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. Author manuscript; available in PMC: 2021 Jan 1.
Published in final edited form as: Curr Mol Med. 2020;20(4):259–274. doi: 10.2174/1566524019666191028122559

Table 2.

KOP blockers and activator.

Synthetic molecules KOP Tissue Effect Ref.
Agonists U50488H Selective Heart Activate Na+-H+ exchanger via PKC activation
Reduces oxidative stress
[36] [43]
Spiradoline (U-62066) Highly selective Cerebral ventricle Protects from epinephrine-induced arrhythmias [117]
Antagonists MR2266 Non-selective Myocardium Reduced severity of I/R induced arrhythmia
Reduced infarct size
Enhanced coronary blood
[112]
Nor-BNI Selective Intrathecal administration Lateral cerebral ventricle Heart Reduces the pressor actions of Dyn A administration
Inhibitory effect on Ang II induced increases in HR and BP via CNS-mediated mechanisms
Reduces isoprenaline-induced cardiac hypertrophy and fibrosis
[142]
[75]
[42]

Ang II; angiotensin II, I/R; ischemia/reperfusion, Nor-BNI; Norbinaltorphimine (nor-BNI; 17,17′-Bis (cyclopropylethyl)-6,6′,7,7′-tetradehydro-4,5:4′,5′- diepoxy-6,6′- (imino)[7,7′-bimorphinan]-3,3′,14,14′-tetrol), PKC; protein kinase C