FIRDAPSE IS THE FIRST FDA-APPROVED, EVIDENCE-BASED TREATMENT FOR PATIENTS WITH CANCER-ASSOCIATED LEMS SCLC1,7

FIRDAPSE is the first FDA-approved therapy that contains amifampridine, a voltage-gated potassium channel blocker targeting the presynaptic nerve terminal of neuromuscular junctions.2,22,23

FIRDAPSE works by blocking potassium channels on the presynaptic nerve terminal that cause action potential termination. This results in sustained calcium influx and increased ACh release at the neuromuscular junction.1,2,23,24

FIRDAPSE has been tested in >70 clinical and nonclinical studies, including 2 positive phase 3 studies, over a period of 9 years.1-3,24

FIRDAPSE demonstrated clinically meaningful muscle strength preservation and patient satisfaction in clinical trials.1-3

patients in the United States are living with the challenges of LEMS24

patients have put their lives back in motion with FIRDAPSE24

The mechanism by which FIRDAPSE exerts its therapeutic effect in patients with LEMS has not been fully elucidated.1

FIRDAPSE is a broad-spectrum potassium channel blocker.1

Watch the full MOA animation video to better understand normal neuromuscular transmission, how LEMS disrupts this process, and how FIRDAPSE helps restore it.

  • Anti-VGCC antibodies target voltage-gated calcium channels on the presynaptic motor neuron in those with LEMS, reducing calcium influx during an action potential9
  • FIRDAPSE blocks presynaptic voltage-gated potassium channels that open and help terminate the action potential, resulting in prolonged calcium influx2,23,25,26
  • As influx of calcium increases, it allows for more ACh transmission across the neuromuscular junction2,23,25,26
  • Muscle contraction and muscle strength are restored with increased ACh signaling23