Activation of ATP-sensitive potassium channels triggers migraine attacks independent of calcitonin gene-related peptide receptors: a randomized placebo-controlled trial

Bianca Raffaelli, Thien Phu Do, Basit Ali Chaudhry, Faisal Mohammad Amin, Håkan Ashina, Josefin Snellman, Tina Maio-Twofoot, Messoud Ashina*

*Corresponding author for this work
1 Citation (Scopus)

Abstract

BACKGROUND: The present study aimed to investigate whether levcromakalim, a KATP channel opener, induces migraine attacks in people with migraine pre-treated with erenumab, a monoclonal CGRP receptor antibody.

METHODS: In this double-blind, placebo-controlled, two-way cross-over study, adults with migraine without aura received a subcutaneous injection of 140 mg of erenumab on day 1. Subsequently, they were randomized to receive a 20-minute infusion of 0.05 mg/ml levcromakalim or placebo on two experimental days separated by at least one week (between days 8 and 21). The primary endpoint was the difference in the incidence of migraine attacks between levcromakalim and placebo during the 12-hour post-infusion period.

RESULTS: In total, 16 participants completed the study. During the 12-hour observation period, 14 (88%) of 16 participants experienced migraine attacks after levcromakalim, compared to two (12%) after placebo (p < 0.001). The area under the curve for median headache intensity was greater after levcromakalim than placebo (p < 0.001). Levcromakalim elicited dilation of the superficial temporal artery during the first hour after infusion, a response absent following placebo (p < 0.001).

CONCLUSIONS: The induction of migraine attacks via opening of KATP channels appears independent of CGRP receptor activation.Trial Registration: ClinicalTrials.gov, Identifier NCT05889442.

Original languageEnglish
Article number3331024231222916
JournalCephalalgia : an international journal of headache
Volume44
Issue number1
ISSN0333-1024
DOIs
Publication statusPublished - Jan 2024

Keywords

  • CGRP
  • human models
  • KATP-channel
  • migraine
  • pathophysiology
  • trigeminovascular system

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