News|Articles|May 4, 2026

Ersodetug misses primary endpoint in phase 3 sunRIZE trial for congenital hyperinsulinism

Phase 3 sunRIZE trial of ersodetug in congenital hyperinsulinism missed its primary endpoint but showed CGM-based glycemic gains.

Expanded analyses from the phase 3 sunRIZE trial of ersodetug (Rezolute, Inc.) in patients with congenital hyperinsulinism (HI) demonstrate consistent improvements in glycemic control across multiple continuous glucose monitoring (CGM)–based endpoints compared with placebo, according to data presented at the Pediatric Endocrine Society (PES) 2026 Annual Meeting.¹

The findings come despite the trial's failure to meet its primary endpoint, raising questions about the path forward for this first-in-class therapy in a disease with limited treatment options.

Key facts

  • Drug: Ersodetug (monoclonal antibody)
  • Class: Allosteric insulin receptor antagonist
  • Indication: Congenital hyperinsulinism
  • Trial: sunRIZE (RZ358-301), phase 3
  • Primary endpoint: Not met (SMBG-based)
  • CGM outcomes: Nominally significant improvements
  • OLE retention: 57 of 59 completers ongoing
  • FDA status: Data submission requested
  • Geography: Multinational (12+ countries)

"These results underscore our confidence in the potential of ersodetug to transform the HI treatment landscape and embolden our mission to achieve alignment with FDA on an acceptable path to approval in this indication, so that we can keep delivering ersodetug to patients and families living with congenital HI," said Brian Roberts, MD, chief medical officer of Rezolute.

The sunRIZE study (RZ358-301) was a multicenter, randomized, double-blind, placebo-controlled, parallel-arm trial enrolling 63 participants aged 3 months to 45 years across more than a dozen countries.¹ Patients with congenital HI who continued to experience hypoglycemia on standard of care (SOC) were randomized to receive ersodetug at 5 or 10 mg/kg or matched placebo, administered as add-on therapy. Dosing occurred every other week during a loading phase and then every 4 weeks during a 6-month controlled treatment period.

The primary endpoint—change from baseline in average weekly hypoglycemia events measured by self-monitored blood glucose (SMBG) — was not met. Rezolute attributed this failure to functional unblinding of the SMBG endpoint, which the company believes led to divergent glucose-modifying behaviors between treatment groups and a pronounced placebo effect.

However, the expanded analyses presented at PES focused on CGM-based outcomes, which showed nominally statistically significant improvements across multiple timepoints. In the full analysis set (FAS), ersodetug-treated patients demonstrated reductions of greater than 50% in average daily percent time in hypoglycemia compared with placebo. In the per-protocol set (PPS), these reductions ranged from approximately 60% to 80%. Average weekly hypoglycemia events by CGM were reduced by approximately 50% to 65% in the FAS and 50% to 80% in the PPS. Additionally, exposure to normoglycemia (area under the curve for blood glucose 70-180 mg/dL) increased by approximately 25% to 50%, and average blood glucose levels rose by approximately 10 to 15 mg/dL compared with placebo.¹

The secondary endpoint of percent time in hypoglycemia by CGM did not achieve statistical significance at the prespecified Week 24/end-of-treatment evaluation window. Notably, however, the company reported that larger glycemic improvements were observed during other periods of the maintenance dosing phase.

All 59 study completers elected to enter the open-label extension (OLE), with 57 participants continuing in active follow-up. Cumulative ersodetug exposure now ranges from approximately 6 to 24 months. Preliminary OLE observations suggest continued glycemic benefit, including clinically significant improvements among former placebo participants after crossover. The company also reported a significant overall reduction in background SOC therapies—including diazoxide, somatostatin analogs, and regular tube feeds—with a notable number of patients transitioning to ersodetug monotherapy.

Congenital HI is a rare genetic disorder characterized by excessive insulin secretion, leading to recurrent and potentially severe hypoglycemia. Current treatment options are limited and often inadequate, with diazoxide serving as first-line therapy but proving ineffective in a substantial proportion of patients, particularly those with diffuse forms of the disease.² Surgical pancreatectomy remains a last resort but carries significant morbidity, including the risk of insulin-dependent diabetes.²

Ersodetug is a fully human monoclonal antibody that binds allosterically to the insulin receptor, reducing receptor overactivation by insulin and related substances such as IGF-2. Because it acts downstream from the pancreas, ersodetug has potential applicability across all genetic subtypes of congenital HI.¹

The regulatory path for ersodetug remains uncertain. During a Type B meeting held on March 17, 2026, the FDA acknowledged challenges associated with the SMBG-based primary endpoint and requested that Rezolute submit the broader study data for comprehensive evaluation.¹ This represents a critical juncture: the agency has not yet committed to an alternative approval pathway based on CGM data alone.

Clinicians should note that the CGM-based improvements reported were largely derived from pre-specified secondary and post-hoc analyses, which carry inherent limitations in statistical rigor.¹

References
  1. Rezolute, Inc. Rezolute announces oral presentation of results from its phase 3 sunRIZE study of ersodetug in patients with congenital hyperinsulinism at the Pediatric Endocrine Society Annual Meeting. Press release. May 1, 2026. Accessed May 1, 2026. https://www.globenewswire.com/news-release/2026/05/01/3286124/0/en/rezolute-announces-oral-presentation-of-results-from-its-phase-3-sunrize-study-of-ersodetug-in-patients-with-congenital-hyperinsulinism-at-the-pediatric-endocrine-society-annual-me.html
  2. Banerjee I, Salomon-Estebanez M, Shah P, Nicholson J, Cosgrove KE, Dunne MJ. Therapies and outcomes of congenital hyperinsulinism-induced hypoglycaemia. Diabet Med. 2019;36(1):9-21. doi:10.1111/dme.13823
  3. De León DD, Stanley CA. Congenital hypoglycemia disorders: new aspects of etiology, diagnosis, treatment and outcomes. Pediatr Diabetes. 2017;18(8):633-642. doi:10.1111/pedi.12580