alinidine

{{Short description|Chemical compound}}

{{Drugbox

| Verifiedfields = changed

| verifiedrevid = 477317415

| IUPAC_name = N-(2,6-dichlorophenyl)-N-(prop-2-en-1-yl)-4,5-dihydro-1H-imidazol-2-amine

| image = Alinidine.svg

| tradename =

| pregnancy_category =

| legal_status = Uncontrolled

| routes_of_administration =

| bioavailability =

| metabolism =

| elimination_half-life =

| excretion =

| CAS_number_Ref = {{cascite|changed|??}}

| CAS_number = 33178-86-8

| ATC_prefix = none

| ATC_suffix =

| PubChem = 36354

| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}

| ChemSpiderID = 33429

| UNII_Ref = {{fdacite|correct|FDA}}

| UNII = E7IDJ8DS1D

| ChEMBL_Ref = {{ebicite|correct|EBI}}

| ChEMBL = 278581

| C=12 | H=13 | Cl=2 | N=3

| smiles = Clc2cccc(Cl)c2N(/C1=N/CCN1)C\C=C

| StdInChI_Ref = {{stdinchicite|correct|chemspider}}

| StdInChI = 1S/C12H13Cl2N3/c1-2-8-17(12-15-6-7-16-12)11-9(13)4-3-5-10(11)14/h2-5H,1,6-8H2,(H,15,16)

| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}

| StdInChIKey = OXTYVEUAQHPPMV-UHFFFAOYSA-N

}}

Alinidine (ST567) is a negative chronotrope that was developed in the 1970s and 1980s. It causes bradycardia by inhibiting the pacemaker current by altering the maximal channel conductance and alter the voltage threshold.Snyders DJ, Van Bogaert P-P: Alinidine modifies the pacemaker current in sheep Purkinje fibers. Pflügers Arch 1987, 410:83-91 The development of alinidine was halted because it was not sufficiently specific for its target. It also has a blocking effect on calcium channels and potassium channels. It also causes elongation of re-polarisation after an action potential.Current Opinion in Pharmacology 2007, 7:208–213

Alinidine did not improve outcomes among patients with acute myocardial infarction in a randomized controlled trial.{{cite journal|vauthors=Van de Werf F, Janssens L, Brzostek T, Mortelmans L, Wackers FJ, Willems GM | title=Short-term effects of early intravenous treatment with a beta-adrenergic blocking agent or a specific bradycardiac agent in patients with acute myocardial infarction receiving thrombolytic therapy. | journal=J Am Coll Cardiol | year= 1993 | volume= 22 | issue= 2 | pages= 407–16 | pmid=8335810 | doi=10.1016/0735-1097(93)90044-2|display-authors=etal| doi-access=free }}