Vamorolone – the first dissociative corticosteroid with mineralocorticoid antagonist activity in man: evidence from LIONHEART and VBP15-004 biomarkers


Topic:

Clinical Trials

Poster Number: LB439

Author(s):

Paula Clemens, MD, University of Pittsburgh, Ana de Vera, MD, Santhera, Utkarsh Dang, PhD, Carleton College, Catherine Dutreix, PharmD, Santhera, Ekaterina Gresko, PhD, Santhera, Michela Guglieri, MD, Newcastle University, Laura Hagerty, PhD, ReveraGen, Yetrib Hathout, PhD, Binghamton University, Karim Wahbi, MD/PhD, Hospital Cochin, Eric Hoffman, PhD, Binghamton University

Background: Mineralocorticoid receptor antagonists (MRA) (eg. Eplerenone) are used for managing DMD patients with cardiac dysfunction or fibrosis. Vamorolone, approved for treatment of DMD, has MRA activity in-vitro and in animal models. It remains unknown whether vamorolone is an MRA in humans.

Objective: To characterize MRA effect of vamorolone in healthy volunteers and establish biomarkers of MRA activity in DMD patients.

Methods: The LIONHEART study is a single dose, open-label, randomized, 3-arm, mechanistic trial to confirm the anti-aldosterone MRA activity of vamorolone assessed by changes in sodium to potassium (Na/K) ratio in urine after a fludrocortisone challenge in 30 male healthy volunteers. Subjects received vamorolone 20 mg/kg, or no drug, or eplerenone 200 mg as positive control. In addition, blood biomarkers for MRA activity from VBP15-004 pivotal trial in 4 to <7 yr DMD participants were analyzed. Results: In LIONHART, the log10 Na/K ratio by treatment arm showed both eplerenone and vamorolone to effectively reverse the decrease in Na/K ratio induced by fludrocortisone. There was no significant difference on urinary Na/K ratio between vamorolone and eplerenone at 4 to 6 hours post-dose, confirming MR antagonistic effect of vamorolone in humans. Vamorolone showed a significant natriuretic effect with no evidence of potassium retention. Both treatments were well tolerated. In DMD participants in the VBP15-004 registration trial, vamorolone at therapeutic dose (6 mg/kg) (but not prednisone) increased serum renin, calcium and phosphate, as well as the protein carriers of these inorganic ions (ASHG [Fetuin A], and Fetuin B), consistent with MR antagonism. Two serum proteins involved in inorganic ion signaling via FGF23 pathways were also increased by vamorolone (klotho, Anosmin-1), but not by prednisone. Conclusions: Taken together, these data confirm vamorolone as an MR antagonist with a potential reduced risk for clinically relevant hyperkalemia. Future research will evaluate its cardioprotective benefits in DMD.