| Stereochemistry | ACHIRAL |
| Molecular Formula | C19H22ClN3O5S2 |
| Molecular Weight | 471.978 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CNC(=S)NS(=O)(=O)C1=CC(CCNC(=O)C2=CC(Cl)=CC=C2OC)=CC=C1OC
InChI
InChIKey=VXTKXGKPBOLHRY-UHFFFAOYSA-N
InChI=1S/C19H22ClN3O5S2/c1-21-19(29)23-30(25,26)17-10-12(4-6-16(17)28-3)8-9-22-18(24)14-11-13(20)5-7-15(14)27-2/h4-7,10-11H,8-9H2,1-3H3,(H,22,24)(H2,21,23,29)
The novel compounds clamikalant (HMR 1883) or its sodium salt HMR 1098) have been shown to block selectively Kir6.2/SUR1-composed K(ATP) channels. Clamikalant is under development by Aventis Pharma (formerly Hoechst Marion Roussel) for the potential treatment of heart arrest and ventricular arrhythmias. Nevertheless, clamikalant and its sodium salt did not pass the clinical trials
Originator
Approval Year
Overview
| CYP3A4 | CYP2C9 | CYP2D6 | hERG |
|---|---|---|---|
Drug as perpetrator
Drug as victim
Sourcing
PubMed
Patents
Sample Use Guides
HMR 1883 (Clamikalant) blocks KATPs in cardiac muscle cells with 10-50 fold higher potency than in pancreatic beta-cells and has little effect on the coronary vascular system. HMR 1883 has pharmacological selectivity for cardiac myocytes and thereby may be a promising substance for the prevention of ischemia-induced ventricular fibrillation. The rilmakalim-induced shortening of the APD90 in guinea pig right papillary muscle was antagonized half-maximally by HMR 1883 with 0.6 uM. The rilmakalim-induced shortening of the APD90 was half-maximally antagonized by HMR 1883 with 0.4 uM. The rilmakalim-induced whole-cell current (at 0 mV clamp-potential) was inhibited by HMR 1883 half-maximally 0.8 uM. Addition of HMR 1883 depolarized the cell potential half-maximally with concentrations of 20 uM.
ACTIVE MOIETY
SALT/SOLVATE (PARENT)
