ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2022 and some content may be unavailable. To unlock all content for 2022, please visit the archives.

Abstract: FR-PO142

FDA-Approved Drug Lasmiditan Promotes Mitochondrial Biogenesis and Accelerates Recovery of Renal Function After Ischemia/Reperfusion Injury

Session Information

  • AKI: Mechanisms - II
    November 04, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Hurtado, Kevin A., The University of Arizona College of Pharmacy, Tucson, Arizona, United States
  • Janda, Jaroslav, The University of Arizona College of Pharmacy, Tucson, Arizona, United States
  • Schnellmann, Rick G., The University of Arizona College of Pharmacy, Tucson, Arizona, United States

Acute kidney injury (AKI) is an abrupt loss of renal function that can result from sepsis, ischemia and toxicant induced injury. AKI incidence has become more prevalent in the last few decades and is linked with the progression into chronic kidney disease (CKD). Mitochondrial dysfunction is associated with development of AKI and mitochondrial biogenesis (MB) has been shown to recover mitochondrial homeostasis and promote recovery from AKI. We studied the effect of lasmiditan, a 5-HT1F receptor agonist that was previously shown to induce MB in-vitro and in-vivo, in a mouse model of AKI.


Electron microscopy was utilized to examine mitochondrial number and morphology 48 h after two daily lasmiditan treatments (0.3 mg/kg). Mice underwent ischemia/reperfusion (I/R) to induce AKI. After 24 h, serum creatinine was measured and I/R treated mice were divided into two groups and dosed with lasmiditan. Mice were treated daily for 144 h or 288 h and serum creatinine measured. KIM-1 and mitochondrial markers were measured using immunoblot analysis. Histopathology analyses were performed to measure tissue damage and fibrosis.


Lasmitidan treatment increased mitochondrial number in murine renal cortices. Serum creatinine levels where similar between the vehicle+I/R and lasmiditan+I/R groups at 24 h. At 144 h, serum creatinine was restored to sham levels in the lasmiditan+I/R group compared to vehicle+I/R group. KIM-1 protein decreased by half in the lasmiditan+I/R group compared with vehicle+I/R at 144 and 288 h. PGC-1α was restored to sham levels at 144 h and increased at 288 h in the lasmiditan+I/R group. Collagen-1 protein and interstitial fibrosis were decreased in the lasmiditan+I/R group at 288 h.


We demonstrate that the FDA approved drug lasmiditan stimulates MB and accelerates recovery of renal function after I/R and prevents interstitial fibrosis.


  • Veterans Affairs Support