Novel nonpeptide agents potently block the C-type inactivated conformation of Kv1.3 and suppress T cell activation

Mol Pharmacol. 1996 Dec;50(6):1672-9.

Abstract

The nonpeptide agent CP-339,818 (1-benzyl-4-pentylimino-1,4-dihydroquinoline) and two analogs (CP-393,223 and CP-394,322) that differ only with respect to the type of substituent at the N1 position, potently blocked the Kv1.3 channel in T lymphocytes. A fourth compound (CP-393,224), which has a smaller and less-lipophilic group at N1, was 100-200-fold less potent, suggesting that a large lipophilic group at this position is necessary for drug activity. CP-339,818 blocked Kv1.3 from the outside with a IC50 value of approximately 200 nM and 1:1 stoichiometry and competitively inhibited 125I-charybdotoxin from binding to the external vestibule of Kv1.3. This drug inhibited Kv1.3 in a use-dependent manner by preferentially blocking the C-type inactivated state of the channel. CP-339,818 was a significantly less potent blocker of Kv1.1, Kv1.2, Kv1.5, Kv1.6, Kv3.1-4, and Kv4.2; the only exception was Kv1.4, a cardiac and neuronal A-type K+ channel. CP-339,818 had no effect on two other T cell channels (I(CRAC) and intermediate-conductance K(Ca)) implicated in T cell mitogenesis. This drug suppresses human T cell activation, suggesting that blockade of Kv1.3 alone is sufficient to inhibit this process.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • HeLa Cells
  • Humans
  • Lymphocyte Activation / drug effects*
  • Mutation
  • Potassium Channel Blockers*
  • Potassium Channels / chemistry
  • Protein Conformation
  • Shal Potassium Channels
  • T-Lymphocytes / drug effects*
  • T-Lymphocytes / immunology

Substances

  • KCND2 protein, human
  • Potassium Channel Blockers
  • Potassium Channels
  • Shal Potassium Channels