Clinical Evidence Supporting the Role of Lonidamine for the Treatment of BPH

Rev Urol. 2005;7 Suppl 7(Suppl 7):S27-33.

Abstract

Glandular prostate epithelial cells of the peripheral zone are unique among normal cells in their dependence on glycolysis for energy production, due to a zinc-mediated enzymatic block in the citric acid cycle. Lonidamine (LND), a derivative of indazole-3-carboxylic acid, is thought to disrupt energy metabolism by interfering with glycolysis and to cause cell apoptosis. We evaluated the efficacy of oral LND treatment in subjects with symptomatic benign prostatic hyperplasia (BPH). The following reports the findings of an open-label study of orally administered LND. Thirty subjects with symptomatic BPH received oral LND (150 mg/day) once daily for 28 days. Subjects were assessed at baseline, at active-therapy assessment visits (days 14, 28), and 1, 2, 3, and 6 months post-therapy, for prostate volume (PV) by transrectal ultrasound (TRUS), maximum flow rate (Q(max)) on uroflowmetry, postvoid residual urine volume (PVR), International Prostate Symptom Score (IPSS), prostate-specific antigen (PSA) levels, serum chemistry, and adverse events.