Oral Nicotinamide Mononucleotide Increases Platelets in Refractory Immune Thrombocytopenia

Managing immune thrombocytopenia (ITP) often requires long-term, non-specific immunosuppression, forcing clinicians to balance therapeutic efficacy against the risk of opportunistic infections [1]. Recent evidence suggests that dysregulated homeostasis of nicotinamide adenine dinucleotide (NAD+, a coenzyme essential for cellular energy metabolism) is a common feature in several autoimmune conditions, driving aberrant immune cell activation [2, 3]. Specifically, the CD38 enzyme acts as a major consumer of NAD+, and its activity has been linked to the pro-inflammatory polarization of macrophages and the subsequent destruction of opsonized cells (platelets marked by antibodies for clearance) [1, 4]. While traditional therapies focus on depleting B cells or suppressing T cell responses, metabolic modulation offers a route to restore immune balance without compromising systemic host defenses [3]. In a recent phase 1/2 trial of 25 adults with steroid-refractory disease, low-dose oral nicotinamide mononucleotide (450 mg twice daily) induced a confirmed platelet response of at least 50 × 10⁹ per liter in 20% of participants within 14 days [5, 1]. These findings suggest that targeting the CD38-NAD+ axis provides a targeted metabolic strategy to manage antibody-mediated cytopenia while preserving stable immunoglobulin levels [5].