Ajmaline
An alkaloid found in the root of Rauwolfia serpentina, among other plant sources. It is a class Ia antiarrhythmic agent that apparently acts by changing the shape and threshold of cardiac action potentials. Ajmaline produces potent sodium channel blocking effects and a very short half-life which makes it a very usefli drug for acute intravenous treatments. The drug has been very popliar in some countries for the treatment of atrial fibrillation in patients with the Wolff Parkinson White syndrome and in well tolerated monomorphic ventricliar tachycardias. It has also been used for many years as a drug to challenge the conduction system of the heart in cases of bundle branch block and syncope. In these cases, abnormal prolongation of the HV interval has been taken as a proof for infrahisian conduction defects tributary for permanent pacemaker implantation.
Structure for HMDB15495 (Ajmaline)
C20H26N2O2
326.4326
326.199428086
(1R,9R,10S,12R,13S,14R,16S,18R)-13-ethyl-8-methyl-8,15-diazahexacyclo[14.2.1.0¹,⁹.0²,⁷.0¹⁰,¹⁵.0¹²,¹⁷]nonadeca-2,4,6-triene-14,18-diol
ajmaline
4360-12-7
CJDRUOGAGYHKKD-HEFSZTOGSA-N
This compound belongs to the class of organic compounds known as ajmaline-sarpagine alkaloids. These are organic compounds containing either of the ajmalan, sarpagan skeleton, or derivative thereof. The Sarpagine (Akuammidine) group, based on the sarpagan nucleus, arises from bond formation between C-16 and C-5 of the corynantheine precursor. Ajmaline alkaloids are based on a 17,19-secoyohimban skeleton (oxayohimban) which is invariably present as an ether.
Organic compounds
Alkaloids and derivatives
Ajmaline-sarpagine alkaloids
Not Available
Ajmaline-sarpagine alkaloids
Aromatic heteropolycyclic compounds
Expected but not Quantified
Solid
Predicted LC-MS/MS Spectrum – 10V, PositiveNot Available
Predicted LC-MS/MS Spectrum – 20V, PositiveNot Available
Predicted LC-MS/MS Spectrum – 40V, PositiveNot Available
Predicted LC-MS/MS Spectrum – 10V, NegativeNot Available
Predicted LC-MS/MS Spectrum – 20V, NegativeNot Available
Predicted LC-MS/MS Spectrum – 40V, NegativeNot Available
Not Available
Not Available
Not Available
None
None
DB01426
Not Available
Not Available
Not Available
Not Available
Not Available
10145712
C06542
Not Available
Not Available
Ajmaline
HMDB15495
HMDB15495
Not Available
441080
Not Available
28462
- Brugada J, Brugada P, Brugada R: The ajmaline challenge in Brugada syndrome: a useful tool or misleading information? Eur Heart J. 2003 Jun;24(12):1085-6. [PubMed:12804922 ]
Enzymes
- General function:
- Involved in monooxygenase activity
- Specific function:
- Responsible for the metabolism of many drugs and environmental chemicals that it oxidizes. It is involved in the metabolism of drugs such as antiarrhythmics, adrenoceptor antagonists, and tricyclic antidepressants.
- Gene Name:
- CYP2D6
- Uniprot ID:
- P10635
- Molecular weight:
- 55768.94
References
- Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. doi: 10.1093/nar/gkp970. Epub 2009 Nov 24. [PubMed:19934256 ]
- General function:
- Involved in ion channel activity
- Specific function:
- This protein mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient. It is a tetrodotoxin-resistant Na(+) channel isoform. This channel is responsible for the initial upstroke of the action potential in the electrocardiogram
- Gene Name:
- SCN5A
- Uniprot ID:
- Q14524
- Molecular weight:
- 226937.5
References
- Barajas-Martinez HM, Hu D, Cordeiro JM, Wu Y, Kovacs RJ, Meltser H, Kui H, Elena B, Brugada R, Antzelevitch C, Dumaine R: Lidocaine-induced Brugada syndrome phenotype linked to a novel double mutation in the cardiac sodium channel. Circ Res. 2008 Aug 15;103(4):396-404. doi: 10.1161/CIRCRESAHA.108.172619. Epub 2008 Jul 3. [PubMed:18599870 ]
- Khodorov BI, Zaborovskaya LD: Blockade of sodium and potassium channels in the node of Ranvier by ajmaline and N-propyl ajmaline. Gen Physiol Biophys. 1983 Aug;2(4):233-68. [PubMed:6088360 ]
- Hermida JS, Dassonvalle E, Six I, Amant C, Coviaux F, Clerc J, Herent D, Hermida A, Rochette J, Jarry G: Prospective evaluation of the familial prevalence of the brugada syndrome. Am J Cardiol. 2010 Dec 15;106(12):1758-62. doi: 10.1016/j.amjcard.2010.07.049. [PubMed:21126620 ]
- Hoogendijk MG, Potse M, Vinet A, de Bakker JM, Coronel R: ST segment elevation by current-to-load mismatch: an experimental and computational study. Heart Rhythm. 2011 Jan;8(1):111-8. doi: 10.1016/j.hrthm.2010.09.066. Epub 2010 Oct 30. [PubMed:20870038 ]
- Leoni AL, Gavillet B, Rougier JS, Marionneau C, Probst V, Le Scouarnec S, Schott JJ, Demolombe S, Bruneval P, Huang CL, Colledge WH, Grace AA, Le Marec H, Wilde AA, Mohler PJ, Escande D, Abriel H, Charpentier F: Variable Na(v)1.5 protein expression from the wild-type allele correlates with the penetrance of cardiac conduction disease in the Scn5a(+/-) mouse model. PLoS One. 2010 Feb 19;5(2):e9298. doi: 10.1371/journal.pone.0009298. [PubMed:20174578 ]
- Hoogendijk MG, Potse M, Linnenbank AC, Verkerk AO, den Ruijter HM, van Amersfoorth SC, Klaver EC, Beekman L, Bezzina CR, Postema PG, Tan HL, Reimer AG, van der Wal AC, Ten Harkel AD, Dalinghaus M, Vinet A, Wilde AA, de Bakker JM, Coronel R: Mechanism of right precordial ST-segment elevation in structural heart disease: excitation failure by current-to-load mismatch. Heart Rhythm. 2010;7(2):238-48. doi: 10.1016/j.hrthm.2009.10.007. Epub 2009 Oct 12. [PubMed:20022821 ]