl group can only be reduced to generate 15-OH-containing product.
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