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KN-92 is an inactive analog of KN-93. KN-93 is the CaM kinase II inhibitor. [1]

Hearts were treated with the CaM kinase inhibitor KN-93 or the inactive analog KN-92 (0.5 μM) for 10 min before clofilium exposure. Early afterdepolarizations (EADs) were largely inhibited by KN-93 contrasted to KN-92. There were little differences in parameters favoring EADs such as monophasic action potential duration or heart rate in KN-92- or KN-93- treated hearts. CaM kinase activity in situ increased 37% in hearts with EADs compared to hearts without EADs. This increase in CaM kinase activity was prevented by pretreatment with KN-93. [1]

In vitro, KN-93 potently suppressed rabbit myocardial CaM kinase activity (calculated Ki ≤ 2.58 μM), but the inactive analog KN-92 did not (Ki > 100 μM). The actions of KN-93 and KN-92 on ICa and other repolarizing K+currents did not illustrate preferential EAD suppression by KN-93. [1]

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