Stereochemistry | ABSOLUTE |
Molecular Formula | C20H26N2O2 |
Molecular Weight | 326.4326 |
Optical Activity | UNSPECIFIED |
Defined Stereocenters | 9 / 9 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
[H][C@@]12N(C)C3=C(C=CC=C3)[C@]14C[C@H]5[C@@H]([C@H]4O)[C@@]6([H])C[C@]2([H])N5[C@H](O)[C@H]6CC
InChI
InChIKey=CJDRUOGAGYHKKD-RQBLFBSQSA-N
InChI=1S/C20H26N2O2/c1-3-10-11-8-14-17-20(12-6-4-5-7-13(12)21(17)2)9-15(16(11)18(20)23)22(14)19(10)24/h4-7,10-11,14-19,23-24H,3,8-9H2,1-2H3/t10-,11-,14-,15-,16-,17-,18+,19+,20+/m0/s1
Ajmaline, (also known by trade names Gilurytmal, Ritmos, and Aritmina) is 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. The class I antiarrhythmic agents interfere with the sodium channel. A class IA agent lengthens the action potential (right shift) which brings about improvement in abnormal heart rhythms. This drug in particular has a high affinity for the Nav 1.5 sodium channel. Ajmaline produces potent sodium channel blocking effects and a very short half-life which makes it a very useful drug for acute intravenous treatments. The drug has been very popular in some countries for the treatment of atrial fibrillation in patients with the Wolff–Parkinson–White syndrome and in well tolerated monomorphic ventricular 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. Ajmaline is used as an antiarrhythmic agent.
Originator
Approval Year
AUC
T1/2
Doses
PubMed
Patents
Sample Use Guides
Adult: 50 mg via IV inj over at least 5 minutes. May also be given by IV infusion, IM inj and oral route.
Route of Administration:
Other
Clinically relevant ajmaline concentrations (1-3 uM) reduced peak I(Na) by approximately 5% but outward I(K) values were reduced by approximately 20% in amphibian skeletal muscle fibres. Peak-I(K) under maintained depolarisation was reduced to approximately 30% of control values by 100 uM ajmaline.